How A Canadian Researcher Is Advancing Breakthrough Therapies
Research and Innovations A Canadian cancer researcher is on the verge of a breakthrough in therapy for cancers, and it could mean the end of conventional chemotherapy.
The strategy for treating cancer has always been fairly straightforward: surgery physically cuts out malignant tumours, conventional chemotherapy kills abnormally dividing cells, and radiation attacks the DNA of cancer cells.
There is no denying that these methods have saved and extended countless lives since they came into standard use. Survival rates for most blood cancers have doubled, tripled and even quadrupled. But despite their effectiveness, these treatments take a huge toll
on patients.
So it’s no surprise that the scientific community is excited at the prospect of a targeted cancer therapy that works in an entirely different way from chemotherapy and radiation, and which has already shown enormous potential.
Breakthrough therapy
At the center of this excitement is Dr. Patrick Gunning, a Scottish-born cancer researcher and associate professor of chemistry at the University of Toronto, who has been funded by The Leukemia and Lymphoma Society of Canada and other cancer charities.
Only 36, Dr. Gunning and his team of researchers are on the leading edge of a new breakthrough treatment for blood cancers that unlike the take-no-prisoners approach on which traditional cancer therapies have been built, is targeted to kill just cancer cells.
“The advantage of such a precise therapy is it doesn’t interfere with healthy cells, which for patients means fewer long-term and permanent side-effects.”
“Conventional chemotherapy targets the fastest dividing cells, and the problem with this type of strategy is that you’re rarely able to selectively target just the cancer cells,” says Dr. Gunning. “So the mechanism by which we are targeting these cells is to switch off a protein over-expressed in cancer cells that prevents cell death. By knocking out this protein, the idea is that cancer cells will be more susceptible to dying.”
Nearly every chemotherapy patient experiences nausea, vomiting, diarrhea, and fatigue. But many also suffer long-term, permanent side effects, including dental and oral health problems, vision problems, learning and memory problems, and organ damage to the heart, lung, liver, or reproductive system.
Targeted treatments
Targeted cancer therapies block the spread of cancer by interfering with specific molecules that are involved in cancer growth, unlike most standard chemotherapies, which attack all rapidly dividing normal and cancerous cells.
In this case, Dr. Gunning and his team have developed anti-cancer molecules that latch onto key proteins STAT3 and STAT5, which have been shown to drive cancer pathogenesis, the process by which the cancers develop and grow. The molecules bind to these proteins inside the cancer cells and “switch off” the tumour growing process.
The advantage of such a precise highly targeted therapy is it does not interfere with healthy cells, which for patients means fewer long-term and permanent side-effects.
“Really what our molecules are seeking to do is make killing the cancer cells easier, so that patients can use lower doses of the treatments that are available right now. So the toxicity of the overall treatment would be less,” says Dr. Gunning.
The next steps
Gunning’s team’s molecules are starting pre-clinical trials now for Acute Myeloid Leukemia (AML), Chronic Myeloid Leukemia (CML), and Multiple Myeloma.
“Our goal is that these molecules will allow people to have a less aggressive cancer therapy regimes, and will prevent tumours from coming back,” Gunning says. “That’s one of our main objectives—to prevent these aggressive cancers from coming back.”
The end of traditional cancer therapies may be near, thanks to Gunning’s research. And, because STAT3 and STAT5 are factors in multiple cancers, such as breast and brain cancer and other diseases, as well as psoriasis, Crohn’s disease and irritable bowel syndrome, his research could lead to new therapies in multiple fields.
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