A new blood test could detect early stage melanoma in more than 80% of patients

Melanoma kills more than 1,700 Australians every year, which is more than the national road toll. But the good news is it’s treatable if caught early enough. And a new blood test might be able to help with faster and easier diagnosis.

Currently, melanoma is diagnosed by an examination of the skin by trained clinicians. Once a lesion is classified as abnormal, a biopsy of the lesion is performed and sent to a pathology laboratory for diagnosis.

Most biopsies (75%) will come back negative, so this is a significant cost to the health system. And biopsies are invasive, requiring excision of the skin under local anaesthetic.

Diagnosis is challenging, particularly in cases of small, thin, early-stage melanomas; in patients with more than 100 moles; and in cases of amelanotic tumours (which don’t have a colour). A blood test prior to a biopsy could provide diagnostic certainty, particularly in high-risk patients.

 

The new blood test

We set out to find ways in which we could detect melanoma by screening patients’ blood. We discovered antibodies produced by the body in response to melanoma, and found these could be detected in blood.

Because the body starts producing these antibodies as soon as the melanoma first develops, the blood test is able to detect the cancer early in its progression.

A total of 1,627 different types of antibodies were examined to identify a combination of the ten antibodies that best indicated the presence of melanoma.
Using an Oxford Gene Technology Array which allows us to identify proteins such as antibodies, we analysed the blood of 105 melanoma patients and 104 healthy people, to compare.

We found 139 possible antibodies that were expressed at higher levels in the patients with melanoma when compared to healthy people. Using high level statistical analyses we identified a combination of ten autoantibodies (what the body uses to fight illness) that can detect melanoma in early stage patients 79% of the time.

 

So how far away is this test from the clinic?

Before we can start using this blood tests on patients in the clinic, there are a few steps we have to take first. While our results have been positive in our first round of testing, we need to test more patients to be sure.

We’ll perform a clinical trial involving 1,000 participants, where we’ll collect blood from patients when a doctor has ordered a biopsy due to a suspicious lesion. We can compare our test results to the biopsy results and we’ll be able to identify how accurate our test is, and improve its accuracy to 90%, which is what should be expected of medical diagnostic testing.

By testing more people we hope to find more, or better, antibodies, and this will bring up the accuracy rate.

We hope to have this completed in three years, and then we’ll work with a commercial company to license a product that can process the tests in clinics.

Hopefully in the not-too-distant future, when a suspicious lesion is identified in a patient, rather than having to undergo a biopsy, patients can just have a simple blood test.

A negative test would give doctors an additional tool to have more diagnostic certainty prior to a biopsy. Biopsies would be required if a test comes back positive.

Many people are aware suspicious lesions found on skin checks will mean they have to undergo a biopsy, and so they may avoid getting checked. This test could alleviate patient concern over skin checks, and allow people in rural and remote areas to get an earlier and more accessible diagnosis.

 

This article was originally published on The Conversation. Read the original article.

Setting sights on pancreatic cancer’s moving targets

In a pioneering study, researchers at the Garvan Institute of Medical Research have discovered a new approach to fight treatment-resistant regions within pancreatic cancer – one of the world’s deadliest cancers. For the first time, they have monitored these drug-resistant regions in pancreatic tumours as they travel, spread and grow in real time – and are finding new ways to neutralise these moving targets.

The findings, which were uncovered in mice, are published today in Cell Reports.

Pancreatic cancer has one of the poorest survival rates of all cancers, and is predicted to be the second-leading cause of cancer deaths by 2030. The 5-year survival rate stands at less than 7.7%, and has scarcely changed in decades.

Regions of low oxygen, which move around within tumours, are a hallmark of pancreatic tumours. Importantly, these travelling pockets of low oxygen are resistant to treatment. Associate Professor Paul Timpson (Cancer Invasion & Metastasis lab head, Garvan), whose team led the study, says these nomadic regions are a major concern in the fight against pancreatic cancer.

“Cancer cells are incredibly adaptable,” says A/Prof Timpson. “Depriving them of oxygen makes them more aggressive, more invasive, and resistant to radiotherapy, chemotherapy and other cancer treatments.

“And the movement of these low oxygen, drug-resistant regions in cancer is incredibly problematic, as it means that those areas are constantly changing – it’s here today, there tomorrow, with no way for us to know where the resistance will be in the future.”

To tackle this problem, A/Prof Timpson and his team have overcome a major technical hurdle and developed an innovative live tracking approach, allowing them to observe the drug response of these treatment-resistant compartments in pancreatic tumours.

“To make real gains in the fight against pancreatic cancer,” says A/Prof Timpson, “we can’t wait for new technology to come to us; instead, we often have to develop it ourselves.”

Using their new live tracking technology, they monitored individual cells within low-oxygen regions of pancreatic tumours, and observed the response to treatment. They saw that cells were resistant to three clinically relevant pancreatic cancer treatments, including the cancer inhibitor AZD2014.

So how do you attack a resistant, moving target?

For James Conway – a PhD student in A/Prof Timpson’s lab and the lead author in this study – the answer lies in precision weaponry. “We took advantage of a tool that is ideal for this situation – TH-302 – a molecular ‘warhead’ that’s activated only in low oxygen regions.”

Using a combination of the low oxygen-activated toxic drug, TH-302, and AZD2014, they precisely targeted low oxygen, drug-resistant tumour regions and observed a marked improvement in drug response and inhibition of tumour growth in pancreatic tumour-bearing mice.

The results from this new study represent an exciting new opportunity for pancreatic cancer, where little progress has been made in the past 40 years.

“The beauty of this new treatment combination lies in the precision of low oxygen-activated drugs.” says James. “Their highly toxic, activated form is triggered specifically in low oxygen regions. This makes them incredibly versatile – they can be given in highly concentrated doses because their toxicity to normal tissues is minimal, but in low oxygen areas of the tumour it is lethal, exactly where the drug resistance occurs.”

The new findings would not have been possible without new technology developed at Garvan. For A/Prof Timpson, investing in new technology is key to furthering scientific discovery.

“Instead of static snapshots,” says A/Prof Timpson “we have a dynamic new way to measure responses in single cells in their native environment – by peering into a live animal. That real time feedback is incredibly valuable. ”

Co-corresponding author Dr Jennifer Morton, of the Beatson Institute for Cancer Research UK, is optimistic about what these results mean for patients.

“Pancreatic cancer is a devastating disease with virtually no effective treatments – but our live imaging showed us that although these areas can move around, we can target them and hopefully reverse resistance to therapy, increasing the options for these patients.

Looking ahead, James highlights the clinical relevance of this study.

“AZD2014 is already being used in clinical trials and, given the potential for use in cancer treatment, we want to find combination therapies that will improve patient responses even further beyond the current standard-of-care. We believe our results bring us one step closer towards application in a clinical setting.”

Beyond pancreatic cancer, these results have the potential to change the wider landscape of cancer treatment. Treatment resistance as a result of low oxygen is a fundamental problem across many cancers, and these findings are likely to have a broad impact in paving the way to more effective, targeted cancer therapies.

What is hypoxia?

Hypoxia refers to areas of low oxygen, whereas normoxia refers to areas with normal oxygenation. In cancer, hypoxia is thought to be associated with insufficient vascularity, a disorganized vascular network, and an imbalance in cellular oxygen demands that leads to limited oxygen diffusion and perfusion. In the 1920s, German scientist Dr Otto Warburg discovered that cancer cells often ignored normal oxygen demands in favour of up-regulating alternative energy sources. This adaptive strategy allows tumours to grow beyond the normal oxygen demands that limit a tissue. However, this also leaves them vulnerable to new approaches using hypoxia-targeted toxic compounds that target tumours, with minimal toxicity to the normal tissue.

Although you might expect to see hypoxic regions primarily in the centre of the tumour (where there may be fewer blood vessels), with fewer and fewer hypoxic regions towards the more vascularized edges of the tumour, A/Prof Timpson and his team saw regions of hypoxia transiently moving around the tumour. For the first time, they mapped the movement of hypoxia in real time over a 24h period, and observed hypoxic regions sporadically travelling around the tumour.

How does the new live tracking technology work?

To get the most precise assessment of drug response, A/Prof Timpson and his team are combining high level imaging technology with oxygen-sensitive nanoparticles that can be read on the order of the microseconds, and whose reach extends deep into tumours to reveal oxygen content at a single cell resolution. In parallel, they are able to overlay this information on oxygen levels with nanosecond readouts of drug performance using fluorescent biosensor technology.

Through live tracking of tumour oxygen content and assessing real time drug response, A/Prof Timpson’s team determined that hypoxic regions in pancreatic tumours are resistant to three clinically relevant drugs in development for pancreatic cancer, including the AstraZeneca drug AZD2014.

In a previous study, co-corresponding author Dr Jennifer Morton, of the Beatson Institute for Cancer Research UK, demonstrated that AZD2014, a dual mTOR inhibitor – “dual” because it blocks two cellular pathways that lead to cancer cell growth – is as effective as the current standard-of-care for pancreatic cancer, Gemcitabine. In this study, live tracking experiments showed that even AZD2014 is subject to hypoxia-induced resistance, but this resistance could be alleviated in combination with a hypoxia-activated toxic drug TH-302.

