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Scientists Announce Finding Key Gene in Suppressing Cancer

April 13, 1994 GMT

SAN FRANCISCO (AP) _ A key gene that normally suppresses cancer has been identified by researchers, offering an important new focus for treating the disease, scientists reported Wednesday.

Loss of the gene was detected in a broad range of cancers, including 60 percent of breast cancer cases and 82 percent of one type of brain tumor.

″It’s very close to the action of cell division. When it’s broken, destroyed, mutated, cell division is left out of control,″ said Dr. Mark Skolnik of the University of Utah Medical Center.

The newly identified tumor-suppressing gene, p16, appears even more significant that the previously identified p53 gene, which is believed to be a major factor in colon, breast, liver and other cancers, said Alexander Kamb of Utah-based Myriad Genetics Inc., who helped lead the p16 research.


P16 controls the production of an enzyme that inhibits cell growth in cancer genes, while p53 does not, he said.

Cancer researchers are increasingly turning their attention to suppressor genes, which brake uncontrolled cell division.

Damage to these suppressor cells - by chemicals in cigarette smoke, ultraviolet light, radiation or other carcinogens - may be the chief cause of cancer, Kamb said at the annual meeting of the American Association for Cancer Research in San Francisco.

P16 may not be the ″magic bullet″ that ties all cancers together, but it’s a major step, Kamb said.

″It looks really promising as a major player in human cancers,″ he said.

Discovery of the p16 gene - called MTS1 by the Utah team - was first announced by David Beach of Cold Spring Harbor Laboratory in New York late last year.

The Utah team researched the gene’s role in fighting tumors and is publishing its findings in the April 15 issue of Science.

Beach said he felt p53 and p16 were among a small number of key suppressor cells that cause cancer when they fail. Scientists aren’t certain how many such cells exist.

Dr. Michael Kastan of Johns Hopkins University in Baltimore, who wasn’t involved in the research, said testing for missing or damaged p16 - along with p53 and other suppressors - offers hope both for diagnosing and eventually treating cancers.

″For example, this will add tremendously to deciding how aggressively we need to treat a breast tumor,″ he said. Women showing greater suppressor-cell damage after an operation would probably get closer monitoring and more therapy, he said.


But Kastan cautioned that the research was still a long way from providing definitive evidence that p16 can be tied to specific cancers.

Kamb said a slide test measuring p16 damage - similar to a pap smear - could be on the drawing boards in a year or so. Similar tests for p53 are already being prepared.

Ultimately, p16 may eventually provide a vehicle for treating cancer genetically, Kamb said.

″It’s a very simple molecule,″ he said. That eases the task of inserting healthy genes into an organ to replace missing or malfunctioning copies.

The Myriad Genetics-University of Utah team tested 290 types of cancer and found significant p16 mutations in about 50 percent. Skolnik said he believes that percentage will increase as their techniques improve.