Cancer researchers ‘switch on’ Natural Killer cells to fight cancer Posted on June 8, 2016February 25, 2018 by Carly du Toit Walter and Eliza Hall Institute (WEHI) researchers, led by Dr Sandra Nicholson and Dr Nicholas Huntington, together with colleagues from the Queensland Institute of Medical Research (QIMR), are investigating ways to ‘switch on’ our Natural Killer (NK) cells to fight cancer. The researchers identified a protein ‘brake’ within Natural Killer cells that controls their ability to destroy their target tumour cells. “Natural Killer cells exist to detect and then destroy any deviant cells in our bodies before those cells go on to develop into tumours or before infection spreads,” Dr Nicholson said. “Natural Killer cells are a key part of our immune system they work by locating other cells posing a danger to health either because they are infected or because they are becoming a cancer cell,” she continued. Our bodies are constantly and successfully fighting off the development of cells that lead to tumours – but when there is disruption to this process cancer is free to develop. In their paper published in Nature Immunology, they showed that when the brake was removed in an experimental model, the NK cells were better able to protect the body against metastatic melanoma. Natural Killer cells rely on a growth factor called Interleukin 15 (IL15) to activate. Dr Nicholson and Dr Huntington’s research has shown that an inhibitor protein made inside the Natural Killer cells limits the ability of the NK cell to respond to IL15 and therefore kill cancer cells. By identifying for the first time how this protein inhibits NK cell responses, they now hope that a drug can be developed that will improve the response of NK cells to this growth factor and help patients fight cancer with their own immune system. “This is about learning how to activate the NK cells of the individual patient and boost their immune system to tackle the disease,” Dr Huntington said. “We are hopeful our research will lead to new immunotherapies that supercharge the body’s Natural Killer cells and maintain it in a highly active state to more efficiently and specifically fight cancer.” The Australian Cancer Research Foundation has supported WEHI by providing three grants, totalling AUD 5.5million towards cutting edge cancer research equipment and technology. The original news post including the YouTube video was published on WEHI website.
Breakthrough in predicting the spread of cancer Posted on January 14, 2016February 25, 2018 by Carly du Toit A team of cancer researchers from Australia and the UK have bred a biosensor mouse that has enabled them to watch as pancreatic cancer cells ‘unzip’ right before they begin to spread. “Our biosensor mouse makes it possible to look at a primary tumour that has not yet spread: in real time, in 3D, and in a living tumour. Using state-of-the-art laser technology, we can see, at a molecular level, whether the contacts that hold tumour cells in place have started to unzip – and that’s a sign that the cancer is about to spread,” says Dr Paul Timpson of Sydney’s Garvan Institute of Medical Research. To understand how unzipping contributes to the spread of pancreatic cancer, the researchers implanted a genetic model of invasive pancreatic cancer. Remarkably, the researchers were able to successfully rezip these cancer cells by treating them with anti-cancer therapies, stopping the spread of cancer before it had begun. To make the biosensor, the researchers bred a mouse in which a key “zippering” protein that holds cells together – called E-cadherin – was linked to a protein from jellyfish that glows green in fluorescence microscopy. This allowed for them to pinpoint when key changes occured. Which is incredibly important given that five-year pancreatic cancer survival rates stand at just 6.1% – a figure that has barely changed in the last 40 years. “Many patients present with pancreatic cancer at a very advanced stage, when the cancer has already spread to other tissues such as the liver,” says Dr Timpson. “But sometimes, the cancer is detected before it has spread – and that’s the point where we have an opportunity to intervene and stop it in its tracks. If we give a drug early enough, we can rezip those cells together.” Dr Timpson says the most exciting part of the study was the fact that the existing treatment – an anti-invasive drug called dasatinib – allowed us to stabalise the primary tumour. “We treated mice that had developed pancreatic cancer that had yet to spread with the anti-invasive drug [and] within three days of treatment, we saw cells within the tumour had re-zippered, and the tumour had stabilised.” Similar results were achieved with a second therapy, saracatinib. “The biosensor mouse is a powerful tool for anti-cancer drug discovery,” Dr Timpson says. “It makes it possible to evaluate the effect of new therapies on tumour spread, in real time and in a system that reflects human cancer as closely as is currently possible.” Dr Timpson points out that this is just the beginning for the biosensor mouse. “We now have a model that is one step ahead of the invasion process in pancreatic cancer – but we are also already using this model in our laboratory for other aggressive and highly invasive cancer types, such as breast cancer. “Ultimately, we expect to use the biosensor mouse to explore zippering and cancer spread in a wide range of tumours throughout the body.” The Garvan Institute of Medical Research has received three ACRF cancer research grants totalling $6.13m. To read the original article, click here.
