LEBANON, NH – Colon cancer is the second most common cause of cancer-related deaths. The APC protein has long been known for its critical role in preventing colorectal cancer. When APC is inactivated, the development of colorectal cancer is triggered. Inactivation of APC is responsible for the vast majority (80%) of all colorectal cancers. Researchers from the laboratory of Yashi Ahmed, MD, PhD at Dartmouth’s Norris Cotton Cancer Center, in collaboration with the groups of Ethan Lee, MD, PhD at Vanderbilt University and David Robbins, PhD at the University of Miami’s Sylvester Comprehensive Cancer Center, have identified a new function for this colon cancer gene: APC stops several colon cancer activators.
APC works in a pathway that allows one cell to communicate with its neighbors. When APC is inactivated, this pathway goes into overdrive and that triggers colon cancer development. Exactly how APC acts in this pathway has remained a mystery. The long-held view was that the sole function of APC is to cause the destruction of one activator of the overdrive activity. “The surprise from our research is that APC actually has a second role in putting the brakes on several other activators in the pathway,” says Ahmed.
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