Study: Fixing a single gene turns colorectal cancer cells into normal cells

Before (cancerous) and after (normal).
Before (cancerous) and after (normal).
Image: Kevin P. O'Rourke
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Cancer is caused by genetic mutations that force normal cells to grow abnormally. Often, however, these mutations are too many to even think about stopping or fixing them. But what if the mutations responsible for causing the cancer were only in a single gene? A new study shows, at least in colorectal cancer, that is the case, and offers hope for a cure.

Colorectal cancer—also called bowel cancer—is among the most common cancers afflicting people. It kills more than 700,000 every year.

Scientists at the Memorial Sloan Kettering Cancer Center (MSKCC) knew that mutations in a gene called APC, short for “adenomatous polyposis coli,” were found in 90% of colorectal cancer tumors. But they weren’t sure how the mutations played a role in causing cancer.

Reversing cancer

To understand APC’s role, they used RNA interference (RNAi) in genetically engineered mice to turn off the APC gene. RNAi technology works by using an agent—in this case an antibiotic—that disrupts the APC gene pathway, and thus stops it from producing proteins that it normally would. These APC proteins have the ability suppress tumors, so when the gene is turned off the mice developed colorectal cancers.

When they stopped feeding the mice the antibiotic, the gene pathway was restored and APC was turned on. Within four days, tumors stopped growing. Better still, the mice intestine, which had the tumors, started functioning normally. After a few weeks, the tumors had regressed and months later the mice were completely free of cancer. The results of the study were published in the journal Cell.

Experiments like these are the closest step yet to curing cancer. Of course, as Nell Barrie, Cancer Research UK’s senior science information manager, tells Quartz, “Correcting a fault like this in humans is currently impossible. Despite that, these results still hold great potential—highlighting that the APC fault in bowel cancer is a crucial weakness that could be exploited in other ways to help treat the disease.”

Beyond the bowels

Most often a gene’s role is to kickstart a cascade of processes that will help the cell do some of its tasks. In the case of APC, one of those tasks is to suppress tumors. MSKCC scientists found that the suppression of tumors happens further down the cascade through something called the WNT pathway, which gets deactivated because of mutations in APC.

Kevin O’Rourke, one of the MSKCC scientists behind the study, tells Quartz that he and his colleagues are now looking for drugs that can activate the WNT pathway. If they are successful, they would have found a treatment for colorectal cancer without having to do a much more difficult job of fixing genetic mutations.

And the finding has implications for other types of cancer. Pancreatic cancer, for instance, presents a similar case, where mutations in a single gene are found in 90% of tumors. A similar kind of investigation could yield treatments for it, too.