Samantha Shaves ‘Shiny Bald’ for ACRF

My name is Samantha and I’m 20 years old. I love acting, dancing and adventures. I have a big heart and always see the best in people. I’m always supported by friends and family. Life to me is a story and I’m trying to write a great one if I help people along the way I couldn’t be happier. I started striking up the conversation with people and found that everyone is guaranteed to know someone who has been affected by cancer, whether that be through work, family, friends or simply someone serving you at a store.

I chose to fundraise for the ACRF because it supports research into all forms of cancer. It was hard for me to pick just one with so many organisations out there. I know this will touch people’s hearts because it relates to everyone.

I chose to shave because I wanted to make a big impact. I thought “what can I do to make a difference?” So, I went all out and I was determined to go shiny bald if I raised my goal of $700. I wanted to prove that no amount of hair means more to me than this. I was ready for a close shave, a fresh start and to bring hope to everyone.

At least I had a choice to shave my hair where imagine having no choice and losing it. The statistics are so high that there is a chance I may have cancer throughout my lifetime, the same with everybody. Now if it happens to me in the future, I already know what it’s like to have no hair.

The impact of cancer motivated me to act because they are so staggering. In 2019 there is estimated to be 144,713 new cancer cases diagnosed.
If you’re thinking about fundraising for ACRF and cancer research, ‘think’ no longer. Actions speak louder than words. We are all human and we have passions and the ability to care about important matters involving each other. Whether it’s colouring your hair, shaving, donating or volunteering, it’s as simple as that. You can do it.

My goal was $700 and I raised that in just 3 days. By the fourth day, I had reached $1000, my mind was blown. Before my big shave, I had raised $3000 by word of mouth and sharing on social media. I had collaborated with my local Bracken Ridge Tavern. They were on board, especially because their staff member is currently going through breast cancer.

I gathered more than 80 people to this event and held raffles, it was spectacular.
It was an emotional night, I had people come up to me and tell me their cancer stories, some currently happening,

I cried four times before I even shaved my head. I had three extra shavers, including my dad, who surprised me and made me cry. The gaming bar manager also shaved her head for the breast cancer lady on a bid that raised $1,121 in 10 mins.

I have currently $7,150 well more than my original goal and my heart is full of love and support. I feel liberated with my bald head and my hair is growing exceptionally fast but this will be something I will remember for the rest of my life.

Feeling inspired by Samantha’s bravery and ready to raise life-saving funds for cancer research? Find out more about fundraising for ACRF here.

New Cancer Laboratory Launches

The ACRF Tumour Metabolism Laboratory – part of the ACRF Centenary Cancer Research Centre – has been officially launched with the laboratory sporting the latest in advanced equipment and technology to help support the innovative cancer research. Cancer is the second leading cause of death globally.


The laboratory, established by a $2.5M grant from Australian Cancer Research Foundation (ACRF) and in collaboration with the Centenary Institute, is dedicated to the study of tumour cell metabolism, at a molecular level. The team then utilise this knowledge to develop new cancer diagnostics, treatments and cures.

“Cancer cells, like all the cells in our body, require nutrients from our diet to survive and to flourish,” says Professor Philip Hogg, Deputy Director, Centenary Institute and Head, ACRF Centenary Cancer Research Centre.


“While our healthy cells mostly produce energy from these nutrients, cancer cells use them to suit their malignant purpose – which is to divide as rapidly as they can. They aggressively soak up the nutrients in their environment and convert them into the components of new cancer cells – that is DNA, protein and lipids. The focus of this laboratory is to understand how cancer cells change their metabolism. If we can successfully stop the cancer cells from changing their metabolism then we can use this knowledge as a basis for developing exciting new anti-cancer therapies.”
The state-of-the-art equipment now available to the researchers at the ACRF Tumour Metabolism Laboratory allows for the precise measurement – down to the nanoscale – of the sugars, proteins and lipids that are consumed by the cancer cells.


“Our equipment enables our scientists to remain at the forefront of research in the cancer metabolism field. We have mass spectrometers to measure glucose and lipid metabolites in tumour cells, a specialised microscope to measure glucose metabolism in tumour infiltrating T cells, a live-cell platform for measurement of tumour cell metabolism as well as a hi-tech instrument to measure protein-drug interactions,” says Professor Hogg.


The team of researchers at the ACRF Tumour Metabolism Laboratory have an impressive history of success as well as proven experience in developing potential new therapeutics that have been tested in cancer patients in Australia and the United Kingdom.

“We have gathered a committed team of first-rate cancer scientists who will make discoveries that will that will benefit our children and our children’s children,” says Professor Hogg.

“ACRF is delighted to have backed this program which will return significant research findings. Our support, through the provision of equipment for the research, has been supplemented by a collaborative funding arrangement with Cancer Institute NSW who have assisted with complementary funding for research personnel. We so value the work that Professor Hogg and his team do to help deliver our supporters’ ambition to Outsmart Cancer,” says Kerry Strydom, CEO, Australian Cancer Research Foundation.

QIMR Berghofer Scientists find new Immunotherapy has Promise

Queensland scientists from QIMR Bergfoher are helping to speed up the development of a new type of immunotherapy by discovering how it activates the immune system to fight cancer.

It’s hoped the antibody therapy – which entered phase I clinical trials in the United States in early 2019 – could in future treat a broad range of cancers.

The head of QIMR Berghofer’s Immunology Department, Professor Mark Smyth, and his colleagues have been testing the antibody, which was developed by US company Tizona Therapeutics.

The findings have been published today in the journal Cancer Discovery, a publication of the American Association for Cancer Research.

“This antibody is designed to block the activity of an enzyme called CD39, which sits on the surface of harmful inflammatory cells,” Professor Smyth said.

“Blocking CD39 with the antibody releases an extracellular chemical signal called ATP.

“In laboratory tests, we’ve shown that this sets off a chain of events that ultimately kills the cancer-promoting inflammatory cells and releases proteins – called cytokines – that help immune cells called T cells fight the cancer.

“In other words, the antibody eliminates some of the enemy soldiers and helps to rally the immune system’s own troops.

“We’ve shown that this is a new way we can target the immune system to fight cancer.”

It was already known that CD39 is the first enzyme in a cascade chain reaction that converts ATP into adenosine, a cancer-promoting and immune suppressing metabolite.

“In this study, we have shown in laboratory tests that inhibiting CD39 with an antibody helps to fight cancer, not just by stopping the generation of adenosine, but also through the immune-activating functions of extracellular ATP,” Professor Smyth said.

“Importantly, our laboratory tests have also shown that it works well in combination with existing immunotherapies.”

The team’s findings will help to guide the design of future clinical trials of antibodies targeting CD39.

The study was primarily funded by the National Health and Medical Research Council of Australia, the Melanoma Research Alliance and Tizona Therapeutics Incorporated.

This article originally appeared on the QIMR Berghofer website. Australian Cancer Research Foundation has provided three grants for cutting-edge technology to facilitate cancer research, totalling $7.05 million.

Penrith Anglican College supports cutting-edge cancer research

Penrith Anglican College is a Pre-K- 12 school located in Orchard Hills. We believe Service and Community Engagement are vital in developing students to be well-rounded people.

ACRF is close to our heart as many of our students have been affected by the devastating impact of cancer. Year 10 chooses a charity to fundraise for each year. Students nominate a range of charities and voted for the cause they would most like to support, and this year chose to fundraise for Australian Cancer Research Foundation.

Students completed a range of fundraising activities from February – August raising $6000 for ACRF. We held a bake sale, movie and pizza nights, a mufti day, sausage sizzle and breakfast. It turns out teenagers like fundraising with food! Thank you to our school community, especially our parents, for supporting our efforts. The efforts culminated in a Charity Ball, which was a great evening. Our students loved the opportunity to dress up and celebrate the achievements of our fundraising

We want to see a world where no family has to endure the devastating impact cancer has. Research is key to finding a cure, and in the future, preventing cancer. That’s why we support ACRF.

ACRF have been great to work with and a worthwhile cause. ACRF are quite stringent in the way they allocate funds, so we are confident that all our funds raised will be making a direct impact.

We would also like to also say thanks to Signwave for their support in printing our giant cheque.

The Annual Gala Ball to help Outsmart Cancer

It’s going to take all of us to outsmart cancer. This is something that ACRF supporter Thu Thao Le puts into action, and for the second time, she has organised an annual gala dinner to raise funds for cutting-edge cancer research. We’re so thankful for her dedicated support.

On October 11, at Crystal Palace in Canley Heights, the Vietnamese community came together for an evening of entertainment, food and music. A record-breaking 620 guests attended the event.

With different performances including a Lion Dance, and different individual singing acts, the night was a fun-filled and memorable one.

The community gathered together to offer their support for cancer research, and we would like to thank the generous supporters, donors and sponsors, who contributed to make the evening such a successful evening for all.

Many thanks to IGA Dulwich Hill, Home Caring, Maoine Skincare and Vuly Play Trampolines, the sponsors for the evening, and to the MC, Thu Thao Luu and Ms Thu Thao Le.

‘Let’s Beat the Bastard’: the ride to Outsmart Cancer

Wayne is a dedicated ACRF supporter who continually goes above and beyond to support cancer research. His annual event, ‘Beat the Bastard’, is a 400km motorbike route that spans north-eastern NSW, this year travelling through Gunnedah, Bendemeer, Walcha, Uralla, and Manilla.  

Like many of us, Wayne has been touched on a personal level. He shares the reason is so passionate about supporting Australian Cancer Research Foundation below.

“Even after losing my sister, brother in-law, and countless close friends and acquaintances, I really didn’t realise how horrible cancer is, mainly because of the distance we lived apart and the fact I didn’t get to see them in their final months.

Then in 2013 my brother Dale was diagnosed with cancer. Over the course of two years, he underwent major surgery, skin graphs and radiation. He never gave up and was determined to beat the bastard.

Over this time, I witnessed just how destructive and devastating cancer can be.

In early September 2016, Dale told me ‘I think the bastard has me this time mate’. Three weeks later we lost him and over the next couple of months, I found myself in a very dark place, alienating myself from my family and friends, sitting for hours in a haze and each day becoming angrier and angrier knowing this bastard had taken my best mate. To help me with my grief and to be honest out of self-pity, I came up with the ‘Let’s Beat the Bastard’ ride. But after the ride started to gain pace, I realised I wasn’t alone, and I most certainly was not the only person in this situation.

I have been absolutely humbled by the response to the ride and have met some extraordinary people, some who are fighting the fight, some who have won the fight and those whose family or friends have lost the fight.

I am so proud to be a part of this event and urge everyone to get involved and help to raise funds so we can finally beat the bastard!”

A lotto I didn’t want to win’: Sydney mum’s story of breast cancer, chemo and recovery

Photo: Amelia Bromley
Photo: Amelia Bromley 

This article originally appeared on Essential Baby in support of our Women’s Appeal for 2019. To show your support for women like Amelia, donate here.

When Sydney mum Amelia Bromley discovered she was pregnant with her second baby she was ecstatic. After a dream pregnancy with her first son Toby, she and her husband, Justin, were thrilled to be adding to their family. “I was loving being a mum,” Ms Bromley tells Essential Baby.

The happy news continued – Ms Bromley soon learnt that her best friend was also pregnant with her second bub. But though their babies were due just a week apart, their symptoms were very different. While her friend complained of sore breasts, Ms Bromley wasn’t experiencing any soreness at all.

And it left her wondering why. 

Photo: Amelia Bromley
Photo: Amelia Bromley 

Later that evening, while examining her breasts, Ms Bromley found a lump. “It was like a little ball bearing,” she recalls. Thinking it was simply mastitis, a condition she’d experienced before, the 36-year-old expected to be given a script for antibiotics. Instead, her doctor sent her for an ultrasound and a biopsy.

The results came as a shock.

“I was so unconcerned that I’d booked Toby in for his 12-month vaccinations,” Ms Bromley says of the day she was told she had cancer – a type called HER2-positive.

She was seven weeks pregnant. 

“The chances of getting breast cancer under 40 are so slim,” she says. “And the chances of getting breast cancer while you’re pregnant are so slim. It’s a weird version of a lotto I didn’t want to win.”

But while the mum was told by her doctors that treating cancer during pregnancy would be “trickier”, choosing not to have her baby was never an option.

“I said to the doctor, ‘If you’re telling me that I need to make a choice between being pregnant and being treated … do I have to make that choice? Can I have both? Until you tell me I can’t, we’ll take the trickier road.”

Taking the “tricker” road saw Ms Bromley book an emergency appointment with her obstetrician. “I needed someone to make sure my baby was okay,” she says, adding that she had a team of amazing doctors looking after her, but needed someone focusing on her growing bub. “I said to her, ‘I need to know you’ll go into bat for the baby when things get tough.'”

While nine weeks pregnant, Ms Bromley underwent a lumpectomy. “I remember saying to my husband, ‘I’m not going to feel this good for a while,” she recalls. 

What followed was a gruelling course of chemotherapy, which began when she entered her second trimester. “I spoke in detail to both doctors about whether it was safe and I was assured that the placental barrier is stronger than the barrier between the brain and the body, so none of the chemo drugs would get through to the baby.”

Despite this reassurance, however, Ms Bromley says she still found herself worrying about whether the treatment would affect her baby. “Sometimes, I still think, Is that because of the chemo? It’s definitely something that plays a bit of havoc with you, especially while you’re pregnant.”

With her husband often travelling for work, Ms Bromley says she was fortunate to have a network of supportive friends who helped her parent her toddler and care for her two-stepchildren while undergoing treatment. She was also buoyed by the regular scans she saw of her baby. “I think I had more scans than anyone has ever had,” Ms Bromley laughs, explaining that hearing her baby’s heartbeat and seeing her moving, helped her feel “like a pregnant woman and not a cancer mum.”

Baby Beatrice, ‘Bea’ was born on 10 October, 2013 at 33-and-a-half weeks  “She was 10/10,” the proud mum laughs.

 A day after welcoming her daughter, Ms Bromley began radiation – in the same hospital.  “I went from maternity on level three down to the basement,” she says. And, in the blur of those first few days, recovering from a c-section and undergoing radiation – a process she describes as “soul-destroying”, the mum says the baby blues hit – hard.

“I felt guilty,” she says. “It was unexpected. I thought, why am I so upset when I’ve got this baby? But I couldn’t stop crying.”

After four weeks of radiation, five days a week, her treatment was over. 

“You’re not supposed to be sick any more,” Ms Bromley says. “Everyone says, ‘well you should be back to normal’. But in reality it takes a really long time to feel normal again.”

Reaching the five-year milestone last year was a turning point for the executive producer who says it’s only now that she feels comfortable talking about her experience and saying, “I had cancer.” But while “life goes on,” Ms Bromley admits that “it’s always there in the background”.

“I always fear [the cancer] coming back,” she says. “I live with the fear of it returning.” The fear however, is tempered by the knowledge that treatments for cancer are evolving at a rapid rate. “If it was to happen again, the chances are better,” she says. “There are things available now, that weren’t available even for me five years ago. ” 

Photo: Amelia Bromley

Ms Bromley says she’s found strength in sharing her story – and hopes people see it as an uplifting one. “Cancer rates are going up,” she says. “We have to talk about it. If we don’t, we won’t fight it. When it comes to funding it comes down to public awareness.”

And she’s fiercely proud of her family.

“We’ve got through the worst of it,” she continues. “Look at us! Bea started school and she’s doing really well… I want other people to know how fortunate we are to live in a time where you can have horrible things happen and go on to live full, happy, amazing and incredibly ordinary lives.”

Philippa’s Moreton Island Adventure

“My name is Philippa, I am 58 years old and work as a teacher aide at Brisbane School of Distance Education.

When I first planned to do the Moreton Island Walk, an 80km journey circumnavigating Moreton Island in Queensland, it was with a friend for fun. But when we realised it was quite a challenge, we decided it would be something that would be fun to do as a group and that the charity was something that would be well supported.

I gathered a team, and we set off. All the team had lost loved ones to different types of cancer, so supporting ACRF felt very personal. We couldn’t decide which branch of cancer research to raise money for, so decided ACRF was a good compromise as they support research into all types of cancer.

It’s a very rewarding accomplishment to feel that you have made a difference, while doing something that is challenging. But nothing feels like the challenges faced by people with cancer.

We all felt the walk was the hardest thing we had ever done.  We were all proud of our achievements.  I was particularly proud of my two daughters who completed the walk with me. Having done this walk and raised what we considered a significant amount of money we would like to make the walk an annual event and involve more people.”

Feeling inspired and ready to help outsmart cancer? Find out more about fundraising for Australian Cancer Research Foundation here.

Jeremy shaves for ACRF

“My name is Jeremy. I’m a 45-year-old father of two boys, and husband to Tonia. I work in the state head office of Australia Post and coach my youngest son’s soccer team.

Originally, I was just going to shave my head to offer my wife Tonia some moral support as she lost her hair through chemo. She suggested I see if I can use the opportunity to raise some money for cancer research, and I decided to give it a go.

I have a history with cancer, losing my father to pancreatic cancer when I was 19 and my eldest big sister to breast cancer when I was 31.

My other big sister has been fighting breast cancer for nearly ten years and my wife is just starting out on her battle with breast cancer. I myself am a cancer survivor, having had successful treatment for bladder cancer two years ago.

Cancer research provides help not only for my family, but all those affected by cancer. It is such a worthwhile cause and that’s why I chose to fundraise for ACRF by shaving my head.”

Feeling inspired by Jeremy’s bravery and ready to help outsmart cancer? Find out more about hosting a headshave for ACRF here.

Stopping healthy cells from self-destructing

Australian scientists have developed a world-first compound that keeps cells alive and functioning when they otherwise would have died.

The idea that our cells are set to ‘self-destruct’ is not entirely comforting.

But like all things, it is a question of balance.

Known as apoptosis, this process of programmed cell death is essential for keeping the body healthy; it’s triggered when cells are aged and diseased as well as during development.

Programmed cell death is essential for keeping the body healthy, too little can result in cancer. Picture: Getty Images

In the womb, our hands begin as mittens, so apoptosis directs cells between the fingers to die off, thereby forming our digits.

Fast-growing cells like our skin and gut-lining, which also faces strong digestive acids, are replaced most often. The average adult human loses between 50 and 70 billion cells each day due to apoptosis.

Because programmed cell death is irreversible once it has begun, apoptosis is tightly regulated by the body, and this regulation has been the focus of much research as its implicated in the progression of many diseases.

Excessive apoptosis can cause tissues to waste away or atrophy in conditions like muscular dystrophy, whereas an insufficient amount can lead to uncontrolled cell proliferation or growth, resulting in cancer.

Some proteins known as caspases get switched on to promote apoptosis, but this pivotal step is controlled by members of the BCL-2 protein family.

This family of proteins has been the focus of 11 years of collaborative research at the Walter and Eliza Hall Institute of Medical Research, led by Professor David Huang, Professor Guillaume Lessene and Professor Benjamin Kile (now at Monash University).

The team has recently published preclinical findings in the journal Nature Chemical Biology, highlighting their discovery of a unique compound that can keep cells alive and functioning when they otherwise would have died.

Stopping unwanted cell death would be revolutionary in medicine, such as minimising cellular damage after heart attacks. Picture: Getty Images

The point of no return

Within the BCL-2 family of proteins some promote cell survival, while others drive cell death.

Proteins called BAK and BAX are involved in a critical step of cell death known as the ‘point of no return’ because cells are committed to die once either BAK or BAX is activated.

So, key to the team’s research was understanding how to block BAK activation.

They screened an assembled collection of 250,000 potential small drug molecules for ones that blocked apoptosis.

“Our experiment pushed the cells right to the brink of death and looked for compounds that rescued it,” Professor Lessene explains.

“What we found was that when a compound we named WEHI-9625 binds to the protein VDAC2 in the apoptosis pathway, then BAK can no longer trigger cell death,” he says.

“It’s a bit like a when a person under arrest is handcuffed to a police officer, they are unable to run away or do anything much at all.”

The compound WEHI-9625 is now considered a proof-of-concept drug, and the next step for the team is to understand how it interacts with VDAC2 and BAK at a molecular level.

When compound WEHI-9625 binds to the protein VDAC2 in the apoptosis pathway, then BAK can no longer trigger cell death. Picture: WEHI

Intervening before it’s too late

The finding could give clinicians the ability to intervene and prevent cell death, says Professor Lessene.

The new ‘cell death blocker’ is revolutionary in its ability to keep cells alive and healthy in the laboratory, he says.

“This would be game-changing for medical emergencies and procedures, such as minimising cellular damage after heart attacks, or preserving organs for transplants.”

Professor Kile, Head of Anatomy and Developmental Biology at the Monash Biomedicine Discovery Institute, says that WEHI-9625 is the first compound identified to successfully override apoptosis and keep cells functioning.”

“We have shown it is possible to halt the biochemical cascade that triggers cell death, right at the point where it begins”.

