Newly Discovered Gene Halts Cell Division and May Have Cancer Link

NEW YORK, Oct. 11, 1996 -- Scientists at Memorial Sloan-Kettering Cancer Center have identified a human gene that arrests cell division in the laboratory and, when defective, may lead to the development of cancer. They reported the finding in the Oct. 11 issue of the journal Science.

The study suggests that if the gene's activity is blocked, cell division continues haphazardly and can lead to the formation of new cells that are missing chromosomes -- an event that is notoriously linked to tumor growth.

The researchers suspect that certain genetically unstable breast, ovarian, and prostate tumors may have defects in the gene, known as MAD2. The new discovery may open the door to finding more effective ways to treat such tumors.

"We think the MAD2 gene stops cells from dividing when doing so would leave the newly formed daughter cells without all the chromosomes they need to function properly," says Dr. Robert Benezra, an investigator in the Cell Biology and Genetics Program at Memorial Sloan-Kettering and the study's lead author.

MAD2 is the first human gene to be identified that serves as a checkpoint for cells to progress into the final stages of cell division. Until now, the only other checkpoint gene to be discovered was p53, which allows a cell to copy its DNA at an earlier phase in the cell cycle. Defects in the p53 gene are known to be involved in about half of all tumors.

The MAD2 gene allows a cell to commit to divide only after the gene checks to ensure that chromosomes, which contain DNA's genetic blueprint, are ready to separate normally to form two genetically identical cells.

"If MAD2 is defective and the checkpoint is challenged -- either by drugs or environmental stresses -- cell division can continue out of control and leave some new cells without a copy of each chromosome, which can lead to cancer," Dr. Benezra says.

The MAD2 checkpoint appears to plays an esse

Contact: Chris Westerman
Memorial Sloan-Kettering Cancer Center

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