ACRF has supported Garvan Institute by providing three grants, totaling AUD 6.1 million towards cutting-edge cancer research equipment and technology.

Key cancer-fighting gene’s secret weapons revealed

Melbourne scientists have discovered how the most important gene in preventing human cancer, p53, is able to stop the development of blood cancers.

The findings revealed that a special group of genes that function within the body’s normal DNA repair process were vital to the effectiveness of p53. This new information could help doctors to better identify patients with an increased risk of developing certain cancers. It could also help to develop safer, more effective treatments for patients.

Dr Ana Janic, Associate Professor Marco Herold and Professor Andreas Strasser from the Walter and Eliza Hall Institute led the study, published today in Nature Medicine.

Dr Janic said it was the first time a study had explained how p53 was able to prevent blood cancers such as lymphoma and leukaemia; and potentially other types of cancer as well.

“In an exciting and unprecedented finding, we discovered that the DNA repair gene MLH1 and additional DNA repair genes, are critical to p53’s ability to prevent the development of B-cell lymphomas,” Dr Janic said.

Dr Janic said revealing MLH1 as a powerful weapon for p53 in the fight against cancer could help doctors diagnose patients earlier and prescribe safer, more targeted treatments for their cancer.

“For instance, if a patient has lymphoma with a mutation that disables the DNA repair mechanism, doctors will now know to avoid certain DNA-damaging treatments, such as chemotherapy, that may only make the cancer more aggressive.

“Now that we understand the significance of MLH1 and other DNA repair factors, we can begin to find ways of identifying the vulnerabilities that their loss may impose on cancer cells with the aim of exploiting these for therapeutic benefit,” Dr Janic said.

Dr Herold said the findings demonstrated the importance of conducting detailed functional analyses. “We screened more than 300 downstream targets of p53 in order to identify which genes were important to p53’s tumour-suppressing function.

“It was amazing to find that the loss of the DNA repair gene MLH1 prevented p53 from functioning properly, causing the development of lymphoma. And when MLH1 was put back into the equation, tumour development was significantly stalled.

“This led us to explore other DNA repair genes and it has become clear just how important the whole DNA repair mechanism is to p53’s ability to prevent cancer development,” Dr Herold said.

Professor Strasser said understanding how p53 worked was a ‘holy grail’ for cancer researchers.

“Half of all cancers in the world occur as a result of p53 not functioning as it should. Researchers have long been aware of the significance of p53, but despite many studies, no one has been able to explain how the protein is able to block cancer development until now.

“We are planning to continue our studies into the genes that are regulated by p53, digging deeper into understanding other potential processes that might impact its function,” Professor Strasser said.

Dr Janic said the next steps were to see if the DNA repair process had the same cancer-blocking impact on cancers other than lymphoma, such as pancreatic and colon cancers.

“p53 is mutated in close to 70 percent of colon and pancreatic cancers, so this discovery could have a significant impact on understanding these diseases. We are therefore keen to test whether genes involved in the DNA repair process might also play a role in helping p53 prevent the development of these cancers,” she said.

This story was originally posted on the WEHI website.

ACRF has supported WEHI Institute by providing three grants, totalling AUD 5.5 million towards cutting-edge cancer research equipment and technology.

Major study uncovers new breast cancer genes and opens the door for more discoveries

An international team of researchers has used a new scientific method to discover at least 12 new genes that influence the risk of developing breast cancer.

It is one of the first published transcriptome-wide association studies in the world to examine cancer risk and provides evidence to support this relatively new method for studying genes. The method is expected to help to speed up the discovery of more genes associated with cancer and other diseases, as well as drugs to target those genes.

The study was co-led by Professor Georgia Chenevix-Trench and Dr Wei Shi from QIMR Berghofer Medical Research Institute and has been published today in the prestigious journal Nature Genetics.

“One of the research methods used by many geneticists worldwide over the last decade is the genome-wide association study. These studies have allowed us collectively to discover hundreds of genetic variants, or genetic markers, that influence our likelihood of developing certain cancers or of having certain traits, like being tall or being a coffee drinker,” Professor Chenevix-Trench said.

“While genome-wide association studies have advantages, there is a lot of information they don’t provide. For example, we can’t tell whether the genes associated with disease risk are expressed at a high or low level. In other words, we can’t tell whether the gene is turned up high like a very bright light, or is turned down low like a dim light.”

In the latest study published today, the researchers used a relatively new method known as a “transcriptome-wide association study”.

They examined approximately 8500 genes and determined whether they were likely to be turned up high or down low.

“We then looked at a much smaller group of these genes to find out what effect being turned up or down had on the risk of developing breast cancer,” Professor Chenevix-Trench said.

“In laboratory experiments, we found when we turned these 12 genes down, the cancer cells didn’t grow as well. This is an important finding because these genes were not previously known to influence the risk of developing breast cancer, and because no one has validated results from transcriptome wide association studies like this.

“In future, we hope drugs can be developed targeting those specific genes, and others like them, to turn them down and reduce the risk of developing breast cancer.

“These findings are also significant because they show that transcriptome-wide association studies are likely to be very useful in helping us to find new genes to examine for cancer risk.

“This method also has several other advantages. It allows us to look at whole genes, rather than individual markers on the genes, and to study a much smaller number of genes.”

This article was originally published on the QIMR Berghofer website.

ACRF has supported QIMR Berghofer Medical Research Institute by providing three grants, totaling AUD 8.4 million towards cutting-edge cancer research equipment and technology.

Setting sights on pancreatic cancer’s moving targets

In a pioneering study, researchers at the Garvan Institute of Medical Research have discovered a new approach to fight treatment-resistant regions within pancreatic cancer – one of the world’s deadliest cancers. For the first time, they have monitored these drug-resistant regions in pancreatic tumours as they travel, spread and grow in real time – and are finding new ways to neutralise these moving targets.

The findings, which were uncovered in mice, are published today in Cell Reports.

Pancreatic cancer has one of the poorest survival rates of all cancers, and is predicted to be the second-leading cause of cancer deaths by 2030. The 5-year survival rate stands at less than 7.7%1, and has scarcely changed in decades.

Regions of low oxygen, which move around within tumours, are a hallmark of pancreatic tumours. Importantly, these travelling pockets of low oxygen are resistant to treatment. Associate Professor Paul Timpson (Cancer Invasion & Metastasis lab head, Garvan), whose team led the study, says these nomadic regions are a major concern in the fight against pancreatic cancer.

“Cancer cells are incredibly adaptable,” says A/Prof Timpson. “Depriving them of oxygen makes them more aggressive, more invasive, and resistant to radiotherapy, chemotherapy and other cancer treatments.

“And the movement of these low oxygen, drug-resistant regions in cancer is incredibly problematic, as it means that those areas are constantly changing – it’s here today, there tomorrow, with no way for us to know where the resistance will be in the future.”

To tackle this problem, A/Prof Timpson and his team have overcome a major technical hurdle and developed an innovative live tracking approach, allowing them to observe the drug response of these treatment-resistant compartments in pancreatic tumours.

“To make real gains in the fight against pancreatic cancer,” says A/Prof Timpson, “we can’t wait for new technology to come to us; instead, we often have to develop it ourselves.”

Using their new live tracking technology, they monitored individual cells within low-oxygen regions of pancreatic tumours, and observed the response to treatment. They saw that cells were resistant to three clinically relevant pancreatic cancer treatments, including the cancer inhibitor AZD2014.

So how do you attack a resistant, moving target?

For James Conway – a PhD student in A/Prof Timpson’s lab and the lead author in this study – the answer lies in precision weaponry. “We took advantage of a tool that is ideal for this situation – TH-302 – a molecular ‘warhead’ that’s activated only in low oxygen regions.”

Using a combination of the low oxygen-activated toxic drug, TH-302, and AZD2014, they precisely targeted low oxygen, drug-resistant tumour regions and observed a marked improvement in drug response and inhibition of tumour growth in pancreatic tumour-bearing mice.

The results from this new study represent an exciting new opportunity for pancreatic cancer, where little progress has been made in the past 40 years.

“The beauty of this new treatment combination lies in the precision of low oxygen-activated drugs.” says James. “Their highly toxic, activated form is triggered specifically in low oxygen regions. This makes them incredibly versatile – they can be given in highly concentrated doses because their toxicity to normal tissues is minimal, but in low oxygen areas of the tumour it is lethal, exactly where the drug resistance occurs.”

The new findings would not have been possible without new technology developed at Garvan. For A/Prof Timpson, investing in new technology is key to furthering scientific discovery.

“Instead of static snapshots,” says A/Prof Timpson “we have a dynamic new way to measure responses in single cells in their native environment – by peering into a live animal. That real time feedback is incredibly valuable. ”

Co-corresponding author Dr Jennifer Morton, of the Beatson Institute for Cancer Research UK, is optimistic about what these results mean for patients.