Invaluable for future of medicine

Professor Huang, a laboratory head in the Institute’s Blood Cells and Blood Cancers division, adds that the ability to stop unwanted cell death could be invaluable for the future of medical care.

“Acute injury can cause cells to die rapidly leading to the loss and weakening of tissues and muscles. In such circumstances, being able to prevent uncontrolled cell death could improve a patient’s recovery, or even their chances of survival,” he says.

The pivotal step that begins apoptosis is controlled by members of the BCL-2 protein family. Picture: Ms. Etsuko Uno, WEHI

“The Institute’s research into cell death spans more than 30 years, beginning with the landmark discovery in the late 1980s that the protein BCL-2 could enable prolonged cancer cell survival. This critical discovery helped to inform the development of an anti-cancer treatment for patients with leukaemia.”

“Our latest research shines light on ‘the other side of the same coin’, offering hope that one day drugs that successfully intervene to block apoptosis could be used to treat conditions such as cardiovascular diseases and degenerative disorders.”

The researchers are now looking to apply the knowledge to developing cell death blockers that are effective and safe in humans.

Professor Huang says the next steps would also involve applying the knowledge to more advanced models of disease.

“There could be applications for keeping cells alive to prevent degenerative diseases,” he says.

The research was supported by the Australian Cancer Research Foundation, Australian National Health and Medical Research Council, Brownless Trust, DHB Foundation, HEARing CRC, MuriGen Therapeutics, Sylvia and Charles Viertel Foundation and the Victorian Government.

This article was written by By Dr Nerissa Hannink, University of Melbourne and originally appeared here.

Tassie Devils Hold Clue for How Human Cancers Evade the Immune System

Melbourne researchers from Peter Mac, in collaboration with Cancer Research UK, have uncovered a new way that some human cancers can hide from the body’s immune system, a feature they share with tumours from an unlikely source – the Tasmanian devil.

In this new study just published in the journal Cancer Cell, scientists discovered that some human, mouse and Tasmanian devil cancers can reduce the amount of immune-stimulating MHC Class I (MHC-I) proteins present on their surface, effectively masking them from being recognised and destroyed by killer immune cells.

“By avoiding recognition by immune cells, some cancers can continue to grow unchecked and are less likely to respond to new types of immune-based cancer therapies,” says Dr Marian Burr, who began this research at the University of Cambridge, UK, and completed it at Peter Mac.

“Identifying how and why some tumours undergo this process of hiding from the immune system may help to improve treatment outcomes.”

Peter Mac's Dr Marian Burr
Peter Mac’s Dr Marian Burr

Whether or not MHC-I appears on the cell surface can depend on the activity of other proteins inside the cell. By systematically knocking out all the genes in the human genome using cutting-edge CRISPR-Cas9 technology, the researchers looked for clues as to which proteins were important in controlling MHC-I at the surface.

They found that a group of proteins that collectively form an epigenetic protein complex – known as PRC2 – acts inside the cell to switch off the genes required for MHC-I production.

When they looked in human cancers such as lung cancer, neuroblastoma and Merkel Cell Cancer they found that tumours with high levels of PRC2 proteins had reduced MHC-I and this was associated with an impaired ability of tumour-killing immune cells to recognise these cancers.

What was especially surprising is that they found the exact same process also occurs in mouse models of lung cancer and in Tasmanian devil facial tumours, a deadly cancer of the mouth and face that has decimated the wild Tasmanian devil population.

“Similar to some human cancers, a defining feature of Tasmanian devil facial tumours is a remarkable ability to evade recognition and destruction by the immune system,” says Dr Burr who was lead author on the study.

“This feature of devil facial tumours, and some human cancers, is a powerful mechanism of immune evasion that is conserved in different species throughout the process of evolution.”

When the researchers used targeted drugs to effectively shut down the PRC2 pathway in a mouse model of small cell lung cancer, they found they could re-establish MHC-I expression which led to more effective immune-mediated tumour cell killing.

Professor Mark Dawson, Consultant Haematologist and head of the Cancer Epigenetics group at Peter Mac, said this discovery suggests a new way to make the human immune system see cancers that are currently invisible.

Professor Mark Dawson
Professor Mark Dawson

“The good news here is that suppression of MCH-I in this context is reversible, which means that cancers previously invisible to the immune system could be re-exposed using approaches to increase levels of the MHC-I components,” says Prof Mark Dawson, who is senior author on the study.

“It is hoped this discovery may lead to a rationale for combining drugs that shut down the PRC2 pathway with immunotherapies to treat some aggressive cancers. This is especially important for solid cancers that are notoriously resistant to immune-based therapies, such as small cell lung cancer and some types of paediatric cancers, that have low expression of MHC-I.”

The paper, titled ‘An evolutionarily conserved function of polycomb silences the MHC class I antigen presentation pathway and enables immune evasion in cancer’, has been published online by Cancer Cell.

This article originally appeared on the Peter Mac website. Thanks to the generosity of our supporters, Australian Cancer Research Foundation has provided four grants to Peter Mac, totalling $9 Million for cutting edge cancer research equipment and technology.

Publication demonstrates why chemotherapy is only effective in some patients

Researchers at Children’s Medical Research Institute have demonstrated why chemotherapy drugs work better with some types of cancers than with others.

Pragathi Masamsetti, the lead author of a new paper published in Nature Communications, has been studying the pathways of cell death caused by chemotherapy drugs for the past five years after a surprise initial discovery piqued her interest. Now that her PhD is finished, she is optimistic that her research will form the groundwork for other scientific or clinical developments in cancer treatment.

“This research could influence which class of chemotherapy is used for each cancer by giving doctors and scientists a better understanding of how the mutations in each type of cancer respond to various chemotherapy drugs.’’

Chemotherapy drugs work by causing a lethal level of stress on the processes occurring when cells are rapidly dividing, a hallmark of cancerous tissue. But these drugs, which attempt to stop rapid cell division, are a blunt solution and are not always effective.

“Chemotherapy can be very powerful in the right situation, but we are only beginning to understand the mechanism behind why some cancer cells die and why some proliferate when targeted by chemotherapy.

“Depending on the type of mutation in a patient, the cancer cells can avoid dying. These cells may go on to proliferate and actually promote the cancer.”

Pragathi’s research revealed that cancers avoid cell death via a range of cellular pathways. The exact pathway the cancer cell uses depends on the particular mutations and other factors present in the cell. Cells with certain cancer mutations, such as the common p53 mutation, are adept at avoiding their own death and go on to create further instability in the genome, making the cancer even more diverse and hard to eradicate. Pragathi’s research paints a picture of what must be present or absent in the cancer cell in order for a cell to avoid its own death via one pathway or another.

Cancer cell chromosomes in blue (telomeres, green; centromeres, pink)

“I feel like this will give a lot of scope for future study into what is happening when chemotherapy is effective and when it’s not. Building on previous knowledge with new techniques has allowed a new level of detail, so now hopefully other labs can better understand the relationship between cancer cells, chemotherapy and genetic mutations. This will be a big bridge to connect all the stories.’’

The research made extensive use of live cell imaging, adding chemotherapy drugs to cells in real time in the ATAC facility at Children’s Medical Research Institute. While this study was fundamental scientific research, Pragathi sees her work as assisting clinics on the path toward personalised medicine.

“By knowing the ways in which cancer cells avoid cell death, it will help us to identify cancer treatments in the future. Once we can identify the mutations involved in each cancer then we can tailor our treatment approach as specifically to the instance of cancer as possible.

“Ultimately this is a step towards more personalised medicine, but we have to do more fundamental scientific research in order to understand how cancer works.

This article originally appeared on the Children’s Medical Research Insitute website. Australian Cancer Research Foundation has given $12M worth of grants to CMRI, including our 2015 major grant.

Jocelyn and Ella team up to chop for cancer research

“My name is Jocelyn, I’m a full-time working Mum with a wonderful husband and 3 beautiful children. Ella is my eldest at 9, and she is the driving force behind the big chop. It’s been tough the last few months finally getting to the length we need to donate our hair.

Jocelyn and Ella show their hair growth to donate to cancer research
Jocelyn and Ella saw first hand the impact cancer has on Australians, and are taking action

Unfortunately, cancer has touched our lives too closely and too often. I lost my sister when she was only 38 and my father was diagnosed just after she was. My father in law has also fought cancer three times. Thankfully both my Dad and father in law are still with us, although my Dad will need another stem cell transplant, we are just not sure when.

It’s pretty confronting to watch loved ones suffer with this horrible disease. My sister tried to keep her hair as long as possible, but eventually, she had to shave it off. An authentic, high-quality wig made all the difference to her self-confidence at a time when her body was failing her.

For a while, my kids thought they would lose their hair if they had a sore throat because it seemed that everyone close to them lost their hair when they were sick. Although we could see the humour in the situation at the time, we knew it was a lot for our little people to experience and process.

I’ve donated my hair before, and it is good hair for wigs. Ella has been asking for a haircut for a while now and when I told her about donating it, she was excited to do it and is not afraid of cutting it really short.

I am certain every person I know has been touched by the devastating impact of cancer in some way. I know that we can make a difference if we all jump in and make it happen.

Ella and her grandfather

Ella is so proud to be contributing and she understands that doctors receive grants that help them research new treatments that could help keep loved ones around a lot longer. I researched ACRF when we were looking for a beneficiary for the money that was raised after my sister’s funeral. It was an easy choice as they have that goal in sight also.”

Support Ella and Jocelyn here

Inspired and ready to cut, colour or shave for cancer research? Find out how here.

Rare ovarian cancer confirmed as not seeded from elsewhere

An international study led by Peter Mac has revealed the origin of mucinous ovarian cancer (MOC) confirming, unlike other types of ovarian cancer, this rare cancer is not seeded from elsewhere in the body.

The research provides new insights that could lead to a tailored treatment for MOC, which accounts for around 3% of all ovarian cancers. Importantly, the study found MOC is a true gynaecological cancer and not a distant metastasis of a cancer that started elsewhere – like the pancreas, bowel or breast.

“Recently our understanding of ovarian cancer changed dramatically and we now recognise the ovaries can act like a sponge for roaming cancer cells,” says Dr Kylie Gorringe who is a Group Leader in the Cancer Genomics Program at Peter Mac and senior author on this study.

“Some cancers masquerade as ovarian cancers when in fact they originated in other organs, and by identifying where these cancers come from we’ve been able to improve treatments and prevention.

“We still have a way to go before we have addressed this question for all types of ovarian cancers, especially the rarest forms, but in the case of MOC we have now confirmed this is not a metastatic tumour but it develops at the ovary from an early stage.”

The genetic events observed in MOC were compared to other tumours from many different tissue types, and this ultimately showed MOC as a unique cancer of the ovary. Benign and borderline mucinous ovarian tumours were also sequenced, revealing these were genetically related to MOC in a way that indicates MOC could have evolved from these less aggressive tumours.

MOC affects less than 80 women each year in Australia, and over 500 samples of MOC and related tumours had to be sourced from around the globe to complete this research.

Results of the study – titled “The molecular origin and taxonomy of mucinous ovarian carcinoma” – were published online this week in the high impact journal Nature Communications.

The analysis – which involved an international collaboration and sequencing DNA from hundreds of genes up to the whole genome – also revealed new potential therapeutic targets that could support a tailored treatment for MOC.

“Building on our study findings, there is a strong case to involve women with MOC in clinical trials of drugs already in development and which target solid tumours with genetic similarities to MOC,” Dr Gorringe also says.

This includes drugs that target cancers with KRAS or TP53 mutations, and HER2 amplifications.

Around 1,500 Australian women will be diagnosed with ovarian cancer this year. The most common type – high-grade serous ovarian cancer – accounts for about 65% of cases. For decades, and without a tailored treatment, MOC has been treated the same way as high-grade serous ovarian cancer.

National collaborators include the WEHI in Melbourne, and international collaborators were based at institutes including the Mayo Clinic in the USA, University of British Columbia, and University of Montreal in Canada, the UK’s Centre for Ovarian Cancer Research at the University of Edinburgh.

Thanks to the generosity of our supporters, Australian Cancer Research Foundation has provided Peter Mac with four grants for technology and equipment for cancer research, totalling $9M.

This article originally appeared on the Peter Mac website.

Numbers count in the genetics of moles and melanomas

University of Queensland scientists have identified a way to help dermatologists determine a patient’s risk of developing melanoma.

UQ Diamantina Institute researcher Associate Professor Rick Sturm said the team uncovered the specific gene variations affecting the number and types of moles on the body and their role in causing skin cancer. 

“The goal was to investigate the genetic underpinnings of different mole classes or ‘naevi types’ and understand how these affect melanoma risk,” Dr Sturm said.

“Based on our work, the number of moles in each category can give a more complete assessment of melanoma risk rather than just the number of moles alone.”

Three key mole classes, reticular, globular and non-specific were magnified under a dermoscope to assess their pattern and risk factors.

“We found people who had more non-specific mole patterns increased their melanoma risk by two per cent with every extra mole carried,” he said.

“As we age, we tend to increase the amount of non-specific moles on our body, and the risk of developing melanoma increases.”

Dr Sturm said globular and reticular mole patterns were also found to change over time.

“Globular patterns were shown to decrease as we get older, typically petering out after the age of 50 to 60,” he said.

“Reticular moles also decreased over time but were likely to head down a more dangerous path and develop into the non-specific pattern.”

A cohort of more than 1200 people, half melanoma patients, were recruited into the almost nine-year study. 

Their results were then overlayed with genetic testing, which found variations in four major genes.

“We found some major relationships between genes and the number of moles and patterns when looking at the DNA,” Dr Sturm said.

“Certain gene types influenced the number of different naevi types — for example, the IRF4 gene was found to strongly influence the number of globular naevi found on the body.”

The findings will help dermatologists to better understand mole patterns and provide more holistic care to patients who may be at risk of melanoma.

“For a long time, clinicians have been interested in how pigmented moles relate to melanoma and melanoma risk,” he said.

“With the availability of dermoscopes and imaging, these results provide a new layer of understanding to guide clinical practice.”

This article originally appeared on the University of Queensland website.

Australian Cancer Research Foundation has provided four grants to the University of Queensland’s Diamantina Insitute for research into Melanoma. This includes the 2018 Major Grant of $9.9M to establish the ACRF Australian Centre of Excellence in Melanoma Imaging and Diagnosis.

Emma runs City2Surf to fund life-saving research

My name is Emma, I’m a mother of three and I’m from Burradoo, NSW. I work in the mental health field, as a social worker, and also at Western Sydney University, supporting students and staff mental health and wellbeing.

My family has been directly impacted by cancer in the last few years.

My beautiful sister Kate was diagnosed this year with Leukaemia (CML) and is now gratefully benefitting from wonderful cancer research that means she is on a drug trial, working towards recovery.

I love the direct impact cancer treatment research can have on a diagnosis. Without research and studies, there may be very different outcomes for my family.

Emma and her daughter Gabriella, who encouraged her to enter City2Surf

I didn’t think I would be running City2Surf this year – to be honest, I signed up two weeks before the race. I last ran this event when I was 15 years old, back in the mid-1980s! But with some convincing from my daughter, I decided I would attempt it this year.

With family fighting cancer you become more aware of how precious life is. Although I am a generally fit person, I wasn’t sure I’d be able to make it through the race – the last time I ran 14km was 35 years ago!

Race day came, and guess what – I actually surprised myself at how much fun it was, and how easy it was once the adrenalin got flowing!

I know cancer directly changes people’s lives so suddenly.

My life has been impacted significantly over the last few years. My lovely mum died of cancer just three years ago, and my sister Kate is now benefitting from a drug trial that is treating her leukaemia.

Running a fun run, on a sunny day in gorgeous Sydney seemed an easy but poignant choice to contribute some money and awareness to the cancer research cause.

Every little contribution will make a difference. If you can choose to donate and encourage friends to join in, why not? It feels worthwhile, and I really felt on the day I had a good reason to try my best when running. Especially as my lovely friends had donated to my Facebook page seeking sponsorship.

I was really excited and humbled as the two weeks progressed, to see how friends added quite generously to my cause. I am so grateful for this support.

I think contributing to research is such a useful way to make an impact for all cancers. I am so grateful that my family has access to the research outcomes such as being on treatment trials, effectively helping to fight cancer and heal from the disease.

Key to targeting the spread of pancreatic cancer

Targeting the tissue around pancreatic cancer cells may be the key to stopping their spread and improving chemotherapy outcomes.

An international team of researchers has revealed how aggressive pancreatic cancer cells change their environment to enable easy passage to other parts of the body (or metastasis) – the main cause of pancreatic cancer-related death.

The researchers discovered that some pancreatic tumours produce more of a molecule called ‘perlecan’ to remodel the environment around them, which helps cancer cells spread more easily to other parts of the body, and also protects them against chemotherapy. In a mouse model, the researchers showed that lowering the levels of perlecan revealed a reduction in the spread of pancreatic cancer and improved response to chemotherapy.

Led by Associate Professor Paul Timpson, Head of the Invasion and Metastasis Laboratory, and Dr Thomas Cox, Leader of the Matrix and Metastasis Group, at the Garvan Institute of Medical Research, the research may provide a promising new path to more effective treatment options for individuals with pancreatic and other cancers.

The findings are published in the journal Nature Communications.

“Pancreatic cancer is very aggressive, and by the time most cases are diagnosed, the tumour is often inoperable,” says Associate Professor Timpson. “What we’ve discovered in this study is a two-pronged approach for treating pancreatic cancer that we believe will improve the efficiency of chemotherapy and may help reduce tumour progression and spread.”

Pancreatic cancer remodels its environment

Pancreatic cancer is one of the most lethal forms of cancer, with a five-year survival of ~9% in Australia. In its early stages, pancreatic cancers often show no obvious signs or symptoms and by the time a cancer is diagnosed, it has often begun to spread outside the pancreas.

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The Garvan-led team investigated why some pancreatic cancers spread, while others appear to stay in one place. In their study, the researchers took an unconventional path – they compared the tissue around tumour cells in both metastatic (spreading) and non-metastatic (non-spreading) pancreatic cancers. This tissue – known as the ‘matrix’ – acts like a glue that holds different cells in an organ or in a tumour together.

Using mouse models, the team extracted fibroblasts – cells that produce most of the matrix – from spreading and non-spreading pancreatic tumours. By mixing these different fibroblasts with cancer cells, the researchers found that remarkably, cancer cells from a non-spreading tumour began to spread when mixed with fibroblasts from a spreading tumour.

“Our results suggest that some pancreatic cancer cells can ‘educate’ the fibroblasts in and around the tumour. This lets the fibroblasts remodel the matrix and interact with other, less aggressive cancer cells in a way that supports the cancer cells’ ability to spread,” says first author Dr Claire Vennin.

“This means that in a growing tumour, even a small number of aggressive metastatic cells – a few bad apples – can help increase the spread of other, less aggressive cancer cells.”

A spotlight on the tumour matrix

To investigate how to stop pancreatic cancer cells from remodelling the matrix around them, the team took an even closer look at the fibroblasts.

Using state-of-the-art mass spectrometry techniques, the researchers discovered several molecules that the fibroblasts from metastatic tumours produced at significantly higher levels than the fibroblasts from non-metastatic tumours.

“What we discovered is a previously unknown set of matrix molecules that aggressive pancreatic cancer cells use to shape the tissue around them, in order to both protect them from chemotherapy and enable easier escape around the body,” explains Dr Cox.

Using gene-editing techniques, the researchers reduced the levels of one of the molecules called perlecan in mouse models of aggressive metastatic pancreatic cancer. Through advanced live imaging techniques, the researchers tracked individual cancer cells and revealed that lowering the levels of perlecan not only reduced the spread of cancer cells, but that tumours also responded better to chemotherapy.

An untapped resource

“We believe that there would be important benefit in targeting the fibroblasts of a tumour in combination with targeting the cancer cells themselves with chemotherapy,” says Dr Vennin. “If we can specifically target the aggressive fibroblasts in patients harbouring precise genetic changes, we can make them more susceptible to our currently approved treatments, which would significantly change how we treat this aggressive cancer.”

The researchers say that targeting perlecan, or other matrix molecules that help remodel the tissue of metastatic tumours, may be effective for not just pancreatic cancer, but also prostate and breast cancers.

“Most cancer therapies today aim to target cancer cells themselves. The environment of tumours is a potential untapped resource for cancer therapy and one which we intend to explore further,” says Associate Professor Timpson.

This article was originally published on the Garvan Institute of Medical Research website. Australian Cancer Research Foundation has given 6.1M in grants to Garvan Institute for cancer research.

Daily coffee doesn’t affect cancer risk

Drinking coffee does not change a person’s risk of being diagnosed with or dying from cancer, a new QIMR Berghofer study has found.

The research findings have been published in the International Journal of Epidemiology.

