Personalizing Colon Cancer Treatment

Tumor suppressing molecule that prevents growth could lead to personalized therapy.

The discovery of a new tumor suppressing molecule may eventually lead to personalized treatment for colorectal cancer, a recent study suggests.

Published in the journal Nature Medicine, the study found the tumor-suppressing protein AIM2 (Absent in Melanoma 2) aids in the prevention of colon cancer by restricting the Akt signaling molecule. As a result, the findings indicate this may provide a potential drug target for patients who lack the tumor suppressing AIM2 protein.

“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 first author Justin E. Wilson, PhD, in a press 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.”

Prior research has found that AIM2 inhibits growth across colon cancer cell lines, in addition to a poor prognosis in colon cancer patients with low or missing AIM2 levels, according to the current study.

“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,” researcher Jenny Ting, a William R. Kenan Jr. Distinguished Professor in the University of North Carolina School of Medicine Department of Genetics said in a press release.

Analysis of colon cancer cells found that AIM2 limits the activation of Akt. Meanwhile, in mouse models that lacked AIM2, the researchers found there were smaller tumors and precancerous colon polyps when Akt was blocked.

Subsequently, drugs that inhibit Akt may offer a personalized therapy for patients who lack AIM2.

“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,” Dr. Wilson said.