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New gene monitors cell division, cancer clinical applications seen

In health, most cells undergo a carefully orchestrated cell-division process in order to replicate. At the heart of this process is mitosis, in which a cell's nucleus duplicates its genetic material and divides. Precisely controlled mitosis is vital to survival, and rigorous checkpoint mechanisms are in place to ensure that each step in the process is properly executed before the cell moves on to the next step. Although not well proven, it is generally believed that many human cancers stem from checkpoint defects in mitosis.

In the July 27 issue of Nature, scientists at The Wistar Institute report identification of a new gene called chfr that establishes a previously unknown checkpoint in mitosis. Further, a laboratory survey of eight human cancer cell lines found chfr to be inactivated, through lack of expression or mutation, in four of the eight -- fully half of the cell lines studied. Mitotic checkpoint genes identified in earlier studies had been linked to cancers, too, but mutant versions had been found in only 1 or 2 percent of cancers.

"The frequency of mutations in previously identified mitotic checkpoint genes is too low to explain the incidence rates of cancers in which troubled cell division is thought to play a role," says Thanos D. Halazonetis, D.D.S., Ph.D., senior author on the study and an associate professor at Wistar. "So, the question was whether there were checkpoint genes we didn't know about and whether those were the genes suffering mutations in these cancers. What we found was a new gene and a wholly new mechanism that monitors progress through mitosis. Further, this gene was disrupted in 50 percent of the cancer cell lines we studied, much higher than the rates for other known checkpoint genes."

Halazonetis emphasizes that studies of tumors from patients will be needed to confirm that mutant chfr is as common in primary cancer cells as it is in laboratory cancer cell lines. If the findings are confirmed, however, clinical a
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Contact: Franklin Hoke
hoke@wistar.upenn.edu
215-898-3716
The Wistar Institute
26-Jul-2000


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