“Pancreatic cancer is a devastating disease with virtually no effective treatments – but our live imaging showed us that although these areas can move around, we can target them and hopefully reverse resistance to therapy, increasing the options for these patients.

Looking ahead, James highlights the clinical relevance of this study.

“AZD2014 is already being used in clinical trials and, given the potential for use in cancer treatment, we want to find combination therapies that will improve patient responses even further beyond the current standard-of-care. We believe our results bring us one step closer towards application in a clinical setting.”

Beyond pancreatic cancer, these results have the potential to change the wider landscape of cancer treatment. Treatment resistance as a result of low oxygen is a fundamental problem across many cancers, and these findings are likely to have a broad impact in paving the way to more effective, targeted cancer therapies.

What is hypoxia?

Hypoxia refers to areas of low oxygen, whereas normoxia refers to areas with normal oxygenation. In cancer, hypoxia is thought to be associated with insufficient vascularity, a disorganized vascular network, and an imbalance in cellular oxygen demands that leads to limited oxygen diffusion and perfusion. In the 1920s, German scientist Dr Otto Warburg discovered that cancer cells often ignored normal oxygen demands in favour of up-regulating alternative energy sources. This adaptive strategy allows tumours to grow beyond the normal oxygen demands that limit a tissue. However, this also leaves them vulnerable to new approaches using hypoxia-targeted toxic compounds that target tumours, with minimal toxicity to the normal tissue.

Although you might expect to see hypoxic regions primarily in the centre of the tumour (where there may be fewer blood vessels), with fewer and fewer hypoxic regions towards the more vascularized edges of the tumour, A/Prof Timpson and his team saw regions of hypoxia transiently moving around the tumour. For the first time, they mapped the movement of hypoxia in real time over a 24h period, and observed hypoxic regions sporadically travelling around the tumour.

How does the new live tracking technology work?

To get the most precise assessment of drug response, A/Prof Timpson and his team are combining high level imaging technology with oxygen-sensitive nanoparticles that can be read on the order of the microseconds, and whose reach extends deep into tumours to reveal oxygen content at a single cell resolution. In parallel, they are able to overlay this information on oxygen levels with nanosecond readouts of drug performance using fluorescent biosensor technology.

Through live tracking of tumour oxygen content and assessing real time drug response, A/Prof Timpson’s team determined that hypoxic regions in pancreatic tumours are resistant to three clinically relevant drugs in development for pancreatic cancer, including the AstraZeneca drug AZD2014.

In a previous study, co-corresponding author Dr Jennifer Morton, of the Beatson Institute for Cancer Research UK, demonstrated that AZD2014, a dual mTOR inhibitor – “dual” because it blocks two cellular pathways that lead to cancer cell growth – is as effective as the current standard-of-care for pancreatic cancer, Gemcitabine. In this study, live tracking experiments showed that even AZD2014 is subject to hypoxia-induced resistance, but this resistance could be alleviated in combination with a hypoxia-activated toxic drug TH-302.

ACRF has supported Garvan Institute by providing three grants, totaling AUD 6.1 million towards cutting-edge cancer research equipment and technology.

Girls night out for ACRF!

For the third year running the wonderful members of the Rotary Club of Rowville-Lysterfield in Victoria have held a fundraising dinner for Australian Cancer Research Foundation. Nothing so remarkable you might think, except for this event all the gentlemen of the club are the waiters and the lady members (wives, girlfriends, mothers, aunts, nieces and female friends) are the guests!

On a chilly evening in May, 71 ladies were wined and dined by 9 men, amusingly dressed in penguin-bibbed t-shirts made specially for the occasion. The venue was the beautifully decorated Tosaria’s Restaurant in Rowville which has been hosting this event since 2016.

Wine and champagne was served on arrival and balloons purchased to unlock a special prize for a lucky punter after dinner, along with plentiful raffle and lucky door prizes contributed by generous local businesses.

ACRF staff member based in Melbourne, Victoria Bonsey, was the Key Note Speaker and spoke about the evolution of cancer research and the history of the organization, leading to the grants awarded most recently and the breakthrough research outcomes. These outcomes are the result of ACRF’s generous supporters helping fund vital cancer research projects. As she explained, we are at a crucial time in the history of cancer research. Our current greatest need is a collaborative effort here in Australia to equip our brightest research brains with the latest tools and technology to outsmart cancer. She then announced in 2018 Australian Cancer Research Foundation will award an additional $10 million grant.

Questions and answers afterwards revealed the depth of concern about the complexities and breadth of different cancers and wholehearted support for the funding of more cancer research.

At the end of the evening President Alan Lunghusen and past President Heather Eddy proudly presented Victoria with a cheque for $3,000 for ACRF. This brings the total raised since 2016 to $8,700! Another great effort to be proud of Rotary Club of Rowville-Lysterfield; your support is truly appreciated.

Melanie clips her plait to raise funds

“There are brilliant minds at work in medical science and surely with continued funding they can solve the cancer problem more rapidly.”

It’s been over 20 years since I started working as a STEM (science, technology, engineering, mathematics) professional. I enjoy helping people work together and realise their leadership and personal potential.

Like so many others, I have friends and family living with cancer. Some are going through treatment and others are in remission. My dad is being treated using a technique developed through research which encourages and motivates me to help out.

When choosing a cancer charity, I looked for one that covered research into multiple types of cancer, and has a good history and governance/system on funds allocation. ACRF ticked those boxes and more. New knowledge that is discovered through cancer research, communicated, and then applied will move us towards ending cancer and alleviating suffering.

I first heard about haircuts to fundraise from my Toastmaster mentor and friend. Since then I have donated my hair three times. To encourage supporters, I set different haircut lengths based on target values reached.

– $1,000, cut to shoulder blades
– $3,000, cut to shoulders
– $6,000, cut to chin

The support of everyone, including from my two Toastmaster clubs, was overwhelming. Donations were generous and it was gratifying to receive the stories of hope shared by supporters who have recovered from cancer.

I would encourage others to raise money for cancer research. It’s a great cause that will help a lot of people. We are fortunate to have our health and we can help change the fate of family and friends who don’t by sharing our resources. Disease does not discriminate; it touches each of us.

New immunotherapy drug trial delivers promising results for previously incurable skin cancers

Previously incurable skin cancers have responded to the new anti-PD1 therapy drug in almost fifty percent of patients on a Peter Mac clinical trial.

Results of the Cemiplimab drug trial, led by Professor Danny Rischin, have shown 29 out of 59 patients with advanced cutaneous squamous cell carcinoma had their cancers significantly reduced.

Professor Rischin announced the results at the American Society of Clinical Oncology annual meeting in Chicago.

Cemiplimab was shown to deliver rapid tumour reduction and durable responses in patients who responded to the drug.

There are currently no approved therapies anywhere in the world to treat this advanced form of the disease.

Cutaneous squamous cell carcinoma, the second most common skin cancer behind basal cell carcinoma, is cured in 95 percent of cases with surgery.

But a small percentage of these tumors reach an advanced stage that is not curable, either because of the development of secondary malignant growths at a distance from a primary cancer site (metastatic)or locally advanced progression is no longer suitable for surgery or radiation therapy.

Advanced cutaneous squamous cell carcinoma is a term that encompasses both of these incurable situations and patients are considered for palliative care in routine clinical practice.

Watch: Prof. Danny Rischin speaking about the trial at Asco in Chicago

Read the full study in the New England Journal of Medicine.

This story was originally posted on the Peter Mac website.

ACRF has supported Peter Mac by providing four grants, totalling AUD 7 million towards cutting-edge cancer research equipment and technology.

Cienne’s birthday donations go to ACRF

Cancer research is something that I am keenly interested in. I recently started training in medical oncology and we see incredible stories unfold constantly: of cure, of relapse, of begrudging acceptance of a slow-growing cancer as an unwelcome housemate. We also occasionally see healthy bodied students, lawyers, builders, musicians, farmers, teachers, engineers – to list a few – who don’t survive the unexpected malignancy. Sadly, their families can do nothing but watch the relentless and devastating effect of cancer on their loved ones. We also see many people whose cancer treatments have been successful; they get back to work and to caring for their family.

Constant improvements in therapy through research are providing outcomes that were once unthinkable. Reflecting on all of this, donations on my birthday for cancer research instead of presents seemed like a perfect idea. Thank you to every one of my amazing generous friends and family; it was thrilling to commemorate my 30th by helping to give others a chance at a few more birthdays too.

Ali and James invite ACRF to wedding

When Ali and James married last year, it was in the beautiful sweeping gardens of Southdown Estate, Burradoo, surrounded by their families and many friends.

The Sydney-based couple, who work in the film and television industry, met at a music festival and share a long-time love of music. Ali says her favourite music moment of the ceremony was dancing with her dad down the aisle towards James to the Beatles – Got to Get You Into My Life – and for James, it was the theme song of comedy film Space Jam as he and Ali were introduced into the reception.