Senior author and head of QIMR Berghofer’s Statistical Genetics Group, Associate Professor Stuart MacGregor, said the large Mendelian randomization study looked at data from more than 300,000 people and showed drinking coffee every day neither reduced nor increased a person’s risk of developing any cancer.

“We know that coffee is one of the most popular drinks in the world, and there continue to be mixed messages about the role it plays in disease,” Associate Professor MacGregor said.

“We also know that a preference for coffee is heritable.

“Our two-pronged research looked at whether cancer rates differed among people with different levels of self-reported coffee consumption, and whether the same trend was seen when we replaced self-reported consumption with genetic predisposition towards coffee consumption.

“We found there was no real relationship between how many cups of coffee a person had a day and if they developed any particular cancers.

“The study also ruled out a link between coffee intake and dying from the disease.”

Coffee contains a complex mixture of bioactive ingredients, including substances such as caffeine and kahweol, which have been shown to display anti-tumour effects in animal studies.

Its potential anti-cancer effect on humans has not been established however, with studies to date producing conflicting findings for overall cancer risk and for individual cancers such as breast and prostate cancers.

The QIMR Berghofer study used cancer data drawn from the UK Biobank cohort for more than 46,000 people who had been diagnosed with most invasive cancer types, including about 7,000 people who died from the disease.

The genetic and preference information from the people with cancer was compared to data from more than 270,000 others who had never been diagnosed with cancer.

QIMR Berghofer lead researcher, Jue-Sheng Ong, said the study also looked at some common individual cancers such as breast, ovarian, lung and prostate cancers and found drinking coffee did not increase or decrease their incidence.

“There was some inconclusive evidence about colorectal cancer, where those who reported drinking a lot of coffee had a slightly lower risk of developing cancer, but conversely examination of data from those people with a higher genetic predisposition to drink more coffee seemed to indicate a greater risk of developing the disease,” Mr Ong said.

“The disparity in those findings would suggest more research is needed to clarify if there is any relationship between colorectal cancer and coffee.”

Associate Professor MacGregor said the study had implications for public health messaging around the world.

“The health benefits of coffee have been argued for a long time, but this research shows simply changing your coffee consumption isn’t an effective way of protecting yourself from cancer,” he said.

“The health benefits of coffee have been argued for a long time, but this research shows simply changing your coffee consumption isn’t an effective way of protecting yourself from cancer,” he said.

This article originally appeared here. ACRF has given $8.4M in grants to QIMR Berghofer for cancer research technology since 2002.

A genomic barcode tracker for immune cells

A new research method to pinpoint the immune cells that recognise cancer could significantly change how we treat the disease.


(L-R) Dr Katherine Jackson, Shaun Carswell, Ghamdan Al Eryani, Dr Mandeep Singh

Researchers from the Garvan Institute of Medical Research have developed a new method to spot rare immune cells that are reactive against cancer cells, from within a patient’s own immune system.

The patented ‘RAGE-seq’ method enables scientists to track how immune cells evolve inside tumour tissue for the first time, revealing unprecedented insight into how to better arm the immune system to target cancer. The technique can be likened to a barcode tracker, able to scan detailed information from thousands of immune cells at a time.

“This method gives us the most detailed view yet of how immune cells behave in the human body,” says Professor Chris Goodnow, Executive Director of the Garvan Institute and co-senior author of the published work. “Immune cells play a critical role in the development of disease. This method shows significant potential to help us personalise cancer treatments to the individual.”

Development of the method, by Dr Mandeep Singh (Immunogenomics Laboratory) and Ghamdan Al-Eryani (Tumour Progression Laboratory) at Garvan, is published in the journal Nature Communications.

Rare immune cells that ‘see’ cancer

Our immune system helps protect us against foreign pathogens, such as bacteria or viruses. But it often responds poorly to cancers, which arise from the body’s own cells – usually too few immune cells ‘recognise’ them to mount an effective immune response.

Immune cells come in many different forms – they mix-and-match different types of ‘receptors’ on their cell surface, which monitor the cell’s environment. When an immune cell’s receptors recognise a potential hazard, the cell replicates to make more copies of itself, able to target the threat more effectively.

“The immune cells that recognise cancer cells are often rare,” says Associate Professor Alex Swarbrick, who heads the Tumour Progression Laboratory at Garvan. “We have to sort through thousands of cells to find these replicating cells that may make up only a small fraction of all the immune cells present in a tumour.”

Building a cellular barcode tracker

Previous methods have made it possible to read the long stretches of genetic output (the RNA) that encodes an immune cell’s receptor, from single cells. But they have not had the capacity to sort through the thousands of cells present in a tumour, at a single time.

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The study authors developed a new method by harmonising four different genomic technologies (Oxford Nanopore Technologies, 10X Genomics, Illumina and CaptureSeq).

They first developed a way to enrich the RNA from single cells, targeting the RNAs encoding the immune cell receptors. They then developed a computational tool to accurately read full-length sequences of the immune cell receptors.

The resulting Repertoire and Gene Expression by Sequencing, or ‘RAGE-seq’, method works much like a barcode tracker. By ‘scanning’ the relevant immune cell receptors in many thousands of cells at once it can provide an accurate snapshot of how the immune cells in a tissue sample are related, and which cells may be effective at mounting a response against cancer.

“This high-throughput strategy is really opening the door to a much more detailed understanding of the cellular dynamics of the immune response,” says Dr Martin Smith, Leader of the Genomic Technologies Group at Garvan’s Kinghorn Centre for Clinical Genomics.

In a proof-of-principle study, the researchers used the method to sample 7,138 cells from the tumour and associated lymph node of a breast cancer patient. The team pinpointed a number of related cells that were present in both tissues, and which revealed specific genetic signatures of the immune response within the patient’s tumour.

A new look at disease

The researchers say the ability to find and barcode these rare cells of the immune system has the power to guide treatment strategies based on the individual.

Immunotherapy is an emerging form of cancer therapy designed to activate the immune system to better target cancer, but not all patients respond well and current methods used to assess a patient’s response give a poor snapshot of the behaviour of their immune cells.

Professor Goodnow says there is significant interest from pharmaceutical companies to better understand the immune system’s response to cancer, at a resolution now available through the RAGE-seq method. “We hope RAGE-seq will be implemented in clinical trials, providing crucial information that will help potential cancer therapeutics get to the right patients more quickly.”

The team is now applying the technique to samples from melanoma patients, to understand why half of patients receiving immunotherapy have a poor response. The researchers believe the method could also be applied to provide a better understanding of autoimmune and inflammatory diseases.

This article originally appeared on the Garvan Institute of Medical Research website.

Marlo Shaves for Cancer Research

My name is Marlo and I am 12 years old and I live near Coffs Harbour. I love the environment and live on an acreage with my family and our chickens, rabbits, a dog and our bees. I’m in year 7 and my favourite subject is Human Society and it’s Environment. I play the violin and I am in two ensembles.

Although I was too young to know what was happening at the time, my grandma has had breast cancer twice, and a very close family friend has also had breast cancer. All I remember from this was my mum being very worried. Cancer affects so many people, and there are so many different types with many having limited treatment options. The idea of a headshave had been mentioned at school, and I thought ‘why not! It’s just hair, and it will grow back’.

For anyone who is considering doing a headshave, I would say ‘DO IT!’. It feels really good to know that you are helping other people. I was really lucky because my family and friends were very generous and supportive, lots of my mum and dads friends who I have never met donated money, and lots of my teachers and other people who live in our small town. Overall I am really glad I did it and if I ever grow my hair I will do it again.


Inspired and ready to do something bold for cancer research? Find out more about hosting a head shave for ACRF here.  

More genetic evidence of what puts people at risk of breast and other cancers

A new international study has discovered that 94 genetic variants, about which little has been known until now, increase a person’s risk of developing breast, ovarian, prostate and pancreatic cancers.

The study, led by QIMR Berghofer Medical Research Institute, also found that hundreds of other genetic variants in the BRCA1 and BRCA2 genes did not cause cancer.

The variants had already been discovered, but it wasn’t previously known whether they increased a person’s risk of cancer or had no effect.

The research, arising from the ENIGMA international consortium, adds to the wealth of genetic knowledge that can help identify those at risk and help doctors and genetic counsellors decide on the best management for people who carry variants in the BRCA1 or BRCA2 cancer genes.

The study involved more than 200 scientists and doctors from 114 institutions around the world, and has been published in the journal Human Mutation.

More than 20,000 variants have previously been identified in the BRCA1 and BRCA2 cancer genes which, when altered, might or might not affect a person’s chances of developing breast, ovarian and some other cancers.

However, the significance of thousands of those variants is still unknown, which is problematic for management of families carrying those variants.

The study collated research and clinical data from around the world for a large number of BRCA1 and BRCA2 genetic variants of unknown clinical significance.

Senior Author and head of QIMR Berghofer’s Molecular Cancer Epidemiology Group, Associate Professor Amanda Spurdle, said it was the single largest study of its type to date.

“We were able to weed out 447 variants as harmless, while showing 94 variants did increase a person’s risk of developing breast, ovarian, prostate and pancreatic cancers”, Associate Professor Spurdle said.

“It’s like separating the wheat from the chaff.

“These findings will help doctors give advice on the frequency of early screening such as breast scans; preventative measures such as risk-reducing surgery or medication; and even personalised treatment with specific drugs (PARP-inhibitors) for people with those cancers.

“The genetic information is also used to decide whether to test close relatives, in a bid to prevent or catch disease early.

“If we can narrow down which variants pose a danger, we can reduce concern for clinicians and patients, and avoid unnecessary testing that unfortunately sometimes occurs for individuals with a variant of uncertain significance.”

Associate Professor Spurdle said clarifying the role of so many variants was only possible because of the international collaboration.

“We pooled clinical and research expertise from around the world and applied statistical methods to tackle this problem, using information from patients and their families spread across 15 countries.

“Importantly, it has also provided a basis for us to further develop our methods for classifying genetic variants in future.”

ACRF has provided QIMR Berghofer with three grants, totaling $7.05M, for research into all types of cancer since 2007. This article originally appeared on their website.

Gwennyth Bravely Shaves for ACRF

“My name is Gwennyth, I’m 9 years old and I am in grade four. I have one brother who is 11 years old. I also have a dog called Brownie who is very naughty and chews apart everything. I love to dance and sing.

Cancer research is really important, and I want to do what I can to help. I decided to shave my hair and raise money for Australian Cancer Research Foundation.

My Nonna had breast cancer and she lost her hair and sadly died. Both my great grandmothers also died from cancer. Luckily my Gran is a cancer survivor, but she had to fight hard to beat it. I got inspired by all of them and others who have had to battle cancer and lost the fight.

I felt very nervous and scared but I went through with it because I was so determined to help other people. I kept telling my mum, ‘It doesn’t matter, it’s just hair and it will grow back – other kids need my hair more than I do!’. After I shaved my head I felt really happy because I knew what I did was able to help so many people.

On the day of the shave, I held a fun morning tea and had all my friends over. My mum’s hairdresser came over, made 33 ponytails, and everyone had a go chopping one of them off (including me!) and then the hairdresser shaved the rest off using a number 1 and 2 blade. I have a very short hairdo now – just like Sinead O’Connor!

Shaving your head is a big responsibility and quite nerve-racking, but when you do it you just feel so much happier that you know you are helping people.”

Inspired and ready to do something bold for cancer research? Find out more about hosting a head shave for ACRF here.

Two new potential cancer therapies identified

An Australian study undertaken by St Vincent’s Institute of Medical Research (SVI) in Melbourne and Children’s Medical Research Institute in Sydney, has uncovered a mechanism of cancer survival and identified not one, but two, potential treatment options that could help kill aggressive cells that lead to both rare children’s’ cancers and common cancers.

“Cells divide throughout our lives to ensure our bodies can keep on functioning; but as they divide, the structures found at the ends of chromosomes called telomeres, get shorter and shorter, until the cell eventually dies,” said senior author, Associate Professor Hilda Pickett from CMRI in Sydney.

Cancer cells find a way around this limitation using one of two approaches to repair the chromosome: 1) the enzyme telomerase is activated to add new telomeres to the DNA ends or 2) through a process called “alternative lengthening of telomeres”, or ALT, which copy/pastes telomere DNA from chromosomes with long telomeres onto those with short telomeres.

“About 40% of soft-tissue cancers including osteosarcoma (bone cancer), liposarcoma (a cancer originating in fat cells), and angiosarcoma (blood vessel cancer), as well as 10% of other carcincoma cancer types, such as breast, ovarian and prostate, occur when the ALT process is activated and the cells become ‘immortal’ and cancerous”, said co-first author Dr Julienne O’Rourke from SVI in Melbourne. “There are currently no specific therapies for ALT-positive sarcomas. People with this type of cancer have a 50% higher rate of death, as these cancers are more resistant to current treatments.”

Associate Professor Pickett said they’d been studying the mechanics of ALT cancers for many years when they identified a protein that is essential for ALT cell viability. The research involved collaboration with Associate Professor Andrew Deans at St Vincent’s Institute in Melbourne to demonstrate that depletion of FANCM was specifically toxic to ALT cancer cells. Together they discovered that by disrupting the function of FANCM, they could put the cancer under so much stress that it stopped proliferating.

Another study by SVI undertaken with international collaborators in Portugal and Switzerland2, also revealed that ALT-positive cancer cells die when FANCM is deleted.

“Both studies, published today in Nature Communications, found that absence of the FANCM enzyme “hijacks” the ALT process and causes very specific cancer cell killing. The FANCM enzyme is not essential in normal (non-cancerous) cells,” said co-senior author Associate Professor Andrew Deans from SVI. “This suggests it could be a good target for new drugs that could eliminate cancer cells, without eliminating other healthy cells.”

“Further, we found that FANCM could be inhibited with specific peptides, or an experimental drug called PIP-199.  The next step is to do new studies with these peptides and PIP-199 to get to the stage where we can begin clinical trials,” said Associate Professor Hilda Pickett.

“We’re all excited by the life-changing and life-saving potential for children and other people with these cancers; it’s not every day you make discoveries that could lead to treatments that could save not a few, but many, precious lives.”

The original article, featured on the St Vincent’s Medical Research website, can be found here.

Researchers reveal key to targeting dormant cancer cells

Researchers from Garvan Institute of Medical Research have identified what keeps some cancer cells dormant – a finding which could uncover new approaches to preventing the spread of cancer.


Dr Weng Hua Khoo, Associate Professor Tri Phan and Professor Peter Croucher

An international team of scientists has uncovered the unique set of genes that keeps some cancer cells dormant. Led by Associate Professor Tri Phan and Professor Peter Croucher at the Garvan Institute of Medical Research in Australia, in collaboration with Professor Ido Amit at the Weizmann Institute of Science in Israel, the research may reveal new therapeutic targets for multiple myeloma (a blood cancer that arises in bone) and other cancers which spread, or metastasise, to bone such as breast and prostate cancer.

The researchers publish their findings in the journal Blood on 25 April 2019 (EDT).

Most will associate cancer with its fast growing cells that spread uncontrollably – but in fact, it’s often the cancer cells that are dormant and inactive that pose the greatest threat. Dormant cancer cells, when ‘woken up’, are a major cause of cancers coming back, or relapsing, after treatment – often as metastases, which are estimated to cause 90 per cent of all cancer deaths.

A ticking time bomb

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Credit: Dr Michelle McDonald

When cancer metastasises, it spreads to different organs in the human body. Some cancer cells can stop dividing and hide in a ‘dormant’ state, tucked-away in niches such as the inner lining of bones. Once dormant, the immune system, our natural protector, cannot find them to target them and conventional chemotherapy is ineffective. There is also no way of knowing how long the cells will remain dormant.

To help prevent dormant cancer cells from being reactivated, Garvan researchers are investigating what makes cancer cells dormant. But isolating the cells to study them has been a challenge – they are rare, often less than one in hundreds of thousands of cells in the bone, and scientists have not known how to identify them.

“What makes our approach different is that we’re looking at the cancer ecosystem as a whole,” says Associate Professor Phan, Head of the Intravital Microscopy laboratory at Garvan and co-senior author of the study. “It’s not just the cancer cell but the other cells in their microenvironment which determine their fate. We are trying to find what genes get switched on by the microenvironment and how those genes make the cancer cell dormant.”

Uncovering cancer’s hiding place

The Garvan researchers first developed a way to track dormant multiple myeloma cells inside the bones of living mice four years ago using a new technique called intravital two-photon microscopy. They have now isolated these rare cells to analyse the dormant cells’ transcriptome – a snapshot of all the genes that are switched on in the cell and control dormancy.

“Having been able to identify the rare dormant cells, we were able to isolate them and work out all the genes which were active. What is exciting is that we discovered many of these genes in dormant cells are not normally switched on in these cancer cells. Now that we know the identity of these genes, we can use that information to target them,” says Dr Weng Hua Khoo, first author of the study.

The team analysed the single cell transcriptomes at the Garvan-Weizmann Centre for Cellular Genomics and confirmed their findings independently with their collaborators at the Weizmann Institute of Science.

Unexpectedly, the dormant myeloma cells had a similar transcriptome signature to immune cells, but which was only ‘switched on’ when the cells were located next to osteoblasts, specialised cells found in bone. “This showed us just how crucial the crosstalk between the tumour cells and the tumour microenvironment is for cancer dormancy,” says Professor Ido Amit, Principal Investigator at the Weizmann Institute.

A new way to target cancer

The researchers are now using their method to collect data on dormant cancer cells from other cancer types, with the hope of finding a common signature that would allow them to target all dormant cancer cells. “The aim now is to bring data from many cancer types together to find a unifying approach to understanding how dormant cells control cancer relapse and metastasis,” says co-senior author Professor Croucher, Research Director at Garvan.

The team is also working to develop potential therapies that target the unique features of dormant cells, now uncovered by this research.

Professor Croucher says, “There are different approaches to targeting dormant cells. One is to keep them dormant indefinitely by creating an environment that stops them from waking up. A second approach is to deliberately wake them up, which can then make them susceptible to being targeted with conventional chemotherapy. But the best approach would be to use this knowledge of what the genes are that keep cells in the dormant state to eradicate them while they’re dormant. This would stop the disease coming back or relapsing – this would be the Holy Grail.”

The original article can be found on the Garvan website.

Kate and Jordan Tie the Knot and Support Cancer Research

Our names are Kate and Jordan and this year marks our fourteenth year together, and our first as a married couple. We live with our dog Oscar in Sydney’s Inner West. We are absolute best friends- even after fourteen years together, we still want to spend as much time as possible together and our favourite thing to do in the whole world is to sit in our garden and have a glass of wine together.

Kate and Jordan on their wedding day

We met in our late teens, in our last year of high school. We were introduced by friends, who were dating at the time, and so began a very slow courtship process. At 19 years old, we dated for a year and then split up for a year. The timing just wasn’t right. We were both young and still finding out who we were. At 21 years old, our paths crossed again and it felt as though it was meant to be. We spent our twenties travelling, living in share houses with friends and partying together, before settling down in our early thirties, buying a house and making it our own.

We are not a traditional couple, and having been together so long, neither of us wanted a traditional wedding. Neither of us wore traditional wedding outfits, we didn’t have bridesmaids or groomsmen, no first dance or wedding cake. This was a wedding PARTY.

As foodies, we sourced the very best food and excellent wines and we had the privilege of having a live singer, Andrew Loadsman (who you may remember from The Voice TV show) and the best celebrant, Todd Mayhew, who kept the vibe fun in his pale blue safari suit. We were married in Jervis Bay amongst coral peonies, smokebush, jewel-toned hydrangeas, and sorbet coloured sweetpeas and delphinium.

It is hard to find someone these days who has had no experience of cancer. It is an unflinching, uncaring, indiscriminate disease and it takes so many great people far too soon. But just as we have had experiences with loss associated with cancer, likewise we are so blessed to say that, thanks to the wonders of modern cancer research and medicine, we still have so many of our dear family members and friends still with us. Kate’s godmother is a survivor, as are many family friends, and Jordan’s dad, who beat Prostate cancer.

The wedding ceremony in Jervis Bay

And beyond this, many more people that were at our wedding thanks to the wonder of modern cancer treatment and we are so grateful for that. So grateful in fact, that we chose not to ask for money for ourselves, but rather to donate that money toward cancer research. If our wedding money can go toward saving just one person in the future it will be worth it.

Cancer research is one of the most important facets of modern medical science and technology, and it is absolutely integral in keeping people alive. We all need to work together to solve cancer. It takes all of us, and even small donations help.

These days we are all blessed with so much. Many of us are already living together before we get married and have no need for the toasters and blenders and crystal glasses that have traditionally been wedding gifts. Honeymoon funds or wishing wells are a popular trend at weddings these days but as you continue through life, you won’t miss that money you got for your wedding – but you will miss the people that shared that day with you. What is more important than anything, if you can afford it, is to give that money where it can genuinely make a difference.

