Magazine article Science News

Bad Brakes in Cell Cycle Linked to Cancers

Magazine article Science News

Bad Brakes in Cell Cycle Linked to Cancers

Article excerpt

Five months ago, molecular biologists tied the tumor suppressor gene p53 to proteins that control the cell cycle--the progression of cells through growth and division (SN: 11/27/93, p.356). Now, two research teams have confirmed an even more insidious relationship between cancer and aberrations in this cycle.

In many tumor types, cells lack functional copies of p16, a protein that puts the brakes on cell division, says Tsutomu Nobori, a molecular biologist at the University of California, San Diego. In these cells, the two copies of the gene that directs production of p16 have either mutated or disappeared, he and his colleagues report in the April 21 NATURE.

They examined 46 cell lines, or groups of tumor cells, for abnormalities in the region of chromosome 9 where the p16 gene lies. About 61 percent of melanoma cell lines, 87 percent of glioma cell lines, 64 percent of leukemia cell lines, and 36 percent of non-small-cell lung cancer cell lines lacked p16 genes, Nobori reports.

The p16 gene contains three regions that direct p16 production, adds Alexander Kamb, a molecular biologist at Myriad Genetics in Salt Lake City. Independently, Kamb's group studied 12 types of cancers and detected no copies of the p16 gene in 133 of the 290 cell lines tested--a frequency of missing genes similar to that of Nobori's group. In Kamb's report in the April 15 SCIENCE, he has named this gene Multiple Tumor Suppressor 1.

The Utah researchers then analyzed melanoma cell lines for alterations as well as deletions in the p16 gene. With both included, the gene's involvement in cancer increased to 75 percent from 58 percent. They expect this trend to hold for other types of cancers, Kamb says. …

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