Colon Cancer: New Discovery Leads To Personalized Approach

First Posted: Jun 29, 2015 10:40 PM EDT

New findings published in the journal Nature Medicine reveal how a certain tumor suppressor molecule that works to prevent tumor growth could actually lead to a new personalized approach in the treatment of colon cancer.

"Several studies and clinical evidence suggest AIM2 functions as a tumor suppressor, but until now, we've had very little direct evidence to explains how this occurs," said study author Justin E. Wilson, PhD and a postdoctoral fellow at UNC Lineberger, the UNC School of Medicine Department of Microbiology and Immunology and the Department of Genetics, in a news release. "We found that AIM2 inhibits tumorigenesis in multiple animal models of colorectal cancer by restricting the pro-survival signaling molecule, Akt, which is commonly hyperactive in many human cancers."

Researchers found that AIM2, a tumor-suppressing protein, helped to prevent colon cancer by restricting a signaling molecule called Akt. Furthermore, the study results build on previous research that suggest that AIM2 limits cancer cell growth in colon cancer cell lines, including how AIM2 limits the activation of the signaling molecule Akt.

"Patients with colon cancer lacking in AIM2 have been found to have poor survival, but we have identified a possible personalized therapeutic strategy to help them," added Jenny Ting, William R. Kenan Jr. Distinguished Professor in the UNC School of Medicine Department of Genetics and a UNC Lineberger Comprehensive Cancer Center member.

The findings showed that AIM2 helped in preventing the activation of the signaling molecule Akt. Furthermore, in mouse models that lacked AIM2, researchers found smaller tumors as well as precancerous colon polyps when Akt was blocked.

"Our research paves the way for future clinical trials that screen for AIM2 expression in colon cancer and possibly other cancers to identify patients who may potentially benefit from personalized anti-Akt therapy," Wilson concluded.

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