Learn more about Donating in Lieu of Gifts

Kathryn’s Bucket-List Fundraiser

My name is Kathryn. I am turning 60 this year and have been happily married for 38 years. I have three beautiful children and five healthy grandchildren. Throughout my life, I have lost too many family and friends to cancer. I don’t like to see anyone suffer. I know every bit of support helps to remedy this.

Hosting a fundraiser for a worthy cause has been on my bucket list. I am pleased to say that I have now achieved this by raising more funds than expected for Australian Cancer Research Foundation. I held a successful fundraiser event with over 150 people attending and we raised over $14,000 that went directly to the cause.

I am surrounded by close family and friends who have suffered or are living with cancer. I, unfortunately, lost my father in law to cancer, my maternal Aunties and mother have suffered from breast cancer, and I have two close family members living with cancer; one has Hodgkin’s lymphoma and the other has multiple myeloma. There are many more that I know of that have battled this dreaded disease.

I believe in supporting the research as it saves lives and hopefully one day we may find a cure.

I chose ACRF as they cover a wide range of cancers. I know of too many family and friends that have suffered or who are currently suffering with cancer. Years ago, it was a death sentence but as a result of research, often it can be beaten, and if not, it can be lived with.

This has been my first major fundraiser. It has taken me well out of my comfort zone.

I don’t normally feel comfortable asking for help. I pushed myself to ask for donations of prizes for silent auctions and balloon prizes. I had quite a few rejects, but I did manage to get corporations, small businesses and individuals willing to support the evening. The outcome was far more than what I was aiming for.

If I can manage to organise a successful fundraiser, I’m sure anyone putting their mind to it can also do the same. It has been a very rewarding experience.

I have been very humbled by the support shown from family, friends and the wider community.  The total raised far exceeded any of my expectations. I am proud knowing that the amount raised will contribute to help save the lives of many.


Want to get involved and support ACRF in our mission to outsmart cancer?

There are many ways you can get involved to raise money if you feel passionate about the advancements in cancer research we are helping fund.

You can host your own fundraiser like Kathryn did. Some ideas for your event include holding a morning tea, a BBQ or a DIY fundraiser.

Another way you can fundraise and help us outsmart cancer is by shaving or colouring your hair and getting family or friends to donate to your cause.

If you are part of a business, we have a business and corporate partnerships program so you can partner with us to raise money as well as creating a partnership that will be a rewarding benefit for your company and staff.

Bacterial toxin research could improve pesticides and help treat cancer

Research into an intricate toxin delivery system found in bacteria could overcome the problem of pesticide resistance in insects, and might even lead to new cancer treatments.

An international team led by Dr Michael Landsberg at The University of Queensland has revealed the detailed inner workings of the newest member of a family of naturally occurring insecticidal toxins.

“This toxin, known as YenTc, is a highly effective toxin-delivering nanomachine,” Dr Landsberg said.

Structure of the YenTcA toxin complex looking down through the central channel.

“We used a high resolution microscopic imaging method known as electron cryo-microscopy to reveal the complex molecular structure that injects highly toxic molecules into targeted cells, triggering cell death.”

The toxin was isolated from a naturally occurring bacterium that targets many commercially significant insect pest species, including the diamondback moth, and has been earmarked as a new biopesticide.

“We found that YenTc contains unique features which decorate its structure, much like baubles that distinguish the appearance of Christmas trees,” Dr Landsberg said.

“We believe these decorations determine which hosts are susceptible to toxins.

“This selection mechanism will ultimately be crucial to the safety of any future biopesticide technology.

“But understanding it might also allow us to engineer bio-inspired toxins that could be used for therapeutic purposes.”

UQ’s Dr Sarah Piper, said the findings had helped researchers understand why YenTc specifically targeted insects.

“This is an important step, which may eventually allow for YenTc or related toxins to be engineered to target different insect species, or perhaps even selectively target and kill unhealthy cells in animals or people, such as cancer cells, without harming healthy cells,” she said.

“So what began with the goal of trying to prevent insects from destroying vegetable crops might one day lead to us having the capability to design and test new therapeutic approaches for treating cancer.”

The work involved researchers at UQ’s School of Chemistry and Molecular Biosciences and the UQ Institute for Molecular Bioscience, Griffith University, AgResearch New Zealand, the University of Auckland, the University of Basel and the Cambridge Institute of Medical Research.

Original article can be found on the University of Queensland website.

200ks in 5 Days | Chelsea’s Story

Mesothelioma.

A form of cancer that I know a lot of people have never heard of.  

I was one of those people, before this horrible illness took someone I loved so much away from me.

Mesothelioma is a form of cancer that comes from exposure to Asbestos; most of the time lying dormant in your body for years. One that burdens its patients or victims, as quickly as it takes them away too.

My name is Chelsea Phillips, I am 25 years old and a passionate, emotional and determined person. In August this year, I’m getting married to my best friend, Ben. I’m extremely family orientated and love my friends.

My Opa (grandfather), to us, seemed like a healthy older gentleman, someone who appreciated everything life had to offer; his beautiful wife, 5 amazing kids, 11 grandkids and so on.

He had always had a shadow on his lungs, something that his doctor was never too worried about. But in the months leading up to his first admission into hospital, he was experiencing severe pain and discomfort around his shoulder and chest. It was mistaken for muscle and joint pain a number of times.

Chelsea’s grandfather and grandmother

The immediate concern came when he saw a different doctor, who sent him straight to emergency at Sutherland hospital on the 12th December, 2016. He spent one and half weeks and his last Christmas lying in a hospital bed, with no answers. We celebrated my Oma’s birthday in January, with Opa at home.

A few months later after visiting a new specialist, my Opa was again admitted into Emergency, where he spent the next few weeks. More and more tests and finally on the eve of Valentines Day 2017, we got the answer that none of us wanted to hear. That shadow on his lungs was Mesothelioma and ‘months’ was the diagnosis.

Within 2 weeks of Opa’s diagnosis, he was transported to a different hospital, where he would spend, what we thought would be his last weeks. But on the morning of the 6th March 2017, just 3 days after he was transferred, we got a call to come and spend the last precious hours with our beautiful Opa. He held out a tough fight for most of the day.

The brutal cancer took him within weeks of his diagnosis. It’s something I would not want anyone else to endure, especially if something can be done about it before it’s too late.

I could have had him around for a century longer and I struggle with the sudden loss of my grandfather every day. I hope that in raising awareness of this sinister cancer, that people will take extra precaution and care, whether they have already been exposed to or are still exposing themselves to asbestos today. They need to get themselves checked and use all the appropriate protective gear.

I asked my beautiful friend and fellow fundraiser, Rachel, if she would be interested in raising money for cancer research and she let me know about the Brisbane Valley Rail Trail. It seemed like a perfect fit for us and we have been planning to do it ever since.

The reason we are taking part in this walk, is to raise awareness of the awful, incurable cancers that have affected both Rach and my families, along with all other forms of cancers. Cancers, that should be much more widely known about and with the help of raising awareness and funds, hopefully avoided and with the help of research, cured.

All funds that are raised from this walk will go straight towards overall cancer research, because although there may not be a cure for this form of cancer yet, this will get us one step closer to curing other types of cancer that are still taking too many lives.

There are too many people in my life alone, that have been affected in some way by cancer, we can all stand up to this horrific killing disease and make a change.

When someone you love is so sick and you hear about so many other people affected by this disease, there is not much that you can actually do and you feel helpless. I have been wanting to do something for two years and I am so lucky I have someone like Rach to go on this journey with.

Support Rachel and Chelsea here

The Fundraising duo! Rachel and Chelsea



200ks in 5 days | Rachel’s Story

My name is Rachel, I’m one half of a studio for architecture and interior design.  I live in NSW with my partner, Micky and our greyhound, Bill. I am 30 years old, with some grey hairs. I’m the first generation Australian in our family, my mother was born in France, and my father in Italy.

In October 2017, my dad, who was then 59, was admitted to Prince of Wales Hospital in Randwick for surgery to remove a cancerous growth on his tongue.  Dad made out like it was no big deal, they were just cutting a small growth off the side of his tongue. But when I went to visit him after the surgery, I could see immediately that it was, in fact, a very big deal.

Dad’s face was a swollen mess, with tubes coming out of various places draining fluid.

The surgery had involved pulling Dad’s tongue through an incision in his upper neck, removing approximately one third of his tongue, and then grafting some tissue from the inside of his wrist to the wound.  The swelling was so bad he couldn’t breathe through his nose or mouth; he had a tracheostomy for nearly 4 weeks.  He had a feeding tube up his nose and had to communicate by writing on a piece of paper. 

Rachel and her father



I nearly fainted that first day I walked into the hospital room; there was my Dad, who wasn’t a smoker, didn’t drink, going through hell.

The positive from this is that the surgeons removed a clear margin, and there was no cancer in the lymph nodes they removed from his neck as a precaution.

Dad then began the long road of recovery from the surgery; his speech was affected, and he had a lot of trouble swallowing. He had regular check-ups, but we were all hopeful that eventually, everything would go back to normal.

Then, in April 2018, we received the news that the cancer had returned, this time in the base of Dad’s mouth and in both sides of his neck. It was very aggressive, and the next course of action was radiation therapy, and chemotherapy; with the likelihood of an ‘all clear’ being given was 5-10%.  Despite those odds, Dads decided to fight the cancer. 

The radiation therapy came with its own set of side effects: nausea, fatigue, dizziness, and pain.  But Dad never complained.  After 8 weeks of treatment at Liverpool Hospital, Dad was feeling better; the swelling in his face had gone down, and we were all hopeful that the combination of radiation and chemo had done the trick. 

The treatment did reduce the size of Dad’s cancer, but didn’t eliminate it.  We were also told that the cancer had also appeared in Dad’s lung.  But he kept fighting.

We were fortunate that around this time (about September 2018), the government subsidised immunotherapy for Dad’s type of cancer – so he gave that a go too.  The side effects from this were bad – intense nausea and vomiting, and extreme fatigue. Dad was hospitalised a few times for 3-5 days each time during September/October, as he could not keep any fluids or food down (all of which went through his PEG – a feeding tube to the stomach). 

Then, in November, Dad was hospitalised again.  The immunotherapy was not working against Dad’s cancer, and we decided that it would best to stop the treatment.  Dad remained in hospital while the doctors tried to manage the side effects of the immunotherapy; and eventually they were able to stop most of the nausea and vomiting.  In December, Dad was moved to palliative care.

Throughout December, I watched as my Dad deteriorated; I witnessed him transform from a person who I loved, into a husk of a man.

On the 19th of December the decision was made to turn off the PEG feeding tube – from then on, Dad would only receive 120mL of water, 4 times per day. He wore a nappy and urinated into a tube. My Dad was skeletal and unrecognisable – he was so thin that his earlobes disappeared, I could see every single one of his ribs, the start and end of his femur; his teeth looked too large for his head. 

I was there when he died on the 2nd January 2019.  I sat by his bed as he breathed his last breath.

What my father went through was horrific, and throughout it we were all helpless, at the mercy of the limits of science.  What I learned while Dad was sick is just how little we know about cancer and how to treat it.  It felt like every time I asked a question, the answer was ‘we don’t know’. I felt powerless. I struggled with being unable to do anything to help; I wanted to magic the cancer away

Rachel, her father and brother hiking

Now, three months on, I have the opportunity to take back some control, and do something to raise money and contribute to research that will hopefully, one day, mean that no one need go through what my Dad went through, what we went through as a family.

I read about a trail in QLD that was 161km long, and bookmarked it, as we were due for a family hike.  In 2016, Dad my brother and I hiked Hinchinbrooke Island over 5 days, and it was one of the best things we did together – Dad really loved it.

So when my wonderful friend Chelsea suggested we do a fundraiser for cancer, I knew exactly which walk we should do.  The extra 39km from Ipswich to Brisbane just made the walk a nice round 200km.  We aim to complete the trek over 5 days, raising money for as they fund research into all types of cancer. ”

Support Rachel and Chelsea here

The Fundraising duo! Rachel and Chelsea

Scientists find link between age and different subtypes of bowel cancer

A study by QIMR Berghofer Medical Research Institute has for the first time identified that bowel cancer has five distinct subtypes that are closely related to a patient’s age.

Senior author from QIMR Berghofer’s Conjoint Gastroenterology Laboratory, Associate Professor Vicki Whitehall, said the new way of classifying bowel cancers may have implications for the kinds of treatments patients are offered.

About 17,000 people are diagnosed with bowel cancer annually in Australia and more than 4,000 die from the disease each year, according to the Australian Institute of Health and Welfare.

Associate Professor Whitehall said the study found bowel cancer could be classified according to methylation of the genes – or simply put, how the genes turned on or off.

“Our study found those changes in methylation of bowel cancers closely track with a patient’s age. This may indicate that bowel cancers occurring in younger and older patients may have different underlying causes,” Associate Professor Whitehall said.

“DNA methylation is a way a cell can turn its own genes on or off, but in cancer this process gets hijacked and it turns on genes that favour growth and turns off genes that are meant to suppress it.

“This study suggests we should now focus on how methylation – the switching on or off of genes – causes these five different subtypes of bowel cancer and look for treatments that reduce DNA methylation to reduce the cancer risk.”

Lead researcher Lochlan Fennell said bowel cancer was generally a disease that struck later in life.

“Previous studies have linked DNA methylation to ageing and bowel cancer but ours is the first study to identify five different subtypes of bowel cancer based on this process,” Mr Fennell said.

“We were interested in finding out which genes were being switched on and off in tumours and that’s how we found the different subgroups.

“Our study indicates that the different genetic changes that cause cancer happen at different ages and that might have implications for different treatments, because we know some types respond better to immunotherapy and other targeted therapies while other types are resistant to these therapies.”

The three-year study involved samples from 216 patients at the Royal Brisbane and Women’s Hospital.

The findings have been published in the journal Cellular and Molecular Gastroenterology and Hepatology. The original article can be found on the QIMR Berghofer’s website.

A marathon for Mum

“My name is Glen, I am an average middle-aged guy. I’ve lived in Canberra most of my life, with my wife, Kristy, and children Haydn and Caitln.

Whilst there are many organisations doing great work to support and research different types of cancers and treatments, few are as ambitious or as bold as ACRF, which is why I have put my support toward an organisation with ACRF’s mission of outsmarting cancer.

Around 2010 my wife Kirsty asked me to participate in a fitness fundraising event. So, to prepare I needed to get fit. I started running during my lunch breaks. The first run I could barely run 1K. But I was determined. I ran as far as I could, about 1K. I took note of the post I just passed, then turned around and walked back. Next run, ok to the post and then a couple of 100m more to the gate. I repeated this over several weeks finding a new point each time. Before I knew it I was doing a 7K loop up and over Mount Ainslie multiple times a week.

So what next? Maybe a marathon? Back to training. More running. 42K, Maybe? There is a longer option, if you are up to it, you can pre-register for the ultra 50K. I’m in. But I didn’t tell anyone as I didn’t know if I could do the 42 let alone 50. So, there we are, friends and family cheering me into each he 42 finishing line, I veer to the ultra lane. I could see them saying, ‘Hey where’s Glen going?! He hasn’t stopped!’ And off I go to complete the ultra.

Glen and his Mother, Jan

After Mum was diagnosed she came to watch me run my next marathon, it was an extremely difficult one for me this time around as I was filled with emotions. On completion, Mum told me how proud she was of me. I whispered back to her, “If you keep coming back to watch me, I’ll keep coming back to run the marathon.”

Mum is still here, I am still running. Mum is a real battler and is the bravest person I know. Running and training is hard, but those with cancer and other illnesses are the real heroes. They don’t get the rest after finishing a run or get to stop after crossing the finish line. It’s like Mum is running her own marathon every hour and day. Keep going Mum until you are ready to cross your finish line.

It is hard to understand the impact cancer has on you until it affects someone close to you. Whilst I am saddened and still a little angry that Mesothelioma will take my Mum well before her time, I am hopeful that one day we will find a cure. If we all do a bit to raise awareness and provide support to cancer research, future generations will be able to live without the fear and sadness that cancer brings.

Since there is no one type of cancer, they fund research into them all. I was pleasantly surprised when ACRF contacted me directly to thank me for my efforts and wanted to know more about my story, they sent me a pack of goodies from sponsoring brands and contacted me to personally thank me. It really made me gratified that I chose ACRF when they showed how appreciative they were of my efforts.”

The Epic Ride to Outsmart Cancer: Postie Trek 2019

4,000km, Postie Bikes and 15 riders on a mission to outsmart cancer and pay tribute to loved ones lost and diagnosed with the disease.

Postie Trek is a biennial event started by Daniel Kranz – a father of two from Firefly NSW, to raise much-needed funds for Australian Cancer Research Foundation. The incredible journey across parts of Australia provides an opportunity for Daniel and the other riders to reflect and remember the impact cancer has had on their lives.

To date, Postie Trek has raised over $77k for ACRF. With a route that spans rural towns across northern NSW and Queensland, the Postie Trek riders

Daniel’s Uncle Den

and support staff will at times quadruple the population size of the communities they are visiting – including Bundarra, Moonie, Mitchell, Blackall, Stonehenge, Old Cork, Winton, Yakara, Quilpie, Byrock, Lightning Ridge and Barraba. The tour kicks off on 26 April 2019.

The first Postie Trek, held in 2016, was in memory of Daniel’s Uncle Den. An avid motorcycle fan, Den spent years working as a postie, and passed away from Pancreatic Cancer six-months post diagnosis – he was only in his fifties. The second event was inspired by his grandfather, Murray, who also passed away from cancer. This year, Daniel has set his fundraising target at 100k.

“I wanted to create something positive out of the negativity of losing them,” says Daniel. “Because we had just lost a family member, we wanted the money raised to go to front line projects, to stop anyone else from going through what we had to. We wanted our kids not to have to worry about it.”

In between Postie Treks, Daniel’s wife Hannah was diagnosed with Cervical Cancer. The young mum in her thirties underwent a hysterectomy to remove her entire cervix. The experience has once again reinforced the impact cancer has on all Australians – with one in three men, and one in four women diagnosed with the disease before the age of 75.

Daniel was motivated to create Postie Trek after he was unsatisfied to see similar events with high overheads. He felt very little of the money raised was going towards the cause. Adamant that 100% of the money raised from the event would go directly to the cause, Daniel and the riders rely on community support wherever possible.

The 2019 Postie Trek route will span from Bundarra to Barraba

“Because of the drought and now the flood, we don’t anticipate as much help as previous years from the local community. It’s so hard to tell how much help we will get,” says Daniel. Postie Trek is rallying support wherever possible, and any donations will be truly appreciated.

At the core of the event, Postie Trek is a family endeavouring to grapple with the impact of this devastating disease. “Postie trek is trying to mend a family that’s still very much hurt” says Daniel.

Support to Postie Trek can be made via their Everyday Hero page or Facebook page.

Libby Cuts her Locks for Cancer Research

My name is Libby, and I was diagnosed with Non-Hodgkin’s Lymphoma just before Christmas last year. I feel very lucky to live in today’s day and age, and I wanted to raise money so that treatment could improve further and maybe help someone like me in the future.

I knew that I was going to lose my hair with the type of chemo I was receiving so it was always my intention to shave my head. Firstly, because I wanted to tell cancer that only I say when I lose my hair, and because I thought it would be gross (and scary) to lose hair when it was longer. 

I then realised I could also raise money and help others.  Another ‘take that!’ to cancer! I set my fundraising target at $700, but so far, I’ve raised $4261!

What I found most surprising about my experience with cancer was how advanced modern medicine had become in such a short time. However, there are still so many types of cancers where treatments have not been refined enough and treatments are very intense. I want treatment to be advanced and targeted to the individual’s situation so that they can get better whilst maintaining quality of life.

When I was first diagnosed, I had a trip booked overseas to the UK and Australia, but a week out I was diagnosed with Lymphoma and was forced to cancel my trip – it was a bummer. I am now a little more than halfway through chemotherapy and have just booked my next trip to Fiji.

I feel a part of me come alive when I am dragging that suitcase through the terminal ready to board my flight to my next adventure. I can’t wait.

Thank you all for your generosity and support — it means a lot to me. Together we can help Australian Cancer Research Foundation create the world we want to see

‘Moving target’ breast cancer cells revealed by new imaging technique

WEHI researchers have developed a new imaging technique to visualise key steps in the evolution of cancer cells within tumours, potentially revealing how breast cancers evade treatment.
Microscopic view of breast ducts
A new imaging technique has allowed our researchers
to view tissues and tumours at high resolution that was
previously not possible. This image shows the three-dimensional
structure of mammary ducts of human breast tissue.
Image from Rios, Visvader et al, Cancer Cell.

Using a laboratory model of breast cancer, the researchers were able to view tumours in three dimensions, at previously unachievable high resolution. This revealed how cancer cells develop from pre-cancerous cells in the mammary ducts, and changes that occur in the tumour over time.