During the months of wedding planning and preparation, Ali and James decided to include supporting cancer research in their special day. Not only has Ali had her own melanoma scare, both of her grandmothers died of cancer. James has also had a family member pass away from cancer.

“On a day of celebration that is primarily focused around two people who are given so much love and attention, we wanted a meaningful reminder that it wasn’t just all about us.”

“It was a good decision to make a donation to ACRF on behalf of our wedding guests. Everyone understood the significance of the ACRF ribbons and favour cards on the reception tables, and now some of our friends are also going to donate to cancer research as part of their wedding favours.”

Revealed: The city of ‘cells’ supporting prostate tumours

Prostate cancer is the most common cancer in Australian men, causing the deaths of more than 3,000 men a year. This new understanding may help increase the accuracy of prostate cancer diagnosis in the future.

The study, led by Professor Susan Clark and Dr Ruth Pidsley from the Garvan Institute and Professor Gail Risbridger and Dr Mitchell Lawrence from the Monash BDI, investigated how cells that are adjacent to tumours differ from those that are more remote.

The team found key changes in the DNA, which may explain how adjacent cells change their behaviour to help tumours grow.

“Most prostate cancer research to date has focused on the cancer cells themselves, the new study set out to explore the ‘city’ of the tumour microenvironment,” said Dr Pidsley.

“What hasn’t been clear until our study was how these changes arise and how they’ve been encoded in the cells,” Dr Lawrence said.

“We’ve uncovered for the first time on a genome-wide level precisely the changes that occur in the surrounding cells. This gives us a much deeper understanding about prostate cancer,” he said.

The findings were recently published in the journal Genome Research.

“Just like people in big cities who rely on a complex network of infrastructure for their daily lives, cancer cells depend on the surrounding tumour microenvironment,” Dr Pidsley said.

“The result of our work is a new molecular map of the cellular infrastructure that the cancer cells rely on,” she said.

The ‘map’ of the tumour surroundings was created by measuring chemical marks on the DNA of the tumour-adjacent cells. These marks determine which genes are turned on and off in the cells, and therefore how they function.”

The researchers hope to use the ‘map’ to understand more clearly how the cancer cells grow and spread and to improve identification of prostate cancer in biopsies to improve patient care.

“We think it has important potential application in increasing the accuracy of prostate cancer diagnosis,” Professor Risbridger said.

Professor Clark said that the collaboration combining the skills of scientists, clinicians assisting with patient samples, and computer scientists had been vital to conducting the study.

The team has started further studies extending this one using a larger sample size of patients.

Read the full paper in Genome Research titled Enduring epigenetic landmarks define the cancer Microenvironment.

This article was originally published on the Garvan Institute of Medical Research’s website.

ACRF has supported Garvan by providing three grants, totalling AUD 6.1 million towards cutting-edge cancer research equipment and technology.

Countrywide supports ACRF

Cocktail Hour at Countrywide National Meeting

At the latest Countrywide National Meeting held in May, Countrywide held a ‘charity hour’ which brought together many of their stakeholders to support Australian Cancer Research Foundation over some cocktails, delicious food, great speakers and a raffle. Guest speakers, Chelsea Ford, founder of Females in Food and Kerry Strydom, COO of ACRF shared some great insight into their experiences. The attendees dug deep and in just one hour, they were able to raise over $2,000 for ACRF.

Attendees were glad to support such a worthy cause and a lot of fun was had, with many people commenting on the value they gained from it. Countrywide look forward to holding more events like this in future.

Women in Business High Tea

Countrywide National Office was beautifully transformed for the Women in Business High Tea they hosted in support of ACRF.

Many people came together to make this event a reality and we thank them tremendously. The Engagement and Culture Team along with other amazing staff at the head office worked together to arrange the presentation space and create the delicious spread that was on offer. Finger sandwiches, tarts, quiches, hazelnut shortbread, scones, cupcakes, mocktails and more were enjoyed enormously by all.

Their guest speakers covered very interesting topics and we are appreciative of the way they opened up and gave attendees valuable insight into the tries and triumphs they have experienced.

Countrywide raised a phenomenal amount of over $2,500 for ACRF!

 

 

Breast cancer: beware of misleading headlines

Findings from a major international clinical trial suggest a significant number of women with the most common form of early-stage breast cancer do not need chemotherapy after surgery.

The results of the so-called TAILORx trial were presented yesterday at the annual meeting of the American Society of Clinical Oncology and concurrently published in the New England Journal of Medicine.

Breast cancer types

The study looked at over 10,000 women with one specific type of breast cancer known as hormone-receptor–positive, human epidermal growth factor receptor 2 (HER2)–negative, lymph node–negative breast cancer.

Not all breast tumours behave the same way, with a number of different subtypes of breast cancer defined by genetic and protein markers. There are five to six main subtypes, depending on the classification system used. But with genome sequencing it’s becoming apparent each patient’s disease has subtle differences at the molecular level. These different subtypes are treated differently, and can have significantly different outcomes for patients.

The subset of breast tumours that form the focus of this study are driven by hormones (oestrogen), do not respond to drugs such as trastuzumab (also known as Herceptin – an engineered antibody that targets HER2), and haven’t yet spread to the lymph nodes. They represent roughly half of the more than 17,000 new cases of breast cancer diagnosed in Australia every year.

Patients with these kind of tumours typically undergo surgery followed by treatment with drugs that target rapidly dividing cells (chemotherapy) and drugs that block the production or action of the hormone oestrogen (endocrine therapy, such as the drug Tamoxifen).

Results from this study suggest many women with this specific type of tumour do not receive any additional benefit from having chemotherapy in combination with endocrine therapy, compared to endocrine therapy alone. This has the potential to spare thousands of women from the awful side effects of chemotherapy, including nausea, hair loss, and heart and nerve damage.

This study used a genetic test (called “Oncotype DX”) to measure a panel of 21 genes that help predict risk of cancer recurrence. Importantly, chemotherapy still showed some benefit in women with higher Oncotype recurrence scores, and in some women under the age of 50.

Although mortality rates have decreased significantly over the last few decades, breast cancer is estimated to cause more than half a million deaths globally every year. Breast cancer remains the second most common cause of death from cancer among females in Australia.

Hope and hype

Cancer is complex and challenging to study, and news reporting on the disease easily lends itself to hype, contradiction and misinterpretation. Clearly communicating research findings are important for helping patients make informed decisions about treatment and modifying risk.

Poor reporting may have serious consequences for public and scientific communities alike. Some of the reports and headlines on this trial have been a little misleading, feeding on an understandable fear. They could potentially encourage patients to incorrectly avoid or stop treatment – with potentially tragic consequences.

False or unmet expectations can also seed disappointment and an eventual loss of trust in science. Another, more sinister, aspect to these headlines is the potential to fuel myths and conspiracy theories about the effectiveness of chemotherapy.

One of the most exciting aspects of this trial is the emergence of robust, large-scale data supporting the use of “precision medicine” – using genetic profiles to dictate treatment and predict outcomes in cancer. Trials like this are critical in balancing the significant hope and hype of precision medicine.

This study supports sparing thousands of women from the sometimes nasty side-effects of chemotherapy, but we must be crystal clear that it applies to a very specific (and significant) subset of women. Patients should not make any changes to their treatment based off this study, and should always consult their doctors.

And while celebrating this genuine advance, we should remember just how far we have to go in finding effective therapies for metastatic breast cancer, and other breast cancer subtypes for which treatment options are still limited.

Darren Saunders, Associate professor, UNSW

This article was originally published on The Conversation. Read the original article.

Jade says goodbye to her hair

“With or without hair, we can still be whole and have our full sense of self.”

 

As a Health and Movement Coach living in Byron Bay, I love inspiring others to lead a full and vibrant life by helping them to establish what works best for their body and health.

The decision to shave my head was made in support of cancer patients who are losing their hair during chemotherapy treatment, and to also make good on my promise to Dad of a few years ago to fundraise. My father was diagnosed with a rare type of Burkitt’s lymphoma in1990 and even though I was very young during his illness, there was still an awareness that it was a truly horrible, dark and stressful time for our whole family.

My father survived his harsh encounter with cancer but the hair he lost during that time has never regrown. It will be a super special moment to shave my head in acknowledgment of Dad’s amazing bravery during cancer treatments – we will be bald together.

I chose to fundraise for ACRF because of their commitment to research into prevention, diagnosis and treatments that encompass all types of cancers. My father’s cancer story is one of the good ones and that naturally motivates me to support others who are affected by cancer.

Our family is truly grateful and blessed that Dad is still in our lives, and I genuinely hope for that same outcome with other families who have a loved one diagnosed with cancer. Raising awareness and funds for cancer research is my way of helping to make it happen.

Structure of protein pair provides blueprint for future drugs

Walter and Eliza Hall Institute researchers have visualised for the first time how the protein SOCS1 ‘switches off’ cell signaling to dampen immune responses and block cancer growth.

The atomic-level structure of SOCS1 binding to its partner protein JAK could guide the development of drugs that alter disease-causing cell signaling pathways, and may have applications for treating some blood cancers, including leukaemias.

