Cardiologist and researcher Associate Professor James Chong has already used human stem cells to repair the damaged hearts of other large primates — a world first.
The achievement and his subsequent work won him a 2016 Metcalf Prize for Stem Cell Research.
Now he’s ready to start a five-year project that aims to bring the therapy to a clinical trial with patients who have had heart attacks.
Heart disease is Australia’s single leading cause of death killing more than 18,500 people a year, or one every 28 minutes.
James, a researcher at the Westmead Institute of Medical Research/University of Sydney and Cardiologist at Westmead Hospital, wants to change those numbers.
“The patients I see affect my thinking every day,” he says. “What I’m working towards is to be able to provide new treatments to extend the quality and length of life of my patients.”
With your support, the National Stem Cell Foundation of Australia wants to help fund James’ research.
The Foundation is aiming to raise provide $1 million for the project, by matching, dollar for dollar, every public donation of $500 or more. Donations must be at least $500 and the total of donations made cannot exceed $500,000.
James Chong (Photo: Westmead Institute of Medical Research)
The approach James and his colleagues are taking involves treating patients with heart failure after heart attack by injecting stem cell-derived heart muscle cells or ‘cardiomyocytes’ directly into the injured region.
It follows on from animal trials James conducted while working in the US — the results of which were published in a landmark Nature paper.
He’s since been working on two challenges ahead of trials in humans: producing stem cells in large enough quantities to be useful, and understanding any arrhythmias that might appear in the repaired heart.
For this Foundation-funded project, he will be collaborating with the University of Queensland’s Professor Peter Gray and Dr Andrew Prowse, who have experience using bioreactors to produce stem cell-derived cardiomyocytes.
Recent studies suggest arrhythmias detected in the initial animal trials were less sinister than first thought.
“The heart muscle cells we produce are a mix of cells, and they beat spontaneously in the dish when we grow them,” James explains.
“And the reason why they beat is because some of them have this pacemaker activity. We think a lot of those previous arrhythmias we saw were just these cells triggering off independently.”
Put simply, the cells were marching to the beat of their own drum because they hadn’t yet realised they were part of an ensemble.
“We’ve found that arrhythmias decrease over time and we think this is because the injected cells are getting used to their environment,” he says. “As they integrate better with their host, arrhythmias decrease.”
With the assistance of the Foundation’s matched funding program, James and his colleagues hope to start enrolment for Phase I clinical trials towards the end of the five-year funding period.
“We don’t have the kind of resources that some other countries do, so funding like this is crucial for us to try to get to this stage,” says James.
“In Australia, we do great quality medical research, and that’s well-known. I’d like to see Australia play a more important role, particularly with clinical translation of cardiac therapies.”