The research, which was published in the journal Cancer Cell, suggests that breast cancer cells are inherently changeable, morphing from one cell type to another at the molecular level – resembling cells that are more likely to spread.

At a glance

  • A new imaging technique has provided detailed new views of cells in tumours, revealing the changes that occur as breast cancer develops.
  • The research revealed that ‘pre-cancerous’ cells in the mammary gland only rarely develop into cancer cells, but that once a cancer forms, the cancer cells appear highly ‘changeable’, a feature that may promote resistance to certain therapies.

Viewing cancer cell evolution

The transformation of normal cells in the mammary gland to cancer cells occurs in many stages, with ‘pre-cancerous’ cells evolving into early-stage cancer cells, which may then undergo changes that make the cells more likely to spread away from the tumour. Until now, it has not been possible to visualise individual clones – ‘sister’ cells that descended from a single pre-cancerous cell – within a whole tumour. 

Microscopic image of colourful mammary ducts
Pre-cancerous clones (coloured green, yellow or red)
could be viewed in mammary ducts (blue) using the
new imaging technique. Only a few of these
pre-cancerous clones developed further to form a tumour. 
Image from Rios, Visvader et al, Cancer Cell.

Imaging technology enabled the research team to examine the frequency of pre-cancerous cells that develop into tumours in the mammary gland, and address the behaviour of cells within tumours. The study was led by Dr Anne Rios with Professor Jane Visvader and Professor Geoff Lindeman at the Walter and Eliza Hall Institute. 

“Using a new imaging technique, we revealed that only a small proportion of pre-cancerous cells will develop into tumours,” Professor Visvader said. “In contrast, once a tumour has been formed, we discovered it was very likely for its cells to undergo a so-called ‘epithelial-to-mesenchymal transition’ (EMT). This is a change in the ‘molecular landscape’ – the genes that are switched on or off – within the cell, transforming it from an ‘epithelial’ form, to a ‘mesenchymal’ form that could have a growth advantage.

“Our models suggest that EMT is not a rare event but is an inherent feature of mammary tumour cells.”

Microscopic view of mammary duct
Mammary duct in the breast: The new technique
allows researchers to see into tissues at high resolution. 
Image from Rios, Visvader et al, Cancer Cell.

The results were obtained in laboratory models that closely resemble human breast cancer, and the team suspects human breast cancers are likely to also show a high rate of molecular EMT, said Professor Lindeman, who is also a medical oncologist at the Royal Melbourne Hospital and the Peter MacCallum Cancer Centre. 

“If EMT frequently occurs in breast cancers, it means the cells are a ‘moving target’ – they can evade one set of weapons we have to fight the cancer, meaning we need to develop strategies that are more broadly targeted,” said Professor Lindeman. 

New views into tumours

Researcher with computer
Dr Anne Rios led the study at the Walter and Eliza
Hall Institute

A new three-dimensional imaging technique was critical for the discoveries said Dr Rios, who now works at the Princess Máxima Center for Pediatric Oncology in the Netherlands. 

“Until now it has been challenging to visualise the intricate structures of complex tissues such as breast tissue, or to see the true arrangement of cells within tumours,” Dr Rios said. “We developed a new, rapid way to prepare tissue samples that retains their intricate architecture but allows us to distinguish individual cells and the three-dimensional structure of the tissue.

Microscopic view of a human breast duct
The researchers were able to reveal the intricate structure
of mammary ducts in human breast tissue. 
Image from Rios, Visvader et al, Cancer Cell.

“Our method enabled us to capture previously unseen images of breast tissue and mammary tumours – this was crucial for us to discover the frequency of EMT within the tumours.

“We expect there will be many other applications for our new imaging method, to study normal and cancerous tissue samples,” Dr Rios said.

“We expect there will be many other applications for our new imaging method, to study normal and cancerous tissue samples,” Dr Rios said.

The research was supported by funding from the Australian National Health and Medical Research Council, the National Breast Cancer Foundation, Cure Cancer Australia, the Australian Cancer Research Foundation and the Victorian Government.

Original article published on the Walter and Eliza Hall Institute website.

Cheers to 20 years!

My name is Cameron, and I’m from Aspendale, Victoria. I have a beautiful wife Deb, and two young boys – Koby and Lenny. I love the great outdoors, fishing and hunting.

Cancer struck me at 17 years old, and I was certainly not given good odds of survival. I was diagnosed with Burkitt’s Lymphoma, a form of non-Hodgkin’s lymphoma. In my early years prior to cancer, I was an extremely fit and healthy teen, enjoying multiple games of AFL at school and club level.

After I was diagnosed was certainly the darkest part of my life, and I spent four months in Royal Prince Alfred Hospital on an intensive trial program that was released at the time.

I still today thank the team at the Alfred and my primary nurse. It’s this level of dedication from doctors and nurses that drives me to want to help others.

It was made apparent to my wife and I a long time ago that the ACRF use the funds raised in the most important way – injected directly into research which will ultimately help find a cure.

The initial commencement of our donations was originally started by my beautiful wife, Deb and her mum decided to climb Mount Kilimanjaro after the passing of Deb’s dad and Karen’s husband, Bob Short. Both Deb and Karen started something pretty special with their fundraising.

Although there are many charities out there all doing their bit, we found ACRF to be the best choice. We have been donating for approximately five years now with over $85,000 raised to date. I would like to personally thank all my family and friends for their continued support financially to raise this incredible amount.

We recently held a ‘Cheers to Twenty Years’ party in honour of my 20 years of remission. All the businesses, contacts and in some cases strangers that volunteered their services, made donations for auctions and contributed their time to ensure the night was a massive success. It was a huge joint effort with over 250 people raising $40,310.10 on the night!

Everyone is touched and affected by cancer. It’s becoming too common and it’s a painful process to watch or go through. It’s a disease I personally wouldn’t wish upon my worst enemy, and certainly something you don’t want your loved ones going through. More research is required, and more funding is required – that’s why I support ACRF.

Moonie’s March

“My name is Sarah. I’m the eldest of three children, work in the sports industry and currently live in Melbourne. My Dad, Gary (or ‘Moonie’ as he was affectionately known), passed away from kidney cancer after an 18-month battle in 2018. He was 56.

Unfortunately, Dad’s kidney cancer was Stage Four, and aggressive by the time he was diagnosed. We watched as he tried numerous treatments, and as the cancer took away our strong and healthy Dad.

He was lucky enough to try some trial drugs in some form, but in some cases the cancer was too far progressed in order for him to meet the requirements. Research, treatments and medications have come so far in the last few years, but I still believe that they need as much support as possible to ensure that everyone is given a chance to fight this beast.

Growing up in the small town of Coolamon in NSW, with just over 1500 residents, there was a real sense of local community. My dad spent countless hours volunteering at both the local AFL club, and community showground. When I decided to organize an event to raise money for the Australian Cancer Research Foundation in Dad’s honour, I chose a route that circled these locations to represent the contribution he made to the community on what would have been his 57th birthday.

Moonie’s March is a 5km walk, followed by a BBQ, activities, live music and entertainment. The community is showing incredible support, and we are expecting 250 people to attend. Our goal was to raise $10,000 and we have already hit $11 500 before the event has been held!

They are also using the opportunity to open a new shelter at the local footy oval which will be named after our Dad.

I support ACRF as I don’t want anyone to experience what my Dad or family went through. We are so close to big breakthroughs in cancer research that we can’t slow down – we need to continue to invest and keep momentum in the research that is already taking place. Dad was a big believer in the work that is being done within the cancer research space by doctors and scientists.

Dad’s primary cancer was kidney cancer, but he didn’t have any symptoms until the secondary tumors on his brain started pressing on his nerves. He never had any symptoms, and the doctors said that had no idea how long the kidney cancer had been there. Being diagnosed with Stage Four cancer meant that he was defeated before even starting any treatments. Everyone should be given an opportunity to fight, and win.” – Sarah, ACRF Supporter

‘Cellular barcoding’ reveals how breast cancer spreads

A cutting-edge technique called cellular barcoding has been used to tag, track and pinpoint cells responsible for the spread of breast cancer from the main tumour into the blood and other organs.

The technique also revealed how chemotherapy temporarily shrinks the number of harmful cells, rather than eliminating them, explaining how the cancer could eventually relapse.

Insights from the study, published today in Nature Communications, could lead to new targeted treatments for breast cancer, the most common cancer to affect women.

At a glance

  • A technique called cellular barcoding has been used to understand how breast cancer spreads.
  • The study also revealed how the cancer can relapse by showing that chemotherapy temporarily shrinks harmful cells rather than eliminating them.
  • The precision of this approach could help to focus research efforts and inform more targeted treatments for the prevalent disease.

Dr Delphine Merino, Dr Tom Weber, Professor Jane Visvader, Professor Geoffrey Lindeman and Dr Shalin Naik led the highly collaborative research that involved breast cancer biologists, clinician scientists, biotechnologists and computational experts at the Walter and Eliza Hall Institute of Medical Research.

Pinpointing the ‘seeders’ of disease

Most deaths from breast cancer are caused by the metastasis, or spread, of cancerous cells from the main tumour site into other organs.

Breast cancers consist of thousands of different cell variants with diverse characteristics that may or may not play a role in the metastasis of the cancer. This makes effective treatment a challenge because it is difficult to know which cells are responsible for driving the spread of cancer.

Dr Merino said the ability to pinpoint the ‘clones’ – subpopulations of cells arising from an original patient tumour – responsible for the spread of cancer was crucial for improving treatments.

“Our study revealed that only a select few clones were actually responsible for the metastasis.

“The barcoding technique enabled us to identify the clones that were able to get into the blood stream and make their way into other organs where they would ‘seed’ new tumour growth,” Dr Merino said.

Professor Visvader said the technique also allowed the researchers to see what was happening to the clones after chemotherapy was introduced.

“We used the chemotherapy agent Cisplatin to treat laboratory models developed using donated breast tumour tissue. While the treatment was able to shrink tumours and the size of individual clones, it did not kill them off completely. All the clones, including the nasty seeders, eventually grew again, accounting for cancer relapse.

“These exciting findings would not have been possible without the ability to meticulously barcode and track thousands of individual clones and watch their behaviour over time,” she said.

New technique ‘tags and tracks’

The cellular barcoding technique was developed in 2013 by Dr Naik and Professor Ton Schumacher from the Netherlands Cancer Institute.

Dr Naik said this new technique meant researchers could go from studying thousands of clones, to homing in on the select few variants responsible for the spread of cancer.

“Now that we know which clones are involved in the spread of breast cancer, we have the power to really focus our research to block their activity. For instance, we are curious to understand what is unique about these particular clones that enables them to successfully spread, seed and grow the cancer,” Dr Naik said.

Professor Visvader said the precision of the approach could pave the way for unravelling important mysteries in the field of breast cancer research and equip scientists with the information needed to design highly targeted treatment strategies for the prevalent disease.

“An important goal is to understand the molecular and cellular basis of how breast cancer spreads and, working with clinician scientists like Professor Lindeman, translate this knowledge from the laboratory into the clinic,” she said.

This article was originally posted on the WEHI website.

Hot Rods for Research

“Over the years my wife and I have lost many friends to cancer, as well as knowing many people who have been affected by cancer in one way or another.  To help raise much-needed funds for cancer research, we organized a get together with like-minded Hot Rods and custom cars enthusiasts on the South Coast of NSW.

The weekend starts Friday, with a meet and greet, and on Saturday we head off on a mystery cruise down the coast, stopping to enjoy fish and chips.”

Saturday night we have live entertainment in the Holiday Park until late. Sunday is our major event – the ‘Show n Shine’, where entrants judge six different awards. We have a raffle, and end the weekend at about lunchtime Sunday. It is a great laidback weekend, with great people and cool vehicles. Best of all, we help out two very worthy causes – with everyone who enters making a donation to ACRF and bringing a toy which we donate to Canberra Hospital.

In the last couple of years, my wife lost her sister Vicky. We dedicated this very special weekend to her. We also lost a very close friend to cancer – both had very long battles with cancer and both of them suffered terribly.

Our weekend doesn’t raise a massive amount but they say every little bit helps. Hopefully, someday a cure will be as simple as treating a common cold. There are many kind-hearted people who attend the weekend, many of whom have been affected by cancer. We plan on holding the weekend annually continuing to donate the proceeds to the ACRF.

We were very impressed with what we were told when we called ACRF to find out more about their work. We were also very impressed with how appreciative the ACRF is. You can see how passionate they are about their work.

As I mentioned before, we dedicate the weekend to the memory of my wife’s sister Vicky Hinds. We hope whatever the weekend raises, it is of some help for ACRF’s invaluable research.

– Lee, ACRF Supporter

A new pattern of DNA tags points to a ‘seed’ for cancer

A close-up view of the two meters of DNA inside prostate cancer cells has uncovered new clues about how normal cells turn cancerous.

In a breakthrough study published in Cancer Cell today, a team led by Garvan Institute of Medical Research scientists describes a new pattern of chemical tags found on the DNA inside cancer cells, which reveals new insights into why cancer DNA is read differently than the DNA in normal cells. By better understanding the precise changes that take place when normal cells become cancerous, the researchers hope to uncover new ways to treat or prevent cancer from developing.

“We’ve found a new process in DNA that goes wrong when cancer develops,” says co-senior author of the paper Professor Susan Clark. “We were looking at chemical features or ‘tags’ associated with the DNA that mark which regions are turned on and which regions are turned off.  We found to our surprise a new pattern of chemical tags that spread into regions that are untagged in the DNA of normal cells.”

Uncovering hidden patterns

Uncovering hidden patterns

Cancer cells are the body’s own cells ‘gone bad’ – and the key to stopping the dangerous switch could be hiding in their differences. One such difference, investigated by the Garvan scientists, is the pattern of so-called methyl groups, tiny chemical tags found naturally in cells which can attach to DNA and change how it is read.

In the DNA of cancer cells, some of the regions referred to as ‘CpG islands’ are completely coated with methyl tags – much like heavy snow covering a stretch of road, making it difficult to navigate.

This methyl tag ‘snow’ turns the gene next to the CpG island off by blocking the cancer cell from reading that gene. In normal cells, these CpG islands are untagged, allowing the neighbouring gene to be switched on. “We’ve been interested for a long time in what it is about these CpG islands in cancer cells that allow methyl tags to attach,” says Associate Professor Clare Stirzaker, co-senior author of the paper.

For a more detailed look at these CpG islands, the team used methylation sequencing to analyse all 28 million methyl tags found on the DNA from prostate cancer patients’ cells and compared them with the location of these tags in normal prostate cell DNA.

Lead author Dr Ksenia Skvortsova discovered a surprisingly intricate pattern – around 13 percent of CpG islands were in fact not completely ‘snowed under’ by methyl tags but only partially covered at the borders, like snow spreading into the shoulder of a road.

“We were excited to see this new altered methylation pattern and how common it was in different cancer types – it was something that hadn’t been observed before and provided us with new insights into how DNA is marked and read differently in cancer,” says Professor Clark.

The new pattern pointed the team to a process that regularly occurs at CpG island borders. In normal cells, Dr Skvortsova discovered, CpG island borders are covered in so-called hydroxymethyl tags that are known to remove methyl tags – a ‘cleaning’ process, which the team’s findings suggest is disrupted in cancer.

It’s all in the DNA wrapping

But what is special about CpG island borders that could disrupt the normal methyl tag cleaning process in cancer? To address this question, the team investigated the histones – the molecules around which DNA wraps like a spool, and which help package up the two-meter-long string of DNA found inside just one microscopic human cell.

The team discovered that the histones around which CpG island borders are wrapped have a separate, so-called mono-methylated tag on them. “Interestingly it is these histone tags in normal cells that seem to predispose certain CpG islands to the spreading of methyl tags we see in cancer cells,” explains Dr Skvortsova.

While it is not yet known how the mono-methylated histones might control how methyl tags are added to DNA, the researchers propose that these histones are the key to a sensitive balance of how DNA is correctly read, and which can provide a ‘seed’ for cancer to develop.

“The DNA structure was discovered in the 1950s, it was fully sequenced in the 2000s, but interestingly we still don’t understand how it’s read differently in different cell contexts,” says Professor Clark. “The new tools we are developing to read methyl tags and histone tags bring us closer to deciphering the blueprint of life.”

 

Illustration by Nikita Skvortsov. Original article can be found on the Garvan Institute Website.

The Power of a Single Cell: Safer Bone Marrow Transplants for Blood Cancer Patients

The results of the phase I clinical trial have been published today in the journal Clinical Cancer Research.

The research was led by QIMR Berghofer scientist Dr Siok Tey. Dr Tey is also a bone marrow transplant physician at the Royal Brisbane and Women’s Hospital where the trial occurred.

About 10,000 Australians are diagnosed with blood cancers such as leukaemia and lymphoma each year.

QIMR Berghofer has received four grants from ACRF for cancer research including blood cancer, totaling $8.4M.

Bone marrow transplantation is the only chance of a cure for patients with high-risk forms of blood cancer, Dr Tey said, with about 700 Australians undergoing a bone marrow transplant each year.

“However, there are many others who need a transplant but cannot undergo one because they do not have a suitably matched donor,” she said.

“The key to bone marrow transplantation is the immune cells. Immune cells are a double-edged sword – they are necessary for fighting cancer and infection but they can also cause unwanted tissue damage, known as graft-versus-host disease.

“This is why we generally need to use fully-matched donors. In this clinical trial, for the first time in Australia, we used genetic engineering to make transplantation safer so we could use donors who were only partially matched.

“We take the immune cells from the partially matched donors, then we insert a gene into these cells which enables the cells to be killed off if they cause complications, such as graft-versus-host disease.”

Dr Tey said the genetic engineering was performed at QIMR Berghofer’s cell manufacturing facility, Q-Gen Cell Therapeutics and patients received the immune cells after their bone marrow transplant at the RBWH.

“What we found really amazing was that these immune cells can massively grow in number in the patients,” she said.

“We were able to show, using two independent molecular techniques that a single genetically modified immune cell, when challenged by a cancer, could split into millions and millions of cells within a few days.

“This immense capacity for rapid expansion was something that had not been shown before and really demonstrates the ‘power of one’: One cell, if it is the right cell, can grow rapidly and help control cancer or infection.”

Anthony Takken was 53 years old when he was diagnosed with high-risk acute myeloid leukaemia in 2014.

His only chance for a cure was a bone marrow transplant but he did not have a fully matched donor.

He has siblings but none of them was a full match because even brothers and sisters have only a one in four chance of being a full match.

Anthony became the first person to go on the clinical trial in January 2015.

Dr Tey and her team took immune cells from his brother, who was a partial match, and genetically modified them.

Mr Takken then underwent a bone marrow transplant from the same brother, and three weeks later had an infusion of the gene-modified cells.

“My cancer has now been in remission for 3.5 years. I have a few health challenges but I have returned to work, I’m travelling the world and the doctors say that the chances of the leukaemia coming back are very low,” Mr Takken said.

“At the time I was diagnosed, I was faced with leaving my 16 and 17 old sons to grow up without a father. Thanks to the gene therapy trial, I’ve now made it 3.5 years past my original expiry date!

“I’m grateful that Queensland is a significant hub in the world for this kind of research and treatment and I hope it can continue to be well funded because it gives people like me a chance of surviving and living and contributing to society.”

Dr Tey said although it was a small clinical trial, it was critical in demonstrating the ability of even a single cell, to control cancer and infection.

“Cancer immunotherapy is one of the most exciting developments in cancer treatment this decade. Bone marrow transplantation is actually the earliest form of cancer immunotherapy and continues to be a very effective form of treatment,” she said.

“Our trial gives hope to all the people who haven’t been able to find a suitable bone marrow donor in the past.

“Every day we are working hard to find the next line of treatment for people with leukaemia, people needing a transplant and treating complications from transplant.

“It’s exciting that this huge technological development is happening here in Queensland, at QIMR Berghofer and the RBWH. It is also exciting that this study paves the way for the use of other gene-engineering technology that has supercharged the cancer immunotherapy field in the past five to 10 years.

“We are now working on our next generation of clinical trials to use gene-modified cells to fight blood cancer and treat complications of bone marrow transplantation.”

Article sourced from QIMR Berghofer.

Fine-tuning cell death: new component of cell death machinery revealed

An important component of the microscopic machinery that drives cell death has been identified by Walter and Eliza Hall Institute scientists.

Studying the ‘pro-death’ machinery that forces damaged, diseased or unwanted cells to die, the research team revealed a protein called VDAC2 was critical for the function of a key pro-death protein called Bax.

ACRF has provided $5.1M to WEHI in technology grants since 2001.

The team also showed VDAC2 contributed to the killing of certain cancer cells by anti-cancer agents. The research, published today in the journal Nature Communications, was led by PhD student Dr Hui-San Chin with Professor David Huang, Dr Mark van Delft and Associate Professor Grant Dewson.