The research, led by Dr Nick Liau, Dr Nadia Kershaw, Associate Professor Jeff Babon and Professor Nick Nicola, was published in the journal Nature Communications.

At a glance

  • The SOCS1 protein binds to JAK proteins to ‘switch off’ cell signaling, which dampens processes including immune responses and cancer growth.
  • Our researchers have used structural biology to visualise how SOCS1 binds to JAK proteins in never-before-seen detail.
  • The detailed structure may guide the development of new drugs that modify JAK activity, amplifying or dampening cell responses, with potential applications in cancer therapies.

Switching off signalling

Dr Liau said the structure of the protein pair revealed for the first time how SOCS1 binds to JAK proteins to disable signalling.

“Using the Australian Synchrotron and the CSIRO Collaborative Crystallisation Centre, we produced an incredibly detailed view of how SOCS1 interacts with the JAK1 protein,” Dr Liau said. “With this image, we were able to explain for the first time why JAK proteins cannot signal when bound to SOCS1. This information could help to underpin the development of new medicine targeting this important cell signalling pathway.”

Above: The structure of SOCS1 (red) bound to a JAK protein (beige) could inform the development of new drugs to treat cancer.


Above: The structure of SOCS1 (red) bound to JAK protein (beige) could inform the development of new drugs to treat cancer.

A blueprint for new medicines

Dr Kershaw said both SOCS1 and JAK proteins had been implicated in driving diseases including cancer and inflammatory conditions.

“In particular, overactive JAK signalling is linked to the development of cancer-like conditions called myeloproliferative neoplasms (MPNs) – which include polycythemia vera, essential thrombocythemia and primary myelofibrosis – as well as certain acute childhood leukaemias.

“Medicines that inhibit JAK signalling are in use for treating MPNs, but they are only able to manage the disease, not cure it. New medicines for these conditions are needed, and we envisage that a drug designed to mimic the SOCS1 protein to switch off JAK proteins might be a more effective treatment,” Dr Kershaw said.

As well as guiding the development of drugs mimicking SOCS1, the team’s research may also underpin the development of a second new class of drugs that inhibit SOCS1, Associate Professor Jeff Babon said. “SOCS1 binding JAK proteins normally applies a ‘brake’ to immune responses – which in a healthy person is a good thing,” he said.

“However, in certain conditions, releasing this brake could be the key to enhanced immune responses. This approach to boosting the immune response could be the key to improving immunotherapies for treating cancer. If we could design a drug that inhibits SOCS1, this might boost anti-cancer immune responses, potentially improving anti-cancer immunotherapies.”

This research article was originally posted on the WEHI website.

ACRF has supported WEHI by providing three grants, totalling AUD 5.5 million towards cutting edge cancer research equipment and technology.

 

A behind-the-scenes look at the ACRF Centre for Lung Cancer Early Detection

Ph.D. student Brielle Parris with the NanoString funded by ACRF.

 

In 2015, ACRF awarded The University of Queensland Prince Charles Hospital with a $1 million grant for the establishment of ACRF Centre for Lung Cancer Early Detection. The centre focuses on the discovery and development of innovative methods for early stage detection of lung cancer. We caught up for a Q&A with one of the Centre’s Ph.D. students, Brielle Parris, to learn more about what goes on behind-the-scenes:

What led you to become a cancer research scientist?

I originally wanted to pursue a career in medicine, but after my undergraduate degree in Biomedical Science, I did a year-long Honours degree at the Centre and was left with too many questions that I needed to answer! I am inspired by the direction that modern cancer research is heading, and its pursuit of combining genomics and technology to diagnose patients earlier and treat patients uniquely according to their genetics. We are currently in a really exciting time in the cancer research sphere, and the advancements are happening at such a rapid rate. My honours year helped me to realise that I didn’t want to just practice medicine – being able to play a role (albeit a relatively small one) in influencing the way that medicine will be conducted in the future excites me much more.

What is your role at the Centre?

I am currently in my second year of my Ph.D., and my thesis will be principally based on the NanoString nCounte. Between my own research, writing grants, assisting with other projects, I am actively involved in the routine processing of patient samples that we receive daily from our kindly consenting patients at The Prince Charles Hospital. All of our research here is based on these samples and would not be possible without them.

Could you give a brief description about the technology that you operate at the Centre?

The NanoString nCounter is an instrument that enables us to directly count the genetic molecules (DNA and RNA) that are contained within the human lung samples that we work with. For example, when we obtain a lung tumour sample from a patient having surgery, I am able to isolate the DNA, attach molecular tags with unique fluorescent spots and count the molecules that we are interested in. This technology can aid our investigation into a variety of nucleic acids within many different patient samples, including lung tumour, blood and sputum (the stuff you cough up when you’re sick) and can identify patterns that may explain certain patient characteristics and why some people develop lung cancer and others do not.

What does it mean to you, to know that you are working towards ending lung cancer?

I’ve often heard people say that your pursuits in life can be meaningless and futile unless you have a strong ‘why’. My mother was a smoker for the majority of my childhood, so she is a constant reminder of my ‘why’. Working towards reducing the incidence of lung cancer by identifying at-risk individuals and through early detection is incredibly meaningful to me.

What is the goal of this new Centre and how does the technology that ACRF provided help achieve this?

The NanoString platform, kindly provided by ACRF, is enabling us to identify patterns in gene expression within lung tumours that may be associated with different survival outcomes, identify gene mutations that predict which drugs will provide most benefit to patients and look at genetic patterns from the blood of patients at risk of lung cancer.

Why do you think it is important to spread awareness around lung cancer?

The stigma that lung cancer is just a ‘smokers disease’, and the consequent nihilism that is associated with the treatment of lung cancer has certainly been a limitation in the funding and support that we have access to. 25% of patients with lung cancer have never smoked, and this proportion is increasing over time. I think that it’s important for the wider community to understand that lung cancer can affect anyone, not just smokers.

Lung cancer is the leading cause of cancer death among both men and women, how will this new Centre help reduce these statistics?

The poor survival outcomes for patients with lung cancer are predominately due to the lack of observable symptoms for early stage lung cancer, meaning that most lung cancers are diagnosed at an advanced stage when treatment options are limited. With a focus on early detection, the core of our work at the Centre is the pursuit of identifying new biomarkers that may identify people at risk or with early stage lung cancer, particularly through non-invasive blood testing. Identifying patients with lung cancer in the very early stages increases their chance of cure following surgery to remove their tumour, and the mortality associated with this terrible disease.

The end of 2018 will mark the third year since the grant was awarded to the ACRF Centre for Lung Cancer Early Detection. What have been the greatest moments of the project so far?

Last year I conducted a study looking at over 400 lung cancer samples from patients at the Prince Charles Hospital to test for cancer-causing DNA mutations. I was fortunate enough to be accepted to present this work internationally at the World Conference on Lung Cancer in Yokohama, Japan last year and then again at the Australian Lung Cancer Conference in Sydney this year.I’m currently working on testing small samples obtained during a bronchoscopy procedure using the NanoString to test for important gene mutations that cause lung cancer, some of which predict benefit from drugs which are designed to target the mutation specifically (targeted therapies). I am hoping to validate this technology to the extent that it may be used in clinical mutation testing, which is now an integral component to lung cancer diagnosis.

Click here to read more about the ACRF Centre for Lung Cancer Early Detection.

 

My cancer is in remission – does this mean I am cured?

So you’ve been through cancer treatment and your doctor has called you in for “some good news”. Satisfied, she tells you your cancer is “in remission.”

What does this mean? Are you cured? Is the cancer gone forever? And what about all those stories you’ve heard of someone who thought they’d “won the battle” – but then their cancer came back?

Detecting cancer

Your cancer is in complete remission when, after treatment, no cancer can be detected. The term “cure” can only be used in hindsight. Commonly, years after the cancer has gone into remission, if it has not returned (or relapsed), it is said to have been cured.

However, a secondary cancer could occur if the same conditions that triggered the first are present.

When a cancer can no longer be detected, it’s cured only if the treatment has killed every cancer cell. But it’s difficult to know if that’s the case due to our inability to detect small amounts of cancer.

A skilled specialist may be able to feel a breast lump that is half-a-centimetre wide. A plain chest X-ray can be expected to detect cancers from 1cm wide. And a CT scan will detect smaller cancers to a few millimetres.

But a cancer 1cm across on a scan has about 100 million cancer cells; even a 0.5cm cancer has about 10 million cells. A 1mm cancer, which would not show up on scans, has 100,000 cancer cells.

So, even when a cancer can no longer be seen and is no longer causing symptoms, there can still be millions of cells remaining. They can keep growing and eventually the cancer will be large enough to be detected again. That’s when the cancer is said to have relapsed.

Some cancers, like testicular cancer, produce proteins (alpha FP and Beta HCG) that can be measured in blood. Measuring these is more accurate than scans in detecting small amounts of cancer.

