Pitt team first to illustrate mechanisms of chromosome missegregation in cancer cells

PITTSBURGH, January 4 - Researchers at the University of Pittsburgh have provided the first graphic illustration of mechanisms by which chromosomes are distributed unevenly during cancer cell division. These results are published in the January 4, 2000, issue of the Proceedings of the National Academy of Sciences.

"This is really the first paper showing a mechanism by which chromosome segregation can go awry in cancer cell division, leading to genetic defects such as abnormal or missing chromosomes," said William Saunders, principal investigator on the study, assistant professor of biological sciences and an investigator in the Oral Cancer Center at the University of Pittsburgh. "By witnessing these events, we can now target for study those activities within a cancer cell that become deranged during cell division. In this way, we can focus on ways to interrupt these abnormal processes with the potential to curb cancerous growth."

During normal cell division, coils of genetic material called chromosomes align neatly in the middle of the cell into 23 pencil-shaped pairs of parallel strands called chromatids. At the same time, two centrioles form at opposite poles of the cell. Thread-like microtubules attach each of the chromatids to the centrioles, forming the spindle. When the cell divides, the chromatids separate and are pulled by the microtubules to opposite poles. Thus, two identical pools of chromatids, the inherited genetic instructions of the future daughter cells, form at the poles. The interior of the cell separates in barbell-like fashion with a narrow bridge that eventually pinches in two to form the two daughter cells.

Using fluorescent markers to label cell structures involved in the division of oral cancer cells, the Pittsburgh team is the first to capture the unusual activities that account for well-recognized genetic derangements characteristi

Contact: John Fedele
University of Pittsburgh Medical Center

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