Cell Death At a glance
  • The death of cells by a process called apoptosis is essential for the removal of unwanted, damaged or diseased cells, and is driven by a finely tuned protein ‘machine’.
  • The protein Bax is a key component of the cell death machinery, forming part of a complex that takes cells to a ‘point of no return’ in apoptotic death.
  • Our researchers discovered a protein called VDAC2 helps Bax to drive apoptosis, and may have a role in fine-tuning cancer cells’ response to anti-cancer agents.
Driving cancer cell death

A failure of the cell death machinery is a hallmark of cancer cells, and is linked to the resistance of cancer cells to anti-cancer treatments, said Professor Huang.

“Bax is important for helping anti-cancer agents kill cells – without Bax and its relative Bak, cancer cells cannot undergo apoptosis when treated with a range of anti-cancer therapies.

“Our research showed that VDAC2 is required for Bax to drive the response of cancer cells to conventional chemotherapy agents as well as the recently developed BH3-mimetics,” Professor Huang said.

Cell Death machinery

Apoptotic cell death is critical for the development and maintenance of our body, and faults in the protein machinery that drives apoptosis have been linked to a range of diseases. Faulty cell death proteins have been linked to both the development of cancer, as well as resistance of cancer cells to treatment.

A key protein in the cell death machinery is called Bax, Dr van Delft said. “Bax helps to take a cell to a ‘point of no return’ when apoptotic cell death is triggered, forming pores in mitochondria, the powerhouses of the cell. This unleashes the final ‘executioner’ proteins that dismantle a cell.

“Understanding how Bax functions could lead to new therapeutics that either promote cell death – with applications for diseases such as cancer – or therapeutics that prevent cell death, which have the potential to save cells in conditions such as neurodegenerative disorders or stroke,” he said.

The team investigated how Bax and a related protein called Bak kill cells, knocking out the function of different genes using CRISPR technology, Associate Professor Dewson said.

“To our surprise we discovered a gene that was essential for the function of Bax but not Bak, despite these two proteins being functionally and structurally very similar.

“We were able to follow up on this research to show that the protein, called VDAC2, was a catalyst that helped Bax associate with mitochondria and form pores in their membranes, to kill the cell,” Associate Professor Dewson said. “Intriguingly VDAC2’s ‘day job’ is to maintain the function of the mitochondria, pumping metabolites in and out of the mitochondria.”

This article originally appeared on the WEHI website.

Cathy Shows her Support for Cancer Research

“My father died of cancer when I was 15 years old.

My mother’s grandmother died of Ovarian Cancer when my grandmother and her sister were young. They died of the same disease.

In the 1990’s, my mother, her youngest sister and one of my cousins all had breast cancer. In 2014, when my mother was diagnosed with Ovarian Cancer, she was genetically tested for the BRCA gene mutation which notably increases the risk of female breast and ovarian cancers.

When her results were positive, her seven children were then advised to have the same genetic test.

So far, six of us have been tested and I am the only one to get a negative result. My brother was diagnosed with prostate cancer before the genetic testing was done.

All my sisters have taken drastic steps to reduce their risks of getting these cancers – and I had to do something to help, somehow.

I decided to shave my head for ACRF. With the community of Echuca, Northern Victoria, rallying around me, I chopped my waist-length hair off to raise vital funds needed for cancer research.

To my surprise, my modest fundraising goal was quickly reached, and then some! Thank you for your generosity and support — it means a lot to me and the Echuca community. Together we can help ACRF create the world we want to see.”

– Cathy, ACRF Supporter

 

A bump in the road

“My name is Jennifer, I am 20 years old. 2018 was a big year for me. I finished my studies, graduated as a nurse, and two days after my final exam headed off overseas for 3 months to celebrate, tired but excited.

I was also diagnosed with cancer – Hodgkin’s Lymphoma to be exact.  

After two weeks of travel, a large lump appeared on my neck. My aunt, who I was visiting, took to me to their doctor as I was heading to Greece, Portugal, and Morocco the following week. I was feeling a little run down from all the studying, but I didn’t feel sick.

Waiting for appointments, travelling to hospital for tests, more waiting for results. I was anxious and toey. My mum, who is a nurse, rang from Australia and asked the doctor if she should travel to Ireland to be with me for the test results.

“I would,” he said.

D-day comes we we’re and off to Dublin to get what I thought would be the ‘all clear’ to resume my holiday, only to be told that I had Hodgkin’s Lymphoma … whatever that is. I guess my newly printed nursing certificate didn’t cover everything.

Up until then, I thought the waiting was the worst thing in the world, but I was wrong.

There’s a certain six-letter word that begins with ‘can’ and ends with ‘cer’ that is way worse. The mere mention of it stops people in their tracks and makes them reflect upon everything that’s gone before. Every possible outcome is contemplated … starting with the worst. But enough of that.

It was time to go home, start my treatment, and get rid of this “bump in the road” (or lump in my neck, to be more accurate).

So back to Melbourne we came, and back to Cabrini Hospital. I say back to Cabrini because one of my jobs while studying was working there as a unit receptionist. Oh, the irony, from a receptionist, to nurse, to a patient. Thankfully, my doctor was amazing and explained every step of treatment so clearly.

There was an upside to this drama – my mum and dad couldn’t say no to a new dog. We rescued a 10-week old kelpie cross, named Isla. But five days later, she came very unwell and didn’t recover.

The vet couldn’t work out what was wrong and to contemplate putting her down. It felt like the worst day ever. But, I was wrong. I phoned again in the morning to be told that she had died overnight. That was the worst day of the worst week. Someone told me that Isla was sent to me to transfer and take away my pain and sorrow. I like that.

I was determined to lose my hair on my own terms. The thought of losing it during treatment was traumatic.

So, I set up a fundraising page to raise money for the Australian Cancer Research Foundation (ACRF). I asked my friends to come and share the “big day” with me. We had some drinks, some food and lots of laughs. It was very comforting to hear your friends say, “Wow Jen, you look good… no, you really do!”. Even I believed it in the end!

My brother Tom let me cut his hair off also in support and solidarity.

I am still undergoing chemotherapy and have some radiation to go through but Rob, my doctor, has given me some great news: the cancer is gone, and I can skip my last chemo cycle – woohoo!

I was lucky enough to also get a new kelpie puppy, named Gigi. Gigi keeps me busy – she’s a whole new world of trouble!

I want to thank everyone for their support, and best wishes.

Love, Jennifer”

Mutation identified as driver of resistance to breakthrough drug

Melbourne researchers have identified a gene mutation in the leukaemia cells of patients who become resistant to venetoclax, a discovery which can be used to identify those at-risk of relapse and help improve outcomes from this breakthrough blood cancer drug.

Venetoclax was developed based on discoveries made in Melbourne at the Walter and Eliza Hall Institute (WEHI) around 30 years ago. The BCL2 inhibitor can induce long-term remissions in many patients with Chronic Lymphocytic Leukaemia (CLL) where other standard treatments are not effective.

Early support by ACRF to WEHI for the development of Venetoclax has been key to the drug’s development.  ACRF has provided three grants, totalling AUD 5.5 million towards cutting edge cancer research equipment and technology.

‘Late Breaking’ research into gene mutation

However in some patients on venetoclax for CLL their disease will progress and, until now, factors leading to this have remained unknown. The study – involving Peter Mac’s Dr Piers Blombery and collaborators at the Walter and Eliza Hall Institute, Royal Melbourne Hospital and University of Melbourne – found a specific genetic mutation developing in the leukaemia cells of seven patients who relapsed while taking venetoclax.

Dr Blombery presented the results of this research in the prestigious “Late Breaking” session at the American Society of Haematology (ASH) annual scientific meeting, in San Diego, overnight.
“We conducted a genomic assessment of cancer cells from relapsing disease in patients and found a very specific single mutation in BCL2, the target of venetoclax, which significantly reduces the drug’s efficacy against the leukaemia in these patients,” Dr Blombery says.

“Importantly, this mutation could be detected in the bone marrow in some cases years before a patient’s disease would clinically progress, so this opens the door for testing to identify those at-risk so we can potentially intervene before overt relapse occurs.”

Key Clue to help develop combination treatments with Venetoclax

Dr Blombery said the study also pointed to other, as yet undiscovered, drivers of venetoclax resistance in patients and the genomics work would continue.
Professor Andrew Roberts, from the Walter and Eliza Hall Institute, said the research was only possible because of long-standing collaborations and fantastic teamwork between clinicians and laboratory scientists from many disciplines.

“Venetoclax remains a very effective treatment for CLL. This key clue should help us develop combination treatments with venetoclax that are even better for people with CLL,” Prof Roberts also says.

Supporters of this research include the Snowdome Foundation – which has a mission to accelerate new therapies for Australian blood cancer (myeloma, lymphoma and leukaemia) patients to help them live longer, better lives – and the Christine and Bruce Wilson Centre for Lymphoma Genomics based at Peter Mac; Vision Super, the Leukemia and Lymphoma Society (USA), the Leukaemia Foundation, NHMRC, Australian Cancer Research Foundation and Cancer Council Victoria.

This article and image originally appeared on the Peter MacCallum Cancer Centre website.

 

Cutting off Melanoma’s Escape Routes

Stopping melanoma from spreading to other parts of the body might be as simple as cutting off the blood supply to the cancer, according to researchers.

Scientists from The University of Queensland’s Diamantina Institute have discovered stem cells which form blood vessels in tumours, and have identified how to ‘switch the cells off’.

Professor Kiarash Khosrotehrani said the study’s findings had enormous implications for cancer patients.

“Blood vessels are vital because tumours can’t grow without them – they feed the tumours and allow the cancer to spread,” Professor Khosrotehrani said.

The Australian Cancer Research Foundation has given $16.1M in funding to the Diamantina Insitute since 1999, including this year’s major grant related to the early detection of melanoma.

Blocking Blood Vessels Development may be Key

“If you get rid of these stem cells, then the blood vessels don’t form and the tumours don’t grow or spread to other locations.”
Professor Khosrotehrani said being able to block blood vessel development could be useful in treating recently diagnosed patients as it may help to prevent the cancer from spreading at an early stage.

“This idea has been around for a while, but it has proven difficult to achieve because blood vessel formation is a fundamental mechanism by which our body responds to injury,” he said.
“Directly targeting the stem cells that form these blood vessels is a new approach that could make the difference.”

The research team will test the ability of a compound to stop these stem cells from forming blood vessels, in a study supported by National Health and Medical Research Council (NHMRC) funding.

Future Research into Melanoma

Researcher Dr Jatin Patel said melanoma’s ability to quickly spread from the skin to other parts of the body was what made it so deadly.

“We know that before tumours spread to places like lymph nodes or lungs, the body starts growing extra blood vessels in these areas – almost as if preparing special ‘niches’ for the cancer,” Dr Patel said.

“Our next study will focus on blocking the development of these niches.

“If the body doesn’t prepare them, then the cancer won’t grow there.”

This article originally appeared on the Diamantina Institute website.  Featured image: Professor Kiarash Khosrotehrani

Charlie’s Bold Act to Outsmart Cancer

My name is Charlotte, but I usually go by Charlie. I’ve just recently turned 18 years old.

Throughout my life, I have witnessed people being destroyed by a loved one’s death due to cancer. I have had firsthand experience myself of losing my grandad and watching him wither away, even if he did do it with a smile. It only makes sense to me to do something to even just make the experience just that slightly less painful.

I knew that I had to do something loud to get people’s attention. You never know when a cancer discovery might be made, and I want to help in any way I can.

Because of this, I decided to shave my head.

When I was around seven, I experienced two major events that motivated me to take action to help outsmart cancer. The first was the death of my best friend’s mum, Anna, and my grandad. When you are so young, you don’t remember the exact details of each diagnosis, but what stays with you is the feeling.

My best friend’s mum, Anna, was just 40 years old when she passed away due to cancer. I remember playing at my friend’s home, running through her parent’s bedroom, where Anna would be most of the time. We were talking to her and, I remember this very clearly – she took her wig off because it was itching her.

As she had some hair growing back, I believed that she was getting better. Not long after, she passed away. My best friend Nefeli, her brother and especially her dad, handled the passing with immense strength. But there are times I remember us crying together, messy cries.

The other event was my grandad, he died a few months before Anna. It was a very different experience. He died very suddenly.

I remember him leaning over the couch to scare me whilst I was watching TV, and as he made me jump, I grabbed onto arm. He didn’t shout but made more of a loud sound that I never heard him make before – I thought he had only hurt his back.

Seven weeks later he passed away from an aggressive form of cancer.

The last time I saw him he was in his hospital bed, looking very skinny and dehydrated, but was still smiling and cracking jokes.

One night in the hospital he was at, I went outside in the corridor and shushed a doctor because “my grandad is trying to sleep!” the next day, I heard that made him giggle.

A few days later he left the world. It affected us very heavily, and everyone that knew him. My grandma moved in with me and my mum, and we had some very sad, but in a weird way, lovely moments together crying.

Shaving my head for cancer research was one of the best things I’ve ever done. It gave me a true sense of purpose by helping other people. ACRF were so supportive throughout, they kept in touch and offered different ways to fundraise.

I felt like I was actually doing something that mattered and was a part of making a better future for everyone. That feeling of satisfaction is hard to find anywhere else.

A legacy of Cancer Research in Joan’s Honour

After 47 years of marriage, Reg Kelsey’s wife Joan passed from breast cancer. Reg chose to honour Kelsey’s life through including a gift in his Will to the Australian Cancer Research Foundation. He encourages others to do the same to help avoid what Joan went through.

Reg was a 23-year-old ambitious young man and rode motorbikes. Joan was a 21-year-old from a good Adelaide family. He spotted her while riding past her house one-day.
“She was standing out front and our eyes locked. Each day thereafter, I smiled at her.

Several months of ‘drive-by-smiling’, Reg asked her out.

He was pleasantly surprised to learn Joan shared his love of motorbikes!

“Not only did she like motorbikes, but she was also an accomplished piano player, was smart and vivacious. I felt very lucky indeed!

As Reg worked his way up the ladder in the motor-industry, he was on the road a lot. Without a permanent address of his own, he boarded with Joan’s parents. On weekends they rode motorbikes.
After three years of courting, aged 23 & 27 years, Reg and Joan married.

“We were very well suited. You don’t have 47 years of marriage unless you’re well matched.”

Joan and Reg had a daughter, then Joan returned to the workforce.

“Joan was a fast learner and quickly gained work as a doctor’s receptionist. We became friends and socialised with the doctor and his wife. This made it easier when the doctor gave Joan the news she had breast cancer. Joan was just 38-years-old. Our daughter was 14.
“When Joan went for her operation, the doctor called me mid-surgery to confirm she needed a mastectomy. I just said, “do what you need to do, Doc.”

Despite the surgery, the cancer eventually returned.

“It spread to the kidneys and finally the spine. After 3 months in hospital, we discussed palliative care and I asked Joan what she wanted. She said she wanted to go home.”

“I fulfilled her wish but she only lasted 3weeks. She passed in our home aged 70yrs. The saddest part is that we didn’t get to enjoy retirement. Joan was just too sick.”

Reg remains thankful for the time they had.

“You can only play the hand you are dealt. I still feel pretty lucky she said yes! After he retired, Reg drew up his Will, and decided to include a gift to ACRF.

A bequest to research is the best way I can think of to help end cancer. “

New Venetoclax combination brings breast cancer hope

Combining two cancer drugs has seen a potential breakthrough for women with metastatic breast cancer.

In a world first, breast cancer researchers at The Royal Melbourne Hospital and Peter MacCallum Cancer Centre, successfully combined a drug that has shown promise in the treatment of chronic leukaemia with therapy used to treat breast cancer.

The Royal Melbourne Hospital’s and Peter MacCallum Cancer Centre’s medical oncologist, Professor Geoff Lindeman, principal investigator of the study, said the combination of the two drugs has given researchers and patients a boost in tackling metastatic breast cancer. Professor Lindeman is also a researcher at the Walter and Eliza Hall Institute.

“The primary aim of the study was to determine the safety and tolerability of venetoclax in combination with tamoxifen,” Professor Lindeman said.

ACRF has awarded The Royal Melbourne Hospital with $1M in grants, and Peter MacCallum Cancer Centre $7M since 2003, for cutting-edge cancer research equipment and technology.

“We tested this combination on the basis of our laboratory findings at the Walter and Eliza Hall Institute. Venetoclax is a drug that switches off BCL-2, a protein that helps keep cancer cells alive. Our findings suggested that adding venetoclax to conventional hormone therapy might boost responses.”

“Although the study was aimed at determining safety and finding the right dose, we found that 75% of the women involved in the study experienced an overall improvement or derived clinical benefit.”

“This result has provided a basis for further studies with venetoclax, where the hope would be to produce deeper and more durable responses for women affected by breast cancer.”

Professor Lindeman added this was the first time Venetoclax has been used on solid tumours. “Venetoclax is not currently approved in breast cancer and further studies will be required to determine its effectiveness,” Professor Lindeman said.

Venetoclax was developed based on a landmark discovery made in Melbourne during the late 1980s by Walter and Eliza Hall Institute scientists, that the BCL-2 promoted cancer cell survival.

“There were 42 women enrolled in the study, which was conducted at The Royal Melbourne Hospital, Peter MacCallum Cancer Centre and Olivia Newton-John Cancer Centre over the last three years.

“The drug was well tolerated, and the majority received the maximum dose with minimal side effects. We have now established a new benchmark dose for future studies.
“We are excited by the findings and what it could mean for patients with incurable hormone receptor-positive breast cancer.”

The research, published today in the journal Cancer Discovery, was supported by AbbVie and Roche/Genentech, the National Health and Medical Research Council, Victorian State Government through the Victorian Cancer Agency and Operational Infrastructure Support Program, National Breast Cancer Foundation, Australian Cancer Research Foundation, The Qualtrough Cancer Research Fund and Joan Marshall Breast Cancer Research Fund.

This article originally appeared on the Royal Melbourne Hospital Website.

$16.4 M to accelerate leading cancer research in Australia

ACRF 2018 Grant News

SYDNEY, NSW – The Australian Cancer Research Foundation (ACRF) has announced this evening $16.4 million in four technology grants to initiate and accelerate further ground-breaking cancer research in Australia.

“Every year ACRF encourages the Australian cancer research community to propose projects that are innovative and have great potential to make a significant impact on cancer prevention, detection and treatment,” Professor Brown said.

A flagship diagnostic centre to improve the early detection of melanoma will be established with a major $9.9 million grant. The ACRF Australian Centre of Excellence in Melanoma Imaging and Diagnosis is set to revolutionise the early detection of melanoma.

“The centre will advance the early detection of melanoma, Australia’s ‘national cancer’, and is a world first,” Professor Brown said.

This project will implement cutting-edge imaging technology in combination with a multi-nodal telemedicine network across Queensland, New South Wales and Victoria and significantly enhance the capability of clinicians and researchers to detect and understand melanoma.

The 3D imaging system takes a total body image in m­­­­illiseconds, giving dermatologists the ability to detect skin cancers in a patient even from the other side of the country. A telemedicine network will significantly benefit rural and remote communities.

Approximately 100 000 individual scans from high risk groups will be completed in the first three years. Australians experience 12 times the global incidence of melanoma. It is the most common cancer in Australians aged 15 to 39.

Three other grants were awarded by the Australian Cancer Research Foundation for 2018.

The recipients include:

  • ACRF Facility for Innovative Drug Discovery – $2 million to develop revolutionary drug discovery technology for cancers with no approved therapy available or requiring improved treatments. Hosted at Bio21 Molecular Science and Technology Institute (VIC).
  • ACRF Centre for Integrated Cancer Systems Biology – $2.5 million for technology to provide new personalised approaches to interrogate cancer biology. This will significantly enhance the translation of cancer research from the laboratory to the patient. Hosted at South Australia Health and Medical Research Institute (SA).
  • ACRF Centre for Compound Management and Logistics – $2 million to establish a transformative acoustic compound management platform with integrated software to enable Australian cancer researchers to access the most advanced drug combinations used in cancer clinical trials. Hosted at compounds Australia, Griffith University (QLD).

“All grant applications are critically evaluated by a team of leading international cancer scientists and clinicians who recommend the projects that will make major impact nationally and globally to the ACRF board,” Professor Brown concluded.

Support for personnel to be involved in the projects has been secured via the NSW government through Cancer Institute NSW ($300,000 over 3 years for the ACRF Australian Centre of Excellence in Melanoma Imaging and Diagnosis) and Ovarian Cancer Research Foundation ($333,000 over 3 years for the ACRF Facility for Innovative Drug Discovery).

The grants were announced at a reception hosted by the Governor General of the Commonwealth of Australia, His Excellency General the Honourable Sir Peter Cosgrove AK MC (Retd) and Lady Cosgrove, tonight at Admiralty House in Sydney.

Carol Shaves her Head in Honour of Friend

We all know someone who has been affected by cancer, and each person’s journey is unique.