Better still, chronic myeloid leukaemia (CML) – a rare form of leukaemia – has a characteristic genetic abnormality, which a very sensitive blood test can detect. This is helpful in determining whether a treatment has eradicated microscopic disease. The holy grail would be to develop such sensitive blood tests for every cancer.


Additional therapies

Because we can’t tell whether remission means cure for most cancers, treatment strategies have been devised to increase the likelihood of cure. If a cancer is being treated with chemotherapy and becomes undetectable, further courses will be given to continue to reduce the remaining microscopic disease.

Some cancers, like breast and bowel cancer, where there is no visible disease after surgery, are given additional treatment in case some cells are still present near the operation site or have spread more widely through the bloodstream. Radiotherapy is given after the cancer has been removed by surgery to kill any remaining cells in the breast.

When it comes to brain cancer, it’s difficult to know if it has been completely cleared. The extent of surgery is limited because of the damage to normal tissues and function, and we don’t have very effective therapies to follow up the surgery. This is why it’s so difficult to cure.

Chemotherapy, hormone therapy (for breast cancer) or both are given to kill any cells that might have escaped to more distant sites. Although we can’t see the cancer shrinking with the additional (adjunct) treatment, we know from trials comparing patients who receive additional treatment with those who do not that the additional treatment results in more patients being cured.

It is common to use multiple types of treatment – surgery, radiotherapy or drug therapy – to improve the chances of a cure.

Chemotherapy may not be able to kill all of a cancer because it kills cells only when they are dividing, which means resting cells escape. Only a percentage of cells are dividing at any one time. In cancer that percentage is higher than in most normal tissues, so cancer suffers more damage than normal tissues with chemotherapy. Multiple doses might catch the resting cells when they begin to divide.

Another problem is that, after initially shrinking some of the cancer, some cells are found to be resistant, or become resistant, to the chemotherapy and are left untreated. Drug combinations are given as cells resistant to one drug might be susceptible to another.


Five-year outcomes

It’s common when reporting cancer outcomes to compare the five-year survival rate, which is the percentage of patients who survive five years after diagnosis. Five years is a convenient interval at which everyone can collect statistics so comparisons can be made between cancers – or the outcomes of cancers between treatment centres, states or countries.

As it happens, with many cancers in remission, to have survived five years does mean they are probably cured. But there are differences for different cancer types.

A person diagnosed with an aggressive lymphoma whose cancer achieves remission is most likely to have been cured if the cancer has not returned in two years. This is because any residual lymphoma would be expected to regrow rapidly.

The opposite is the case for breast cancer. Although the chance of relapse after complete remission is greatest in the first two years and becomes smaller over time, and the five-year survival rate is 90%, relapses have been recorded up to 20 years later.

It is important to note, though, that survival rates have greatly improved over time and are always improving. In the 1970s, only one cancer patient in three made it through the first five years after diagnosis. Today, this figure is around 70%, and exceeds 85% for some cancers that were previously fatal.

The ConversationSo, remission might mean cure but we only know that over time.

Ian Olver, Director, University of South Australia Cancer Research institute, University of South Australia

This article was originally published on The Conversation. Read the original article.

Every cancer patient should be prescribed exercise medicine

Every four minutes someone in Australia is diagnosed with cancer. Only one in ten of those diagnosed will exercise enough during and after their treatment. But every one of those patients would benefit from exercise.

I’m part of Australia’s peak body representing health professionals who treat people with cancer, the Clinical Oncology Society of Australia. Today we’re joining 25 other cancer organisations to call for exercise to be prescribed to all cancer patients as part of routine cancer care.

Published today in the Medical Journal of Australia, our plan is to incorporate exercise alongside surgery, chemotherapy and radiotherapy to help counteract the negative effects of cancer and its treatment.

What are we calling for?

Historically the advice to cancer patients was to rest and avoid activity. We now know this advice may be harmful to patients, and every person with cancer would benefit from exercise medicine.

Most doctors and nurses agree exercise is beneficial but don’t routinely prescribe exercise as part of their patients’ cancer treatment plan.

It is our position that all health professionals involved in the care of people with cancer should:

  1. view and discuss exercise as a standard part of the cancer treatment plan
  2. recommend people with cancer adhere to exercise guidelines
  3. refer patients to an exercise physiologist or physiotherapist with experience in cancer care.

Why prescribe exercise?

Cancer patients who exercise regularly experience fewer and less severe side effects from treatments. They also have a lower relative risk of cancer recurrence and a lower relative risk of dying from their cancer.

If the effects of exercise could be encapsulated in a pill, it would be prescribed to every cancer patient worldwide and viewed as a major breakthrough in cancer treatment. If we had a pill called exercise it would be demanded by cancer patients, prescribed by every cancer specialist, and subsidised by government.

Cancer and its treatment can have a devastating effect on people’s lives, causing serious health issues that compromise their physical and mental well-being.

Here’s why exercise is a new contender in the fight against cancer. TEDxPerth.

Research shows exercise can help cancer patients tolerate aggressive treatments, minimise the physical declines caused by cancer, counteract cancer-related fatigue, relieve mental distress and improve quality of life.

When appropriately prescribed and monitored, exercise is safe for people with cancer and the risk of complications is relatively low.

Implementing exercise medicine as part of routine cancer care not only has the potential to change people’s lives but to also save money. People with cancer who exercise have lower medical expenses and spend less time away from work.

What exactly should be prescribed?

Exercise specialists can prescribe exercise in a similar way that doctors prescribe medications; by knowing how cancer impacts our health, and understanding how certain exercises improve the structure and function of the body’s systems.

These individualised programs involve specific types of exercises, performed at precise intensities and volumes based on a mechanism of action and dosage needed to counteract the negative effects of cancer.

The evidence-based guidelines recommend people with cancer be as physically active as their current ability and conditions allow. For significant health benefits, they should aim for:

  1. at least 150 minutes of moderate intensity aerobic exercise weekly (such as walking, jogging, cycling, swimming)
  2. two to three resistance exercise session each week involving moderate to vigorous intensity exercises targeting the major muscle groups (such as weight lifting).

These recommendations should be tailored to the individual’s abilities to minimise the risk of complications and maximise the benefits.

How will patients fill the prescription?

Getting this much exercise may seem out of reach for many people with cancer. But exercise specialists who have experience in cancer care can help. They’ll design an individual program based on the patient’s disease, how they’ve responded to treatment and the anticipated trajectory of their health status.

Online directories can help find accredited exercise physiologists and physiotherapists practising nearby. These services are eligible for subsidies through Medicare and private health insurance.

Or patients can opt for structured cancer-specific exercise medicine programs such as EX-MED Cancer, which I lead. Such programs are designed to maximise the safety and effectiveness of exercise medicine for cancer patient.

Prue Cormie, Principal Research Fellow in Exercise & Cancer, Australian Catholic University

This article was originally published on The Conversation. Read the original article.

ProCan to receive $41 million funding boost

ProCan, the ACRF seed-funded cancer research project has been strengthened with a $41 million boost to expand research to outsmart cancer.

In 2015, ACRF awarded Children’s Medical Research Institute with ACRF’s 30th Anniversary $10 million grant towards the ACRF International Centre for the Proteome of Human Cancer (ProCan™) research project.

Now, with an extra $41 million dollars in funding provided by the NSW and Commonwealth Governments on Monday, this will further help researchers apply cutting-edge science to detect, diagnose and treat cancers.

The joint investment will support a world-first proteomics project, ProCan, at the Westmead Children’s Medical Research Institute (CMRI).

Premier Gladys Berejiklian said the NSW Government is investing $21 million in the project.

“The NSW Government is proud to support the CMRI and the ProCan project that will support the work to ultimately crack the cancer code.”

Federal Health Minister Greg Hunt said the Commonwealth Government is contributing $20 million to enhance Australia’s international reputation as a cancer research leader.

“This will support ProCan to create an unprecedented database containing massive amounts of molecular information on all types of cancer,” Mr Hunt said.

NSW Health Minister Brad Hazzard said the combined investment would allow the CMRI to make ProCan a truly global and revolutionary project.

“The concept behind ProCan is to make Westmead the home of the world’s first database of the entire cancer spectrum,” Mr Hazzard said.

ProCan is designed to improve the knowledge of cancer and the treatment of patients. This project was immensely strengthened by the link to the ‘Cancer Moonshot’ initiative led by ex-US Vice President, Joe Biden.

The project is analysing and measuring thousands of proteins simultaneously in cancers and using advanced techniques to learn how to predict the most effective treatments for individual cancers.

The technology will generate results within five to seven years, which will help develop a new method of cancer diagnosis and treatment planning that can give clinicians guidance within 36 hours. It will be particularly powerful for rare cancers.

Willa exceeds fundraising goal

I am a 16-year-old girl who has been crazy about dancing, and done classes, for as long as I can remember. I also love the water and used to swim competitively. Now I’m at the beach as a junior member of the local surf life-saving club.

To raise funds in support of the Australian Cancer Research Foundation, my very long hair was chopped off on February 17. It was incredible to exceed my goal and raised $3,000. The generous donations and support from my friends and local community was fantastic and meant a lot to me.

