Reactivation of a single gene turns colorectal cancer cells back into normal tissue

Future cancer treatments may target your genes rather than the cancerous cells themselves. A new study found that reactivating a single gene was enough to stop and reverse colorectal cancer (that's cancer of the colon, or bowels) in mice, with a return to normal intestinal functions within just four days and tumors gone within two weeks. The concept, though not the specific method, could lead to new treatments of a variety of cancers.

Nearly 700,000 people around the world die from colorectal cancer each year, which makes it one of the biggest cancer killers (lung cancer is the most common, at more than 1.5 million deaths, while cancers of the liver result in around 750,000 deaths a year and deaths from cancers of the stomach stand a little over 700,000). In the United States, where colorectal cancer is the third most common cancer in men and in women (or second most common combined across both sexes), diagnoses for the disease numbered over 135,000 people in 2011.

It's highly prevalent, but current treatments at the advanced stages are toxic and ineffective. The researchers noted, however, that 80 to 90 percent of colorectal tumors contain the same gene mutation. They sought to reverse that mutation to see what would happen.

They treated mice with colorectal cancer in their colon, which is where it normally forms in humans, and found that not only did tumors stop growing but the intestinal cells also recovered normal function – even in tumors with Kras and p53 mutations. They then shrank and disappeared or turned into normal tissue within two weeks. After six months of monitoring, the mice remained cancer free.

This does not necessarily mean that the researchers have found a cure for colorectal cancer. The researchers still need to explore the wider consequences of the treatment and to determine why it is so effective in mice, then they need to adapt the technique for human treatments.

The approach may have big implications in broader cancer treatment. "If we can define which types of mutations and changes are the critical events driving tumor growth, we will be better equipped to identify the most appropriate treatments for individual cancers," says study first author Lukas Dow of Weill Cornell Medical College.

A paper describing the research was published in the journal Cell.

Source: Meyer Cancer Center