In honour of my friend Briohne, who did not survive breast cancer, and the many other courageous people who are affected by this disease, I decided to raise funds for the ACRF through a head shave.  My own mother died of cancer 17 years ago and in the years since her death, there have been many advances in cancer therapies owing to research funded by organisations such as ACRF.

Shaving your head is definitely bold – thankfully it’s a great way to encourage donations because it never fails to get noticed! I am extremely proud to have nearly achieved my fundraising goal of $1,000  in honour of my friend and her favourite charity. Plus,  I like my new look.

It was from Briohne that I first learned about ACRF.  Whilst undergoing cancer treatment, she co-created the Silk Rags Project. The project is a stage performance and musical about four women and how they journey through their respective lives, focusing on a recent cancer diagnosis. Silk Rags is about not letting your struggle become your identity, a message that will resonate with so many. Every performance raises funds for cancer research and is a beautiful legacy to her.

Looking forward, I want to continue supporting the ACRF as they can help so many people who are experiencing the effects of cancer.

Caring for the Caregiver

ACRF is pleased to continue a connection with CancerAid – the app which assists cancer patients and their caregivers. One of these caregivers is Lisa, whose father was diagnosed with Stage IV tongue cancer. She shares her heartbreaking story below.

“I wasn’t prepared for the impact of my father’s cancer. The story of my father’s cancer is now our family story. Our story begins when my father was diagnosed with Stage IV base of the tongue cancer.

It is a story I continue to tell, so that other families have the knowledge and the power to help each other.

Our story is a seven-year journey of my father living with chronic pain, losing his ability to eat and drink, spending the last four years of his life surviving solely on a peg tube with severe nerve
damage.

Nerve damage so severe that his entire body would twitch and nothing could help him, nothing could alleviate his pain.

Nerve damage so severe I would walk into my parent’s home and hear my father screaming in pain rendering us all helpless. Nerve damage so severe that my father was housebound the last two years of his life, missing countless family moments.

My mother was my father’s primary caregiver throughout his entire illness, and she did this with unconditional love, dignity and grace. If love could have saved my father he would be here right now. Even as I am writing this, I am not sure how my mother was my father’s sole caregiver for so long.

My mother is the definition of strength and courage while surrounded by heartbreak and human suffering. But caring for a loved one strains even the most resilient, loving people.

When an oxygen mask descends in front of you on an aeroplane, the first rule is to put your own mask on prior to assisting anyone else.

Only when we first help ourselves can we effectively help others and that rule also applies to caregiving. The life of a caregiver is not easy, but when your needs are taken care of, the person you are caring for will benefit as well. Below are some tips on taking care of YOU while caregiving for a loved one.”

Lisa offers the following advice to caregivers going through a similar experience to hers:

1. Set realistic goals – prioritize, make lists and establish a daily routine. Start saying no to requests that are draining, such as hosting holiday meals.
2. Be honest with yourself. Ask ‘am I capable of taking care of my loved one all by myself? Do I need to hire outside help or consider assisted living?’
3. Get connected – Find out about caregiving resources in your community. A support group can provide validation and encouragement, as well as problem-solving strategies for difficult situations.
4. Set personal health goals – Including goals to establish a good sleep routine. Find time to be physically active, eat a healthy diet and drink plenty of water.
5. See your doctor – Get all recommended vaccinations and screenings. Make it a priority to see your GP. Make sure to inform your doctor that you are a caregiver.

The CancerAid app is available for free to download and use on Android and Apple devices.
If you, or someone close to you, are diagnosed with cancer and you wish to use the app, Click Here

Dreamlab delivers a new way of making sense of cancer

Research by the Garvan Institute of Medical Research has revealed a new way to group cancers based on their DNA ‘signatures’.

This discovery, among others, is based on data analysed through Project Decode on the DreamLab app, which was fuelled by the growing phenomenon of citizen science.

The findings, posted on BioRxiv (a preprint server) are the product of analyses of 3750 genomes spanning eight different cancer types.

Researchers have found a new way to ‘cluster’ cancers together, grouping individual cancers in a way that could indicate the best treatment for each one.
While the findings are preliminary, it is hoped that this new way of classifying cancers could bring the medical world a step closer to realising the potential of personalised medicine – providing treatment and monitoring that’s targeted to each individual patient.

DreamLab, an innovation created by Garvan and The Vodafone Foundation in Australia, works by harnessing the idle processing power of users’ smartphones to solve complex cancer problems and send the results back to Garvan for analysis. Over 300,000 people have downloaded DreamLab and joined the ‘citizen science’ movement.

Dr Mark Pinese, Senior Research Officer at Garvan, is encouraged by what these initial findings could mean for future cancer treatment.

“By using the power of DreamLab to crunch genomic data from The Cancer Genome Atlas (TCGA), our team of researchers uncovered a new way of looking at mutations in cancer,” said Dr Pinese. “This is an interesting finding as in the clinic it could help us determine which type of cancer a patient has, and the best treatment for that cancer. This is a key goal of personalised medicine.”

 From body parts to DNA signatures

Traditionally, people think of cancer as being specific to a body part – such as lung cancer or breast cancer. However, researchers now know that it is predominantly the DNA changes in an individual’s cancer, not its tissue of origin, which sheds light on how to best treat and manage it.

Scientists are still in the early stages of understanding exactly how to read a cancer’s DNA for clues as to how best to treat it, and how aggressive it is. So far, researchers have mostly looked for DNA changes in one or a few genes at a time– but the new DreamLab-enabled research takes a more sophisticated approach, looking instead for changes in groups of 7-20 genes.

The DNA-protein connection: uncovering hidden ‘cliques’ 

Genes inside people’s cells code for proteins, and proteins carry out the work of the cell – so gene changes can affect how proteins work. Importantly, proteins are constantly interacting with one another as they carry out the cell’s work.

To achieve this, the researchers used a novel technique, called EPICC (Experimental Protein Interaction Clustering of Cancer), to cluster cancer patients based on DNA mutation profile, leveraging knowledge of protein-protein interactions to reduce noise and amplify biological signal.

The researchers wanted to know whether groups of interacting proteins – which they call ‘cliques’ – might hold the key to how best to treat cancers. They reasoned that the cancers with changes in the same clique of proteins would be controlled in similar ways, and might therefore respond similarly to treatments.

The Garvan team matched the gene changes in 3750 cancers with the corresponding protein changes and interactions across a massive network of about 20,000 proteins.  This revealed 141 different clusters, which were agnostic of the cancer’s tissue of origin.

Dr Catherine Vacher, is the co-first author on the paper.

“We used an algorithm that can detect communities in social networks to identify groups of proteins that interact with one another – which we call ‘cliques’ – that were altered in the cancers,” Dr Vacher said. “We see a future where one day a genomic test could classify a patient’s cancer and give their oncologist insight into the best treatments for that patient.”

 Citizen science doubling the speed of research

Through the assistance of The Vodafone Foundation’s DreamLab app, Garvan was able to harness the idle processing power of thousands of smartphones across Australia, and more recently in New Zealand and the UK, to halve the time it would have otherwise taken to crunch the data in Project Decode.

“With one in two Australians set to be touched by cancer directly at some stage in their life, we see Garvan’s research as vital to improving the health of the nation,” said Megan Retka-Tidd, Head of The Vodafone Foundation. “Garvan’s initial findings are truly exciting and point to the power of handheld technology, combined with leading scientists, to help speed up cancer research. Collectively, DreamLab users donated sixty million hours to Project Decode to speed up this research.”

Dr Swetansu Pattnaik, is the co-first author and bioinformatician at Garvan.

“Citizen Science, such as the contribution of thousands of people to DreamLab, is truly astounding,” Dr Pattnaik said. “While these are early findings, we look forward to the global medical community poring over, critiquing and adding to them.

“We are already working to translate this clustering approach into clinical practice in the future.”

 Project Demystify launches on DreamLab

Coinciding with the release of the initial Project Decode findings, the next research project – Project Demystify has launched on DreamLab.

Project Demystify seeks to understand, or connect the dots, between physical human traits – hair colour, height, blood pressure, and, at times, symptoms of disease – and their genetic basis.

To achieve this, existing data on individuals’ traits (which will be sourced from clinical information and wearable devices such as fitness wristbands) will be correlated with individuals’ genetic information.

However, to do this correlation is not simple. Complex calculations are required to determine correlations between different traits. These calculations need huge amounts of computing power, and it is these calculations that will be computed via Project Demystify on the DreamLab app.

People are encouraged to download DreamLab from the App Store and Google Play Store.

The DreamLab app was built by Transpire, with Amazon Web Services Australia generously powering the DreamLab server.

– ends –

This release originally appeared on the Garvan Institute’s website.

Julie Organises Golf Day Fundraiser

We often read about the importance of listening to our body and to not neglect having health checks.  It is sound advice and something which I ignored until it was nearly too late.

In 2017, I was diagnosed with stage 3 bowel cancer and my doctor said a delay of another month would have meant less than a year to live. I’m happy to report that surgery was successful, and I have now been in remission for just over a year.

Experiencing first-hand the impact of cancer, I decided to get involved in raising awareness about bowel cancer and fundraising. I am hooked on golf and know the game is a great way to reach out to other people so a Ladies Golf Day was organised for September at the Glades Golf Course, Gold Coast.  Several other enthusiastic golfers joined me and the day was a huge success.  $4,000 in donations was collected for ACRF.  Plans are also confirmed for another golf fundraising event in December.

I am confident that scientific research will someday result in an enduring end to cancer.  In the meantime, please learn from me – don’t put off taking advantage of cancer checks!

Saigon Boys Turn Up the Music for ACRF

I’m Duc, the band leader and manager of the Saigon Boys Band, a Vietnamese pop group established in 2015. We perform mostly at local clubs in south-western Sydney during the weekends.

I have family members and friends who’ve passed away from cancer and the other band members all know of someone who has been affected by cancer.  Because of this, we believe the most important thing is to find a medication or vaccine that will ensure a cancer-free future for everyone.  We wanted to help raise money for more cancer research, and we felt the best way for us to do this was putting on a concert.

As a group that’s been performing for a few years, hosting a charity event wasn’t too difficult for us to organise.  We decided on a date in September, the location, and then posted details of the performance on Facebook.  We set up in Freedom Plaza – choosing an outdoor pedestrian mall in Cabramatta’s CBD so weekend shoppers could take a break, sit and listen to our music, enjoy the good weather and learn about ACRF.  Our stage was decorated with ACRF balloons and we had volunteers placed with donation boxes.  There was a great turnout of people on the day, and we were very happy that so many in the community made contributions. The event was a great success.

I would encourage others to fundraise.  Supporting ACRF and their cancer research work is the best way to stop more people dying every day of cancer.

 

Share your story

Chris to run 12 marathons in 12 days for ACRF

Chris Glacken’s dedication to supporting ACRF is inspiring. He is an incredibly selfless individual and is committed to raising $100,000 for cancer research. We could not be more appreciative. His most recent event, the Alanis 12, will see him run 12 marathons in 12 days.

“Both my parents have lost their battle with cancer within the last two years. They were both the same age, diagnosed with the same stage of cancer. Mum passed away only a few months ago in May this year.

I made a promise to my father a few days before his passing that I would continue the battle against cancer. Many other friends, including my sister and brother in law, have also been touched by cancer this year.­­

It was cruel to witness something so heartbreaking and feel so helpless.

I was inspired to create the Alanis 12 as the first Australian event that will challenge anyone who would like to have a crack at completing all 12 marathons. I named the event after my guardian angel, Alanis Morissette, whose music I listen to every time I run.

When I stand at the starting line of my events and brief the participants, it always amazes me to see how many put their hand up when asked if they have been affected by cancer in some way. I believe that if you give people a purpose, they will help – and those who run with me prove this.

It’s tough running so far and so often but nothing compared to what others are suffering through cancer.­

We are running for those who can’t.”

 

Share your story

Jola Adventures in the Arctic for Cancer Research

“My name is Jola, and I have a huge taste for adventure. In the past, this has led me to climb mountains and cycle extreme distances, but to fundraise for ACRF I decided on something a little different: hiking in sub-arctic conditions through Iceland, Norway and Greenland.

Last year, I lost a beautiful friend Michelle to cancer. After her passing, I had one enduring thought that I could not shake: that I could be next.

How is it possible to beat this terrible disease that so many people are affected by? When you lose so many people to this terrible disease, cancer takes on a personal quality. As a scientist, what made sense to me was focusing on raising money for cancer research, with the dream that one day a world without cancer would be possible.

This was the decision that lead me to my life-changing arctic adventure.

Did I mention that I do not like the cold at all, that I’m scared of heights, and that I’ve never even walked with crampons before? Sub-arctic temperatures are no joke – with conditions averaging around -6 degrees Celsius, the icy winds relentlessly beat at you, and your hands and toes start to freeze. It takes so much energy just to function, not to mention what it takes to push yourself physically and mentally through challenges.

But, with my goal in mind, I hiked land and glaciers, scrambling along the uneven frozen terrain. I tried my hand (literally) at ice climbing, scaling frozen glaciers at 700m altitude. I kayaked in between icebergs and even snorkelled through freezing, dark water. Although challenging doesn’t even begin to cover how this felt, in the end, I pushed myself completely out of my comfort zone. It was amazing.

Despite all the physical and emotional challenges that were brought before me, I carried with me a sense of drive that was seeded in all those who were trusting me to complete this trip. I was proud to feel like what I was doing was more important than the immediate challenges before me – it was something important for everyone. And in the end, I felt like a superhero.

 ACRF has one singular goal: To outsmart cancer. By providing the brightest minds in Australia the tools they need to make ground-breaking research discoveries, we believe this is possible. Please, donate today to support people like Jola and their immense contribution to moving forward into a cancer-free world.

Some breast cancers have a pause button

Breast cancer is the most commonly diagnosed cancer in Australia. It claims the lives of eight women every single day.

Tumours that are contained to the breast are usually treatable. Five-year survival rates have risen to an impressive 90% over recent years. But for those diagnosed with aggressive types of breast cancer, there are fewer treatment options and still much that we don’t know.

It’s the spread of breast cancer — or metastasis — that makes it deadly.  When cancerous cells from the tumour break away and move to other parts of the body, treatment becomes much more difficult and less effective.

Preventing metastasis: the spread of breast cancer

A study from Garvan Institute and US researchers has shed new light on the harmful spread of breast tumours. It provides insight into new approaches we might use to stop their growth and spread.

ACRF has provided three grants to Garvan since 2003 for cancer research, totalling $6.1M.

When cancer cells break away from the primary tumour, they travel elsewhere and eventually grow into robust secondary tumours.

The new research has uncovered a natural process: the primary tumour can signal the immune system to follow the breakaway cells and ‘freeze’ them. In this paused state, the cells can’t grow effectively — thereby stopping secondary tumour growth in its tracks.

Although this research was done on mice, there are indications the same process may also happen in people.

Tumour signalling may lead to new cancer treatments

We still don’t know why some tumours pause their own spread; but we know it’s a promising avenue for future treatments.

“We want to understand exactly what the tumour is releasing to activate this immune response, and how immune cells are targeting the secondary sites,” concludes Dr Christine Chaffer who co-led the research. “In principle, all of these steps present therapeutic opportunities that could be used to stop a cancer from developing any further.”

If we can exploit this naturally occurring signalling process in breast cancer, we may eventually find the controls that pause other types of cancer as well. These findings suggest exciting new treatment approaches and avenues for further research.

Broadly considered, these findings suggest a future where people can live with cancers they might otherwise die from.

This article originally appeared on the Garvan Institute website.

At ACRF, we are committed to finding better ways to treat breast cancer and to prevent this cancer from affecting the lives of so many women. To learn more about our commitment to funding world-class breast cancer research, as well as research into other common women’s cancers such as cervical and ovarian cancer, discover Amelia’s story through our Women’s Appeal. Learn how you can help ACRF provide life changing support for women like Amelia.

Study Finds Spider Peptide Slows Melanoma Growth

An international study has discovered that a compound extracted from the Australian funnel-web spider is highly effective at killing melanoma cells, as well as cells taken from facial tumours on Tasmanian devils.

It is believed to be the first time the spider-derived peptide has been found to have anti-cancer properties in melanoma and Devil Facial Tumour Disease (DFTD) cells. The findings mean the compound could potentially become the basis for a new treatment for DFTD and melanoma in future.

The study was led by QIMR Berghofer researchers Dr Maria Ikonomopoulou and Dr Manuel A. Fernandez-Rojo, along with collaborators from the Institute for Molecular Bioscience at the University of Queensland.

ACRF has awarded QIMR Berghofer $8.4 million in grants since 2002 for cancer research.

‘Very promising’ early results

The researchers tested the peptide – which is very similar to the known Gomesin peptide from the Brazilian spider Acanthoscurria gomesiana – in a series of laboratory experiments.
Dr Maria Ikonomopoulou, who led the study, said the early results were very promising.

“We decided to test this spider compound because it was very similar in chemical composition to a compound from a Brazilian spider, which was already known to have anti-cancer properties although it had never been tested in devil facial tumour cells,” Dr Ikonomopoulou said.

“In our laboratory experiments, we found that the Australian funnel-web spider peptide was better at killing melanoma cancer cells and stopping them from spreading than the Brazilian spider peptide. Additionally, the Australian spider peptide did not have a toxic effect on healthy skin cells.

“When we tested the Australian spider peptide on human melanoma cells in the laboratory, it killed the majority of them. We also found the peptide slowed the growth of melanomas in mice.”
Dr Ikonomopoulou and Dr Fernandez-Rojo also tested the compound on cells taken from facial tumours on Tasmanian devils.

“Similar to the effect in melanoma cells, we found that the Australian spider peptide killed the DFTD cells, but didn’t affect the healthy cells as much,” she said.

“We also experimented with different versions of the compound to try to find which one would be best at killing the DFTD cells,” she said.

“When we altered two particular amino acids in the peptide chain, the compound became even better at destroying the DFTD cells”.

“This research is still at a very early stage, but these results are very promising. There are many years of work ahead, but we hope that this compound could in the future be developed into a new treatment for melanoma and DFTD.

“These findings prompt us to continue investigating the potential of bioactive compounds derived from venom to treat melanoma, liver diseases, obesity and metabolism, as well as against the Tasmanian devil tumours in collaboration with the biopharmaceutical industry.”

Dr Ikonomopoulou and Dr Fernandez-Rojo are now based at the Madrid Institute for Advanced Studies, IMDEA-Food.

The findings have been published recently in two separate studies in the journals Scientific Reports and Cell Death Discovery.

This article originally appeared on the QIMR Berghofer website.

Discovery paves way for improved ovarian cancer care

Melbourne scientists have revealed a better way to identify which patients should respond to powerful ovarian cancer drugs called PARP inhibitors (PARPi), resolving an important question in ovarian cancer care about why some patients respond to the drugs, while others do not.

The findings add to a vital ‘checklist’ that helps match ovarian cancer patients with the right therapy for their cancer. Being able to offer targeted treatment is crucial for patient survival rates which have seen little improvement over the past 30 years.

The study, published in Nature Communications, was led by Professor Clare Scott, Dr Olga Kondrashova, Dr Matthew Wakefield and Dr Monique Topp from the Walter and Eliza Hall Institute; in collaboration with Associate Professor Alexander Dobrovic from the Olivia Newton-John Cancer Research Institute and LaTrobe University ­­­School of Medicine.

ACRF has provided $5.5 million in grants to fund research to the Walter and Eliza Hall Institute since 2001.

At a glance

A new ovarian cancer study could help to better match patients with the appropriate therapy for their cancer.

The research identified subtle but important epigenetic differences among ovarian cancer patients that could influence their response to treatment.

There is no ‘one size fits all’ approach for treating ovarian cancer so being able to offer more personalised care is crucial for patient survival rates which have seen little improvement over 30 years.

Subtle yet significant differences

Professor Scott said it was well documented that PARPi could only work when the cancer’s DNA repair process wasn’t functioning as it should.

“For the past two decades, it was thought that ovarian cancer patients whose cancer’s BRCA1 genes are ‘silenced’ – or methylated – had faulty DNA repair and therefore were good candidates for PARPi treatment. Yet the puzzling thing was we were unable to predict the patients for whom the drugs would work,” she said.

Dr Kondrashova said the ‘Eureka moment’ came when the researchers discovered epigenetic differences in some BRCA1 methylated cancers. These subtle yet significant differences explained why some patients would respond to the drug, while others would not.

“It was suddenly clear that all patients in the group could not be treated the same way. We discovered that some of the patients had what could be described as ‘incomplete’ BRCA1 methylation where not every gene copy was ‘switched off’.

“As it turns out, incomplete methylation isn’t enough to cause faulty DNA repair in cancer cells which explains why PARPi isn’t going to be effective.

“At the same time, those in the group who had ‘complete’ BRCA1 methylation in their cancer were responsive to PARPi confirming to us that the treatment should not be discounted,” Dr Kondrashova said.