So many people have died from this terrible disease, including my grandpa. I have so much respect for anyone dealing with cancer and wanted to raise money to help researchers find better treatments and someday the end to cancer altogether. I came across ACRF by Internet search, and liked what they are doing to fund research into all types of cancer.

 

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Mother’s Day is just around the corner!

Wouldn’t a world without cancer be the greatest gift of all this Mother’s Day?

In thinking about meaningful Mother’s Day gifts, we have 3 ideas that will make Mum smile … and help fund research to outsmart cancer!

Donate in lieu of a gift

A Mother’s Day donation is a thoughtful gift idea that will help fund world-class cancer research. We will send your mum a lovely card to acknowledge your generous and thoughtful gift. Make a donation.

Purchase an Entertainment book

Entertainment books are full of deals – things you could do together. And 20% percent of each sale will go directly to cancer research. Order here.

Order a Mother’s Day hamper

Treat your mum to a gorgeous charity hamper filled with luxury products. 10% of proceeds will help scientists advance research into cancer prevention, diagnosis and treatment. View the hampers here.

We are very grateful to have supporters who choose to mark special occasions such as Mother’s Day by contributing to outsmart cancer for good.

 

Donate in lieu of a gift

Odd one out: protein goes against the family to prevent cancer

Melbourne researchers have made the surprise discovery that the ‘odd one out’ in a family of proteins known to drive cancer development is instead critical for preventing stomach cancers.

The research team showed switching off a gene called NF-κB1 caused spontaneous development of stomach cancers, driven by chronic inflammation. The study also revealed that immunotherapy may prove to be a significant tool for treating stomach cancers that are driven by runaway inflammation, warranting further investigation.

At a glance

  • Around 2000 cases of stomach cancer are diagnosed in Australia each year, affecting nearly twice as many men as women.
  • The study showed switching off a gene called NF-κB1 led to spontaneous development of stomach cancer caused by chronic inflammation.
  • Researchers discovered the stomach tumours had ‘markers’ that identified they may respond to ‘immune checkpoint inhibitor’ cancer immunotherapies.

Dr Lorraine O’Reilly, Dr Tracy Putoczki and Professor Andreas Strasser from the Walter and Eliza Hall Institute, with Professor Steve Gerondakis from Monash University, led the research, published in the journal Immunity.

Surprise discovery

Stomach (gastric) cancers are relatively common in Australia, with around 2000 cases diagnosed each year. Twice as many men are affected as women and the disease is often not diagnosed until an advanced stage. Many stomach cancers develop as a result of uncontrolled inflammation over many years.

Dr O’Reilly said the finding was unexpected because previous research had shown that high – not low – levels of activity of other NF-κB family members were drivers of stomach and other cancers.

“Until now, it was thought that abnormally increased activity and levels of any of the members of the NF-kB family was linked to cancer,” she said.

“Now, for the first time, we’ve identified NF-kB1 is the ‘odd one out’ in the family because abnormally low expression – or ‘loss’ – of this family member actually causes the development of spontaneous stomach cancers.

“We found that defects that led to lower than normal levels of NF-kB1 kick-started uncontrolled inflammation in the stomach and, over the long-term, led to invasive stomach cancers.”

The findings have ramifications for the understanding and treatment of human cancers.

“It is well established that long-term inflammation can lead to stomach cancer in humans. The cellular processes that we have identified in this study as being important for the development of stomach cancer provide new targets for therapy that have not been explored before,” Dr O’Reilly said.

Immunotherapy hope

Dr Putoczki said the preclinical model would be very useful for testing new treatment options, such as immunotherapy.

“Stomach cancer is a disease where immunotherapy is still in its infancy. This is the first preclinical model of stomach cancer that repeats the pattern of human stomach cancer development, that involves progression from chronic stomach inflammation through to fully invasive cancer,” Dr Putoczki said.

“We showed that there are markers on these stomach tumour cells that indicate they would be responsive to a type of immunotherapy called immune checkpoint inhibitors, in particular anti-PDL1 immunotherapy, which is already used with great success in the treatment of melanoma and certain other cancers.

“Not only does this research provide compelling evidence for further investigation of immunotherapy for treating stomach cancer, it also provides the first model for preclinical testing of these treatments.”

ACRF has awarded a total of $5.5 million towards cutting-edge cancer research technology at the Walter and Eliza Hall Institute.

Baseball club win for ACRF

On 17 March, the Pine Rivers Rapids Baseball Club in Bray Park, Queensland, hosted their annual President’s Cup fundraising for a charity event. As one of their members, Mark Coates, died of cancer last year, the club dedicated the 2018 event to Mark and proudly nominated the Australian Cancer Research Foundation as their charity to support.

The night was kicked off by the youngest players in T Ball & Rookie Ball playing a match against their coaches and managers; it was a very funny game that saw coaches batting blind and taking a lot of spills. The main event was a match between the President’s Team – junior league players joined by the club’s Division 1 little league players – against a team made up of the club’s major sponsors and community supporters. The President’s Team came out on top this year, perhaps due to a bit of leeway from the umpire!

“We had a wonderful night,” said Club Treasurer Alexa Warren, “and all of us are very happy about supporting ACRF and the great work they do.”

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Poems and prose to raise funds for ACRF

Brian Loughlin was an accountant for all of his working life, and in retirement, he joined a creative writing group at University 3A to improve his writing skills. It was after a trip to China with his wife Pat in 1983 when Brian first started putting his thoughts on paper. He says the Yangtze River was so impressive that he was moved to write a poem about it.

Over the years, Brian’s enthusiasm for writing has continued undiminished. His poetry and prose are purposely upbeat despite the tremendous sadness of losing four family members to cancer.

“My wife died in 2012 after three cancer diagnoses over twelve years, one of our daughters died of leukaemia in 1984, and then both my brother and my sister died of cancer. My son Maurice had cancer in 2009 but he is currently free of this terrible disease.”

Brian says that he made a conscious effort to maintain a positive attitude while his family were going through cancer treatments, as he was there to support them. Brian also believes the positive attitude, and encouragement received from friends, are what kept him going each time one of his beloved family didn’t survive cancer.

At age 90, Brian decided that he could do more towards contributing to cancer research. After hearing about the Australian Cancer Research Foundation at a Cuppa for Cancer event, Brian selected 50 of his poems and prose writings and then designed a book and its cover. The book was published in 2017 by the University of Wollongong Printery, and Brian is donating all sale proceeds to ACRF.

“I like that ACRF has a Medical Research Advisory Committee, headed up by Professor Frazer (co-creator of the cervical cancer vaccine), and the committee recommends where the money goes for best effect. I think that is a better way of handling donated funds.”

Although his life hasn’t been without struggles, Brian says that he still remains positive and continues to attend University 3A and his church.

If you would like a copy of Brian’s great book (his description!) please email fundraising@acrf.com.au and we will put you in contact with Brian. The book costs $10 plus postage.

 

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Pre-cancerous: warning sign or cause for panic?

It might be a spot, lump, bump or polyp you’ve found suspicious or bothersome enough to ask a doctor to have a look at. The doctor sends what she has excised for testing and tells you it’s “pre-cancerous”. But what exactly does that mean, and is it cause for alarm?

A reminder about how cancer occurs

Our bodies are made up of more than 200 types of building blocks, or cells, which form your organs (heart, brain, skin and so forth). Over time, these cells replace each other to keep our organs healthy and functioning normally.

Ordinarily, this cell regeneration (and the controlled cell death) is exquisitely controlled. But occasionally errors are made, particularly in the gate-keeping processes that control how quickly and efficiently the cells regenerate. The process then begins to get out of control.

The older we get, and the more times our cells regenerate and replace themselves, the more chances there are for mistakes. This is why we call cancer a disease of age – one that is more likely as you grow older.

How is pre-cancer different from cancer?

Pre-cancers are abnormal cells which have undergone some changes that we know are associated with an increased risk of becoming cancerous, but are not yet cancer. These changes include alterations to the inherited material (DNA) of the cells and the way those cells talk to their neighbouring cells and the immune system.

As these changes occur, the cells develop the ability to ignore normal cues that would ordinarily signal them to die (or stop replicating). This leads to an increase in the number of pre-cancer cells that may be detectable – for example, a mole on your skin made up of melanocytes (pigmented cells) or a small polyp in your colon that shows up during a colonoscopy.

Additional or more powerful changes occur to switch these pre-cancers to cancer, and the chance of this happening is different for each cancer. Cancer occurs when cells become completely deaf to normal signals that constrain growth and regeneration, allowing them to start moving away from their proper location, upsetting their resident tissue and other organs around the body.

Not all pre-cancers are equal

Pre-cancers can take a long time to develop into cancer, many in fact will not progress but some can progress remarkably fast. It’s this risk of cancer that clinicians and scientists are trying to prevent.

