Colon cancer’s culprit gene

Colon cancer’s culprit gene

Joanne Silberner

Colon cancer’s culprit gene

Last week’s announcement by Britishresearchers that colon and rectal cancers can be triggered by the absence of a normal gene was not the first time such a cancer mechanism has been described –a similar process is known to be at work in several rare childhood malignancies. Never before, however, had a defective gene been tied to so common a form of cancer–one that will kill 60,000 people in the U.S. this year, a death toll exceeded only by lung cancer’s. With rare cancers as models, scientists will next hunt for the exact genetic defect that breeds colorectal cancer, a crucial step toward devising a way to diagnose the disease early and ultimately finding a cure.

Reserchers from the Imperial CancerResearch Fund in London identified a unique chromosomal segment– evidently missing all or part of a key gene–in people with a familial form of colorectal cancer. They found identical segments in over 20 percent of colorectal-cancer victims who had no strong family history of the disease.

Although the scientists know wherethe crucial gene is, they have not yet mapped out its structure. The defect does not by itself cause malignancy, they think. “Cancer is a series of mistakes,’ explains study leader Sir Walter Bodmer. Genes come in pairs, and even with one inherited defective gene it apparently takes a mutation in its mate to set off colon cancer. The mutations can be inherited or caused by ingested toxins that a low-fiber diet allows to languish in the system. Bodmer suggests that the normal genes keep cell growth in check. Defective genes permit cells to grow into small polyps, and a high-fat, low-fiber diet may somehow disturb the growths so that they become cancerous, he says.

Last May, Johns Hopkins Universityresearchers found a different gene linked to colorectal cancer in some patients. In the cases they studied, it was an overactive gene, rather than a nonfunctional one, that was to blame. Dr. Bert Vogelstein, who was involved in the Hopkins study, calls the British research “another important piece of the puzzle.’ Identification of the anomaly may soon prove useful in identifying which members of high-risk families should be closely monitored.

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