The deadly cancer with a survival rate of less than 8%
With a five-year survival rate of just 7.7 per cent, pancreatic cancer is the fifth most common cause of cancer-related deaths in Australia – but awareness of the disease is at an alarmingly low 15 per cent, research from the Garvan Institute of Medical Research has found. As a result, research into pancreatic cancer isn’t receiving the funds it desperately needs to find a potential breakthrough.
It’s not just the cancer that people aren’t aware of, however. A staggering 83 per cent of Australians aren’t even sure of the organ’s function – to secrete digestion-aiding enzymes and produce hormones that help regulate the metabolism of sugar. Furthermore, 77 per cent of people have an incorrect view of the signs and symptoms of pancreatic cancer.
Unfortunately, correct symptoms of the disease, such as upper abdominal pain, jaundice, loss of appetite, weight loss, depression and blood clots, may not present themselves until the cancer is at such an advanced stage that surgical intervention is no longer possible.
We asked members of the Over60 community affected by this insidious disease to share their experiences, and were absolutely overwhelmed by the responses.
“I was diagnosed in 2012,” Over60 member Noreen Wheatley recalls. “I had a Whipple’s [pancreaticoduodenectomy] done. I was one of the lucky ones to survive. I have joined the over-5-year survival group and they are studying our DNA to see if there is a common denominator. Hopefully they can and then be able to diagnose precursors in family genetics and treat it early, and survival rates increase.”
Most, however, are not as fortunate. “I lost dad in 1994 to pancreatic cancer. He had been unwell but ok for several months. He was diagnosed in December and was able to stay at home and live his life, but he lost half his body weight in a couple of months and became frail. I nursed him 24 hours a day, slept in his room for the weeks before he died. He died surrounded by his wonderful family. He was 65 years old.”
So, a recent breakthrough from Australian and UK scientists couldn’t have come at a better time. Associate Professor Paul Timpson, Head of Invasion and Metastasis at the Garvan Institute, and Professor Kurt Anderson of the Beatson Institute for Cancer Research, UK, have created a “biosensor mouse” which allows them to track the disease’s progression – and perhaps even stop it in its tracks.
To find out more about this incredible innovation, Over60 spoke to Associate Professor Paul Timpson. “We’ve made a green glow-in-the-dark mouse that can show a pancreatic cancer tumour getting ready to break apart and spread throughout the body before it even occurs,” he explains.
“For a tumour to spread, it has to lose its contact with adjacent cells, with which it’s zipped together, just like a common zip on a piece of clothing. With this mouse, we can actually watch the process of those cells unzipping (or spreading) in real-time. So, we can say, ‘This tumour has not yet spread, it’s not yet broken apart, it’s just weaker’. And then what we do is give it drugs that we know can control that zip, and kind of re-zip it before it moves.”
Associate Professor Timpson adds, “For pancreatic cancer, which is highly invasive and spreading, when metastasis occurs we do not have a cure. So, if you can increase the number of cases in which that tumour stays in the same place, then the surgeons can go in and take it out.”
In addition to the biosensor mouse, Associate Professor Timpson and his team have created another mouse which could be the key to fine-tuning chemotherapy, increasing drug effectiveness and minimising nasty side-effects.
“The second mouse we’ve got is called a FRET (fluorescence resonant energy transfer) mouse. Using the green and red fluorescent proteins found in glow-in-the-dark jellyfish, we’ve created a mouse that’s basically like a traffic light. Before, drugs were administered with a one-size-fits-all approach to the amount of treatment and length it was given. What we’re trying to do now is fine-tune treatment, so you can watch the cancer-causing molecule switch on and off like a traffic light, indicating whether the chemotherapy is working (the mouse glows amber) or not (the mouse glows red and green). By doing that, we can determine how long to give the drugs, where to give the drugs, and when. This way you maximise the drug response while minimising side-effects.”
Just how does it work, then? Associate Professor Timpson explains: “The behaviour in the solid middle of a tumour is very different to the behaviour out at the edges, when it’s about to spread. What you find is that drugs work way better on the outside of the tumour than they do deep inside because it’s really hard to penetrate. So we can now see not only is the drug working for how long, but how deep it’s penetrating into the tumour.”
“Now imagine the tumour – it’s covered in a meshwork, kind of like collagen (the protein which makes up the shape of your lips and your organs, for example). What happens with pancreatic cancer is that you get a massive deposition of too much collagen all around the tumour. Because it’s covered in this meshwork, any drug you give just cannot get into the tumour – it’s protected.”
“So, what we can do is give a very low dose of a drug that can break up that mesh, we can make it softer, and easier to penetrate so the cancer drug can get in. You can then fine-tune that to get the tumour soft enough to allow the drug in, while still being hard enough to allow the pancreas to still function.”
Garvan is also an expert in patient-derived xenografts, which are tumour samples taken direct from the patients. “We’ve got the largest cohort in the world, with over 400 samples,” Associate Professor Timpson explains. “With these, we can say patients 1 through 15 are going to respond to the treatment, 15 to 200 we have no cure for these people, and then from 200 to 400 they’ve got a different molecular signature that we know we can attack.”
“Using these samples, we can replicate each individual’s tumour in mice and test treatments, fine-tune it and then take it to the human. That’s called personalised therapy.”
But it’s not just one cancer that will benefit from these new breakthroughs, Associate Professor Timpson says. “If this can work for pancreatic cancer, it could also help breast cancer, prostate cancer, colon cancer and even skin cancer. It may even be applicable in diabetes and neuroscience research – it’s always bigger than you ever imagine.”
To find out more about pancreatic cancer and how you can help Associate Professor Paul Timpson and his team at the Garvan Institute continue their research to find a cure, visit garvan.org.au/pancreatic-cancer.
THIS IS SPONSORED CONTENT BROUGHT TO YOU IN CONJUNCTION WITH GARVAN.