Doctors currently use a combination of the size, number, location and appearance of precancers together with molecular changes and patient history (for example exposure to known environmental risk factors such as long-term sun exposure, or a genetic susceptibility such as family history of bowel cancer) to predict the overall likelihood of cancer developing.

This risk assessment determines whether a pre-cancer needs to be removed and the screening interval for follow-up with the patient. This evaluation is based on the best available data and medical researchers are working hard every day to understand more about what contributes to this risk to identify better, absolute markers for pre-cancers that will progress to cancer.

So if your spot, lump or bump wasn’t cancer, you have found it early and this is good news. Having a pre-cancerous condition doesn’t mean you have cancer, or that you will definitely develop cancer. But pre-cancerous conditions might develop into a cancer, so it’s important to monitor your health.

Early detecting

In Australia, cancer screening has been implemented for many decades. We have a number of screening options for skin cancer (regular skin checks by GPs and specialists), breast cancer (mammograms, available free for women 50-74), cervical cancer (screening test, available free for women 25-74) and bowel cancer screening (also known as colorectal cancer), performed through the National Bowel Cancer Screening program (available free to every Australian aged 50-74) through a faeces test.

The same precautions that reduce your chances of cancer are likely to reduce the earliest changes associated with pre-cancer.

In addition to regular screening, quit smoking, protect yourself from excess sun, eat a balanced diet with plenty of fibre and exercise regularly. And as always, if you have any concerns or would like more information, talk to your doctor.

Susan Woods, Senior Research Fellow, University of Adelaide; Hannah Brown, Post-doctoral Fellow; Reproductive Epigenetics, University of Adelaide, and Tamsin Lannagan, Postdoctoral Fellow, University of Adelaide

This article was originally published on The Conversation. Read the original article.

Half marathon burn for Rebecca and Charlie

My husband and I currently live in Sydney after spending the past three years in London. We decided that participating in the 2018 Australian Running Festival would be a great way to celebrate our return home. We both enjoy setting ourselves challenges, and the half-marathon is a good opportunity to test ourselves and work on our fitness.

We also have a more serious reason for wanting to do the run next month in Canberra. While Charlie and I were in London, my father passed away quite suddenly after being diagnosed with pancreatic cancer. Sadly, the disease had progressed quickly without being noticed. As anyone reading this will know, it is heart-breaking when a family member dies of cancer. I am fundraising for ACRF in the hope that any money donated means that we are one step closer to stopping all types of cancer.

Just recently, a handful of people in our social circles have either been diagnosed with cancer, or this devastating disease has claimed someone close. It strengthens our motivation even more to contribute towards cancer research.

There has been an enthusiastic response from friends, family and work colleagues to our upcoming run and to our raising funds for ACRF. I would encourage others who want fundraise in the same way to pick an event and get involved. You will have the incredible achievement of finishing a marathon, and it’s a chance for anyone to cheer you on by making a donation. And if further incentive is needed, you will be running to help wipe out cancer!

 

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Anna combines love of swimming and fundraising

I am a registered nurse and worked in hospital oncology units and hospices where most patients were very unwell or receiving treatments for cancer. Now working in general practice, I continue to see and care for patients and families affected by cancer.

In 2016 my close friend Lynn Cain was diagnosed with advanced stomach cancer; it was heartbreaking to watch Lynn suffer and deteriorate despite treatment and trials. She died just 13 months after diagnosis, leaving behind her 15-year-old son.

Lynn’s death reinforced what I already knew – continuing cancer research is the only way forward. We need to make more progress with finding effective remedies that offer hope, so it’s important to support organisations like ACRF which are funding research.

My love of the ocean and swimming has resulted in doing several long races over the past ten years and fundraising as well. Taking part in this year’s Rottnest Channel Swim would be different though; the swim would be done in Lynn’s memory and I was completely motivated to succeed. Having participated in the 20km open water solo swim event two years ago, doing it again was achievable if I could put in the training which begins six months before. That goal kept me getting up at 4:50 am most mornings to do squad training at the local pool and then longer ocean swims during the weekends. My partner and our three teenagers were fantastic support.

The response from all my family across the world, friends and the local swimming community was tremendous, and Lynn’s family and friends were also keen to be involved.

I’m thankful to everyone inspired by my effort and commitment who contributed to my fundraising endeavour. It’s all about putting yourself out there and going for it! And going for cancer research is vital.

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UQ facility sheds new light on cancer growth and behaviour

Researchers will soon understand how to better target cancer treatments with the opening of a new Australian Cancer Research Foundation facility today (Tuesday April 17) at The University of Queensland (UQ).

The $2.3 million ACRF Cancer Ultrastructure and Function Facility, to be opened by Acting Queensland Chief Scientist Dr Christine Williams, will provide unprecedented visualisation of cancer cells and how they multiply and react to their environment and drugs.

Professor Brandon Wainwright, Director of UQ’s Institute for Molecular Bioscience (IMB) where the facility is based, said it would provide a vast leap forward in our understanding of cancer.

“This new facility, established thanks to the generosity of ACRF supporters, will allow us to marry our knowledge of the genomics that drive cancer cells with a knowledge of how these cells behave in their microenvironment,” he said.

“The ability to view and track cancer cells will enable us to see, in nearly real time, how healthy cells turn cancerous, the changes in surrounding tissues that allow these cells to spread and how cancer cells respond to their microenvironment, including the presence of therapeutic drugs.

“This knowledge will set us on the path of developing new and improved therapies for cancer, and arm doctors with information that will help them recommend the most appropriate treatment for a patient’s individual cancer.”

The facility houses three microscopes at the cutting edge of imaging technology and represents the first time such imaging capability has been combined with expertise in genomics, cancer models, drug development and the clinic.

ACRF CEO Professor Ian Brown said ACRF is proud to continue to support cancer research at IMB. This is the fourth ACRF grant awarded to the Institute.

“The new microscopes at IMB will allow researchers to observe the structure and function of living cancer cells in real time with unprecedented resolution, giving them the opportunity to optimally target and fine-tune cancer treatments,” Professor Brown said.

“It is our hope that this will assist IMB in making significant contributions to the global understanding of how cancers grow and develop to improve treatments and patient outcomes.”

“Thanks to the generosity of many ACRF supporters – individuals, families, organisations and community groups from around Australia –we are able to award high-impact technology grants to advance research into prevention, diagnosis and treatment of all types of cancer.”

“We are proud of our long standing association with IMB. It is our mission to do everything we can to provide Australia’s best researchers with the tools they need to outsmart cancer.”

The ACRF Cancer Ultrastructure and Function Facility will be located at The University of Queensland’s Institute for Molecular Bioscience in Brisbane, and involves researchers from UQ’s IMB, Diamantina Institute, Faculty of Medicine, and Centre for Microscopy and Microanalysis.

ACRF has provided The University of Queensland a grand total of $19.9 million to all their research facilities since 1999.

Joanne on fundraising journey

“You never know what tomorrow will bring, so walk, run, cycle, sing and dance as much as possible.”

I am a French tourist currently cycling across Australia. Bike touring can sometimes be physically challenging but it is a wonderful way to discover a country, its natural beauty and meet its people. In addition to my passion for cycling and travel, I’m a videographer, age 35, adore my family and good food and continue to be an enthusiastic fan of Doctor Who and Harry Potter.

Cycling the vast distances of Australia first started as a crazy idea (still might be) but as I researched it, the more it seemed possible. I have both the time and the savings to do the trip now and thought why not try?

It also seemed like a good time to raise money for a charity along the way and I chose La Ligue Contre le Cancer, which funds cancer research projects in France. Realising that during my trip I could meet Australians who might want to support my fundraising effort but not want to contribute to a French organisation, I started looking for a cancer charity in Australia. It would have to be one that was national as my plan is to see the whole country and I want to get everyone involved. When I came across ACRF on the Internet, it met all the criteria, one of my Aussie friends vouched for the organization, and there it all started. My goal is to collect $1 per kilometre cycled.

Cancer, like any other disease, makes you feel powerless and angry. I’m not a doctor, a nurse, a researcher or anyone capable of helping people with cancer first hand, but I can raise funds for research. Research is the key to curing cancer and whether it’s medicines, machines, or procedures, we’ve come a long way. I’m hopeful that research will take us even further to ending cancer soon!

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Ann Smith’s story

Star ACRF supporter and volunteer extraordinaire, Ann Smith has suffered her share of loss to cancer. She lost her twin sister Rosemarie in 1993 and more recently her husband John in December 2016.

“It is still very hard to grasp he is gone. When it comes to husbands, John was a Rolls Royce. A fastidious organiser, before he got too sick, John made sure I was well set-up in a new smaller home, close to family and friends.

“He also looked after our Wills and ensured that the cause closest to my heart – Australian Cancer Research Foundation – was mentioned.

Apart from mentioning ACRF in her will, at John’s funeral service, Ann’s daughters arranged for donations in lieu of flowers to go to ACRF.

“I now donate each month via direct debit and my girls are fully supportive of my wishes in my Will”, said Ann.

Ann Smith

Find out more how to leave a gift in your will.

Find out more about leaving a gift in your will