At least 70 genetic mutations may be involved in the formation of colon cancer, far more than scientists previously thought, a new study suggests. The study by researchers at University of Texas (UT) Southwestern Medical Center contradicts previous thinking that only a few mutated genes may play a role in the development of colon cancer. "The ways we've been treating patients up to now is to just go after one target when we should be going after three to four different pathways simultaneously," said Dr. Jerry W. Shay, vice chairman and professor of cell biology at UT Southwestern. The new study identified 65 candidate genes and at least five passenger genes whose mutations play significant roles in cancer development. Inactivating the function of any of these tumor- suppressing genes led to a key step in cancer development called anchorage-independent growth, meaning cells piled up on top of each other rather than aligning neatly. According to previous studies, there were 151 candidate genes and that mutations in just eight to 15 of them would lead to cancer. There were 700 other genes classified as passenger genes whose mutations were incidental to cancer growth. Current cancer treatments target just one or two known cancer- driver genes. While patients may get transient tumor burden reduction, almost universally tumor growth returns. "Those numbers are dead wrong," Dr. Shay said, suggesting a new approach to colon cancer treatments targeting multiple genes and pathways simultaneously. The next step is further research to classify more accurately which genes drive cancer and which are merely passengers, the researchers said. Study findings were published in the July 2011 Cancer Research (Priority Reports).
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