09
Dec 2013
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Colorectal cancer advance comes with a challenge

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When Dr. John Dick unveiled his latest cancer discovery last week, he also issued a challenge.

“I think this work will hopefully stimulate (drug) companies to get into the game,” he told the Toronto Star.

Dr. Dick, senior scientist at Princess Margaret Cancer Centre and the McEwen Centre for Regenerative Medicine, led a team of scientists and surgeons that found a way to disarm a gene called BMI-1 that regulates colorectal cancer stem cells.

In his own words: “When we blocked the BMI-1 pathway, the (cancer) stem cells were unable to self-renew, which resulted in long-term and irreversible impairment of tumour growth. In other words, the cancer was permanently shut down.”

Some context:  Dr. Dick was the first person in the world to identify cancer stem cells, the evil twin of the stem cell. Just as stem cells spark the creation of millions of specialized cells to repair and regenerate tissues and organs (while also renewing themselves) throughout a lifetime, cancer stem cells drive the production of millions of tumour cells (while also replicating themselves).

Current cancer therapies — essentially, surgery, chemotherapy and radiation — go after the tumour cells but leave the cancer stem cells unscathed. Which is why, researchers believe, cancer often comes back.

When Dr. Dick discovered the cancer stem cell — first in leukemia in 1994 and then in colon cancer in 2007 — he opened up a new front in the war on the dread disease.  With his latest finding, published in Nature Medicine,  he has provided a schematic diagram for building a major new weapon in that war. One that can be aimed at colorectal cancer, the third leading cause of cancer-related deaths in the Western world.

The discovery, which made news across Canada, is based on research conducted with mice. The team replicated human colon cancer in the rodents and identified BMI-1, a gene implicated in other cancers, as the pivotal regulator of the cancer stem cells, driving the cycle of self-renewal, proliferation and cell survival. Then they put an existing small-molecule inhibitor to work blocking BMI-1.

While the implications are enormous, there is a huge chasm to be bridged between working with mice and testing a drug  with people. It could take years and many millions of dollars.  But an important start has been made.

What happens now?

“So the next step … is to find the best possible drug to target this gene,” says Dr. Dick in a University Health Network video. “We’re actually testing a number of drugs that are able to target this gene. We’re trying to determine which is the best one and working with other investigators and other companies to try to develop and optimize the drugs so they can be delivered to patients in the best possible way.”

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