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Colorectal Cancer Research: Single Gene Can Turn Cancer Cells Back to Normal?

Jun 18, 2015 11:13 PM EDT
(Photo : mgkuijpers / Fotolia)

Scientists have discovered a single gene that can turn colorectal cancer cells back into normal tissue in mice, according to a new study.

Anti-cancer strategies generally involve killing off tumor cells, but findings published in the journal Cell indicate that cancer cells may instead be coaxed to turn back into normal tissue simply by reactivating a single gene.

During the study, researchers found that normal intestinal function was restored within just 4 days and tumor growth stopped with this technique. Remarkably, tumors were eliminated within two weeks, and signs of cancer were prevented months later.

Colorectal cancer is the second leading cause of cancer-related death in developed countries, accounting for nearly 700,000 deaths worldwide each year.

These findings suggest that restoring the function of a single tumor suppressor gene can cause tumor regression and may lead to more effective cancer treatments in the future.

Up to 90 percent of colorectal tumors contain inactivating mutations in a tumor suppressor gene, called adenomatous polyposis coli (Apc). Although these mutations are thought to initiate colorectal cancer, it has not been clear whether Apc inactivation also plays a role in tumor growth and survival once cancer has already developed.

"We wanted to know whether correcting the disruption of Apc in established cancers would be enough to stop tumor growth and induce regression," first author Lukas Dow said in a press release.

To find out, Lowe and his team used a genetic technique to precisely and reversibly disrupt Apc activity in a novel mouse model of colorectal cancer. As see in previous research, Apc suppression in the animals activated the Wnt signaling pathway, which is known to control cell proliferation, migration, and survival.

But when Apc was reactivated, Wnt signaling returned to normal levels, tumor cells stopped proliferating, and intestinal cells recovered normal function.

Tumors regressed and disappeared or reintegrated into normal tissue within two weeks, and there were no signs of cancer relapse over a 6-month follow-up period. In addition, this approach was effective in treating mice with malignant colorectal cancer tumors containing Kras and p53 mutations, which are found in about half of colorectal tumors in humans.

Although Apc reactivation is unlikely to be relevant to other types of cancer, this approach can have important implication in treating colorectal cancer. Lowe and his team hope to one day mimic the effect of Apc reactivation with drug treatments.

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