‘Snap shots’ at key points

Professor Scott said the findings were a result of methodologies developed by Associate Professor Dobrovic at the Olivia Newwton-John Cancer Resarch Institute that could accurately determine the degree of BRCA1 methylation, as well as quality data sets and sophisticated laboratory models called patient derived xenografts (PDX models).

“PDX models are powerful because they mimic the complexity of human tumours at key stages as the cancer progresses. Our models are developed with cancerous tissue donated by patients from the Royal Women’s Hospital, the Royal Melbourne Hospital and the Peter Mac at the time of their cancer diagnosis, or prior to and after treatment with PARPi.

“Like ‘snap shots’ in time, PDX models allow us to accurately track how each patient’s cancer is changing or responding to treatment. The success of this approach shows that a long-term, detailed analysis is invaluable for providing better patient care.”

No ‘one size fits all’

Professor Scott said understanding the various reasons for PARPi resistance was an invaluable approach for developing better, more personalised patient care.

“There is no ‘one size fits all’ approach for ovarian cancer care. We need to keep making these strides in understanding so we can better match patients with the right treatment for their cancer,” she said.

The research was conducted in affiliation with the University of Melbourne and was funded by the Cancer Council Victoria Sir Edward Dunlop Research Fellowship, the Stafford Fox Medical Research Foundation, the Victorian Cancer Agency, Cancer Australia, the National Breast Cancer Foundation, and the National Health and Medical Research Council.

Clinical trials information

Professor Scott’s laboratory is currently involved in studies linked to two clinical trials on PARP inhibitors – the EMBRACE study and the SOLACE 2 study. Find out more about these trials on the Cancer Council Victoria website and at the Australian New Zealand Clinical Trials Registry.

This article originally appeared on the WEHI website.

Image courtesy of WEHI. Research led by (L-R) Dr Olga Kondrashova and Professor Clare Scott is helping to match ovarian cancer patients with the right treatment for their cancer.

ACRF connects with CancerAid: The app that assists cancer patients and their caregivers

Anxiety and fear. From the very first moment after a cancer diagnosis, through treatment and beyond, these are some highly experienced emotional responses recorded by people living with cancer.

Initially, there is often little time to process the shock and suddenness of a diagnosis, especially whilst having to make highly stressful decisions about which course of treatment to take.
In the months following the initial diagnosis, most patients find it difficult to absorb and retain information with so much going on.

The CancerAid app was designed to alleviate anxiety and fear. Developed and launched after a comprehensive amount of research, the app’s features are based on expert advice and patient interviews.

Two oncologists listened to patients expressing these emotions whilst working in a cancer centre in Sydney. They wanted to find a way to empower their patients, and allow them autonomy and control over their care.

The free app CancerAid offers access to personalised, medically reliable information about cancer, treatments and what to expect. Patients can track and share symptoms, feelings and appointments, nominate friends and family for support, access reliable cancer research updates and connect with a community of fellow patients and caregivers. This is all done in the patient’s own time, and on their terms.

The app empowers patients to keep loved ones and doctors up to date with their care needs more efficiently, so that their treatment can be done in the most effective way possible.

The app is continuously developed by healthcare professionals and an in-house team of experienced developers and designers who invite patients to give them feedback on how the app can improve.

ACRF and CancerAid

ACRF is pleased to connect with CancerAid to support our community and those affected by cancer.

CancerAid has assisted more than 20 000 patients with managing their cancer diagnosis.

This immense recognition has led to the app being ranked number one in the US, UK and Australian app store, and being given accolades by Steve Wozniak of Apple, and Sir Richard Branson. CancerAid has also won one of the largest deals in Shark Tank History.

Benefits of the app

Today, it is highly evident that tracking symptoms and activities can result in health benefits. Recent research reveals that cancer patients who track symptoms contribute to improved personal outcomes.

A study recently presented at ASCO, the world’s largest cancer conference, revealed that people with cancer who record their symptoms during treatment and share them with their doctors, enjoy a better quality of life, are less likely to be admitted to hospital, and most remarkably, have a better chance of survival. Basch at al (2017).

It’s no surprise to the CancerAid team that the most used feature is the in-app community where patients and caregivers are encouraged to share their stories to support others.

Isolation is a common feeling amongst patients. In the in-app community, CancerAid allows individuals to connect with others going through similar experiences. It’s no surprise to the CancerAid team that this is the most used feature. The community and symptom manager has been received as a comforting resource where patients and caregivers can express their experience with symptoms, treatments and changes to their lives.

The CancerAid app is available for free to download and use on Android and Apple devices.
If you, or someone close to you, are diagnosed with cancer and you wish to use the app, Click Here

References:

Basch at al (2017). Overall Survival Results of a Trial Assessing Patient-Reported Outcomes for Symptom Monitoring During Routine Cancer Treatment. JAMA, 318(2), p.197.

Convert Points into Life Saving Donations

You can make a difference to people and the planet with your credit card. NAB’s NAB Rewards program means at the click of a button, you can transfer your points to a donation and contribute to our important work. Launched in 2017, NAB Rewards credit card customers can convert their points into donations.

NAB is working with community investment specialist, Good2Give, to support this initiative and ensure the efficient and secure transfer of funds to charities.

Login to the NAB Rewards Store via internet banking or the NAB App to make your donation today – remember, every little bit counts.

Last year, your donations helped fund:

  • New imaging technology which will helps develop new therapies by examining tumors.
  • Equipment that will help build in-depth knowledge of all cell types that make up a tumour, and how cancer cells evolve, leading to improved treatments.
  • Developing manufacturing and monitoring facilities which will support new immunotherapy clinical trials.
  • Building a new facility which supports research into improving long-term outcomes of cancer patients and survivors.

 

Learn More Here

To My Dearest Mum – In honour of women’s cancer month

A mother is someone very special. She ia a friend, a teacher, a protector and many other things in the eyes of her children and grandchildren. In October, we honour all the mothers, grandmothers, daughters, sisters and other women who have been taken away by cancer too soon.

Below you’ll find Michael’s story about the effect her cancer diagnosis and passing away has had upon his family.

 

What I miss most about you Mum

You always began a phone call by saying “Hi love, I was just thinking of you.” You were always thinking of others and, as I sit here writing this letter, I am waiting for your daily call to ask how your granddaughters and I are doing.

Each morning, I still find myself expecting the phone to ring. I wish I could hear your voice, and say hello. I really miss you Mum, and your comforting way of telling me that everything would be okay.

I won’t lie, some days are a lot harder than others. But, I want to tell you that whilst things here are really tough for everyone at the moment, the endless love you had for us gives us the strength to keep moving on exactly how you wanted us to. We are doing our best to make you proud.

There are some darker moments when it feels like the void that you have left in our lives seems overwhelming. On other days it feels like it has all just been a dream, and that I will come to visit you with the girls soon.

My favourite day of the week was always the day when I came to see you and Dad. You always greeted me with huge hugs and kisses.

I am imagining Olivia and Mia begging you to make your famous ravioli. You would always cook whatever the girls wanted for lunch or dinner when they were visiting, always generous with your secret ingredient of love.

And after we all had sat down together to eat, you would sneak them a treat when I wasn’t looking – much to their delight. I am so thankful they have those special memories in the kitchen with their grandmother.

You were always so passionate about looking after others, and your legendary cooking and hospitality displayed this best. This was your space, where you could be creative and nourish those you loved.

The way you cared for others exceeded levels of what I thought was possible.

You were selfless beyond belief, and always put our needs before your own. I am truly grateful that you were such a loving and dedicated mother to me and Steven, and a committed wife to Dad – we could not have wished for anything more.

Back in March 2015, when we received the news about your illness, you didn’t flinch. Instead, you packed up your stuff, left the hospital and carried on with business as usual. Your only concern upon your diagnosis of an inoperable stage IV lung cancer was for Dad, my brother, me, and my girls.

Our entire family could not have been more shocked – we had no explanation for this. You never smoked and were always so healthy. At 63 years old, you were supposed to be enjoying a well-earned break during retirement, not facing this awful disease.

You did whatever you could, immediately taking on daily chemotherapy in tablet form until the cancer overpowered the treatment. In February 2016, we were so thankful that you had qualified to take part in a clinical trial, and we celebrated as your condition improved and you carried on with your life.

At times it was impossible to even believe you were so sick with incurable cancer, but we were never sure of what the future held for you Mum.

I still sit here wondering why and how this happened, and I daydream about what might have been in store for us as a family. But the reality is that we are still learning to navigate this surreal new world without you.

Steven continues to thrive. You had no doubts about that, he was always the strongest. He got that from you Mum.

We are keeping our promise to you and looking out for Dad, and he is doing the same for us and the girls. You would be proud to know he has been brilliant looking after the kids with me and picking them up from school. He has even been making their dinner – I am not joking!

He is doing his best Mum, but I know that he is truly heartbroken and sad without you here. I have never seen anyone miss someone this much. You two had such a magical, unbreakable bond.

Your commitment to him in the 50 years you shared was absolutely unwavering, as his was to you. I loved that you always did things together and that you never left each other’s side. Do you remember how Dad would always say to you “You are so special to me, Krystyna” and you would reply “Joe, I am just like everyone else, but you make me feel special”. I am lucky to have grown up surrounded by this love, and I am thankful my girls have too.

The girls ask about you every day, they miss you so much. They often ask me to send you a big kiss and cuddle, or ‘smoosh’ as they like to say.

Like you Mum, Mia and Olivia loved nothing more than spending time with you, particularly in the garden. They would jump up and down on the trampoline trying to impress you while you tended to your beautiful plants.

In the rare moments when I have to remind them of their manners, you are still the first person they ask for because you always went in to bat for them!

They are growing up so fast, too fast, just like you always said. I continue to treasure every moment with them, just like you told me to.

I plan on taking the girls to a musical each year to keep your love of music, dance and theatre alive in them.

Later this October I will be running the Melbourne Marathon to fundraise for cancer research. I know how much you wanted to be there with the girls and Dad cheering me on, but I’ll be running in your honour Mum.

I am so grateful that advancements in cancer treatment gave you three and a half more years with us.

And, I am determined to continue to do everything I can to make sure this disease can no longer tear loved ones away too soon.

In the end, we knew your last day was coming, but it crept up on us all so quickly. You took your last breaths in Dad’s arms, surrounded by those who loved you most.
All you wanted was to care for your friends and family, and make sure that we would be okay.

Every day your positivity shone through like a beacon of light. Over the years that you were ill, you refused the limelight and the fuss, but the truth is, you were the real star, and I know you are shining brightly somewhere.

Thank you for being my best friend and for loving our family unconditionally.

Rest easy. Mum, I love you.

Donate to cancer research in memory of women affected by cancer

Many Australian women have been lost to cancer. If you want to help outsmart cancer, and make a difference for Australians like Michael and his family, donate to cancer research now.

Your donation will help fund groundbreaking research into the development of new ways to detect cancer and new treatments.

 

Donate Now

Hoover gives hope for nanomedicine cancer treatment

A ten-year-old beagle with prostate cancer is helping researchers at The University of Queensland use nanomedicines to accurately diagnose and target the disease.

Hoover is the first patient in the world to receive the nanomedicine, which the research team hopes will help track and treat his cancer, and lead to better treatment for people with the same disease.

Nanomedicine is the science of developing tiny particles for applications in health – in this case, therapeutics to specifically target a protein found in prostate cancer.

ACRF awarded the University of Queensland’s Centre for Advanced Imaging a $2.5 million grant in 2014, into investigating all types of cancer.

UQ Associate Professor Kris Thurecht said the new technology was important for advancing cancer treatments.

“Chemotherapy is a common treatment for most cancers,” he said.

“Unfortunately, it can also cause serious side effects because it is not always able to differentiate cancer cells from the healthy ones, sometimes damaging healthy cells in the process.

“Nanomedicines with the ability to target specific areas can lead us to target chemotherapy drugs to where they’re needed and kill cancerous cells with minimal impact on healthy cells.

Dr Thurecht said pre-clinical studies had been successful in treating prostate cancer in the laboratory, leading to total remission in some cases.

Our best friends may hold the key

“Validation of this science and technology in companion animals like Hoover is an exciting step forward in nanomedicine and towards human treatment,” he said.

Owner Brenda Douglas with Hoover, the world’s first patient to receive the novel nanomedicine

Dr Rod Straw, Veterinary Oncology Specialist, Brisbane Veterinary Specialist Centre and Australian Animal Cancer Foundation Director with Hoover and his owner, Brenda Douglas

Associate Professor Kris Thurecht and Dr Rod Straw, Centre for Advanced Imaging

Sarah Daniel, CAI Nuclear Scientist, analyses Hoover as he receives the novel nanomedicine; UQ Centre for Advanced Imaging

Hoover was chosen for the trial because dogs – like humans – naturally develop prostate cancer.

Dr Rod Straw, Veterinary Oncology Specialist and Director of Brisbane Veterinary Specialist Centre and the Australian Animal Cancer Foundation, said the beagle could prove to be the vanguard for a revolution in health care.

“Cases like Hoover’s are very important to cancer research,” he said.

“We can learn to develop cancer treatments for not only pets but humans as well.”

This article was published on the Centre for Advanced Imaging website, read the original here.

Prominent cancer research charities join forces

To mark World Cancer Research Day on 24 September 2018, the Australian Cancer Research Foundation (ACRF) is pleased to announce new collaborations with Australian Prostate Centre, Ovarian Cancer Research Foundation (OCRF) and the Snowdome Foundation. This will further enhance cancer research capacity in Australia and increase collaboration between cancer research funders.

ACRF provides outstanding Australian researchers with state-of-the-art equipment they need to improve prevention, diagnosis and treatment of all types of cancer. The new collaborations will provide additional funds to support personnel that operates equipment acquired with an ACRF grant. This ensures that the equipment will be used for maximum impact and efficiency.

ACRF Chief Executive Officer Professor Ian Brown says that the new collaborations are an excellent way to enhance the impact and improve the efficiency of funding for Australian cancer research.

“The benefit of the collaborations announced today mark a significant saving on resources and time for researchers. Less time will be spent on writing additional funding applications, allowing researchers to spend time on what really matters – cancer research.”

ACRF grant applications are assessed annually by the Medical Research Advisory Committee, comprising esteemed Australian and international cancer researchers and clinicians who volunteer their time. The Committee ensures that the most promising and impactful cancer research initiatives in Australia are recommended to the Board of Trustees to receive ACRF funding.

“These collaborations are a tremendous acknowledgement of the reputation and integrity of ACRF and its grant selection and governance procedures. We look forward to giving researchers not only the most advanced tools they need to outsmart cancer, but also simplifying the provision of human power to make it all happen.”

OCRF Chief Executive Officer Lucinda Nolan believes that collaborating with likeminded cancer research charities is a smarter way to progress towards shared goals.
“Collaboration makes us stronger, smarter and more efficient.” Ms Nolan says.

“Joint grants will unlock additional funding for ovarian cancer researchers and improve our ability to support a broader range of projects. This partnership is an exciting development for us and will hopefully accelerate progress within the research field.”

Mark Harrison, CEO at the Australian Prostate Centre says: “We are proud to be collaborating with ACRF in recognising and supporting potentially lifesaving cancer research in Australia. This agreement will accelerate research outcomes to benefit all Australian men with prostate cancer.”

Snowdome CEO Miriam Dexter says “The Snowdome Foundation is pleased to be collaborating with ACRF to advance translational blood cancer research. ACRF brings a national approach as well as a transparent, peer-reviewed grant review process. Further, by leveraging each organisations’ key funding focus, we are able to match hi-tech equipment with vital human infrastructure resulting in fast-tracking next-generation blood cancer treatments and ‘making hope real’ for Australian blood cancer patients.”

The current agreements will be in place until 2020.

The Silk Rags Project

We’re thrilled to announce a new collaboration with The Silk Rags Project, a performance designed to entertain, educate, start conversations and raise vital funds for cancer research.

Whilst undergoing cancer treatments, Briohne Sykes and Dee Handyside separately created two projects which reflected their personal experiences through theatre and music.

Combining their passions, The Silk Rags Project was formed: a one-act musical which guarantees audiences will laugh, cry, and learn. We’re honoured they’ve chosen to fundraise for the Australian Cancer Research Foundation through the project, where profits from performances will be donated.

Described as “poetic and pragmatic” by Ros Johnson of Dramaturg, and a “joyful musical reaction to a deadly serious subject” by Noel Mengel of The Courier Mail, The Silk Rags Project encourages theatre groups to organise a fundraising event and perform the mini-musical, which is simple to organize and is sure to be both challenging and educational.

At the conclusion of each performance, a handout is provided to audiences to provide tools to effectively communicate regarding different experiences of cancer. This has been created in conjunction with Griffith University, and builds on the themes of the play to better prepare audiences in dealing with a cancer diagnosis of a loved one.

We’re very honoured to be working with Scriptwriter Briohne Sykes and Composer Dee Handyside on this inspiring project, which is perfect for Australian theatre group’s 2019 production.

Find out more here, share this post with your local theatre group, and get ready to come along!

Promising Results from Zero Childhood Cancer Clinical Trial

The Zero Childhood Cancer program has just released initial results of its national clinical trial, revealing promising outcomes within its first 11 months.

Of the 128 children enrolled in the trial from across Australia with high-risk and relapsed cancers, 67% were provided with personalised treatment plans aimed at killing their unique cancer cells. For most children enrolled in the trial, there were otherwise few to no treatment options available to them.

Led by Children’s Cancer Institute and the Kids’ Cancer Centre at Sydney Children’s Hospital, Randwick, Zero Childhood Cancer is one of the world’s most comprehensive child cancer personalised medicine studies. The trial uses sophisticated genetic tests to scientifically analyse each child’s individual cancer cells to identify and recommend new personalised treatment options.

ACRF is one of the founding funders of the Zero Childhood Cancer Project, a $1.5 million grant was awarded to the project in 2014.
Associate Professor Tracey O’Brien, Director, Kid’s Cancer Centre at Sydney Children’s Hospital, Randwick says the trial is giving a small group of children a better chance of survival, where current treatment affords little hope.

“Zero Childhood Cancer is about using the best science we have to give hope to children with high risk cancer. We must try a different approach. Accepting the status quo means that 70% of these children won’t survive to celebrate another birthday,” Associate Professor O’Brien said.

“Our early results are encouraging and as we learn more, I see future potential for targeted drug therapies to be used more broadly in all child cancers as a smarter way to achieve cure, while minimising therapy side effects.”

One step closer to personalised medicine

Executive Director of Children’s Cancer Institute, Professor Michelle Haber AM, said the Zero Childhood Cancer program is bringing us one step close to personalised medicine for all childhood cancers.

“Zero Childhood Cancer is giving unprecedented genetic and biological information for children with the most aggressive cancers. It is arguably the most comprehensive personalised medicine program for children with cancer in the world,” Professor Haber said.

“The information we gather will not only benefit children on the national clinical trial but will inform new discoveries and further clinical trials that we believe will impact all children with cancer in the future.”

No story exemplifies the impact of Zero Childhood Cancer more than that of Ellie. At just 11 months old, Ellie was diagnosed with infantile fibrosarcoma, a rare and aggressive tumour that was resistant to chemotherapy. The tumour was so large that she was on life support.

Following sequencing of the entire genetic material of Ellie’s tumour, the whole genome sequencing identified the specific genetic change likely to be driving Ellie’s cancer. The Zero Childhood Cancer team were then able to identify a new drug that specifically targeted that particular genetic change. The drug was sourced, after four weeks of treatment, Ellie’s cancer had shrunk enough for her to be taken off life support and breathe independently. Six weeks later, Ellie was home.

Ellie’s parents, Mina and Rob, know their daughter is only here today because of the Zero Childhood Cancer program.

“We were told to think about saying goodbye, she was so sick we didn’t even know if she would reach her first birthday. Now, to be celebrating her second birthday, when she is such an active, boisterous and energetic two-year-old is beyond our wildest dreams. We can’t thank the teams at the hospitals and research centres involved in the Zero Childhood Cancer program enough,” Mina said.

Outcomes of the Zero Childhood Cancer program over the past 11 months

  • 128 children registered for the trial after just 11 months, each of these are children with an aggressive cancer that is identified as having less than a 30% chance of survival
  • Of these, 36% have been enrolled at the time of relapse, 38% at diagnosis and 26% with progression of disease
  • In terms of cancer types, 36% have brain cancer, 29% sarcoma, 13% leukaemia, 6% neuroblastoma and 16% other rare cancers
  • For 67% of children a personalised treatment plan has been recommended
  • Average turnaround time from receipt of samples to personalised treatment recommendation is 9 weeks

Despite the dramatic increase in childhood cancer survival rates over the last sixty years from virtually 0 to 80%, three children and adolescents still die every week in Australia from cancer.

The original article was published on the Children’s Cancer Institute website,  read the original article here.