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2001 MAR 29 - (NewsRx.com & NewsRx.net) --- To the small list of genes that play a role in the development of breast cancer can now be added the name ZNF217.
Multiple copies of this gene were found to remove natural restrictions on cell growth and thereby increase the chances for malignancy in a study jointly conducted by researchers with the Lawrence Berkeley National Laboratory (Berkeley Lab) and the University of California at San Francisco (UCSF).
"We hypothesize that over the course of evolution, the human body has developed an intrinsic molecular mechanisms to count and limit the number of times breast cells divide as a means of limiting the growth of abnormal cells," says Paul Yaswen, a cell biologist with Berkeley Lab's Life Sciences Division who was the principal investigator in this study. "When expressed inappropriately, ZNF217 appears to compromise this mechanism, the net result being that the affected cells can continue dividing and accumulating additional changes necessary for malignancy."
Normal cells contain two copies of ZNF217, which are located on human chromosome 20. Amplification of the ZNF217 gene (i.e., more than two copies are present) has been found in many different types of tumors, including some 40% of human breast cancer cell lines. The results of this latest study support the theory that over-activity of the ZNF217 gene contributes to the development of breast cancer by promoting cell "immortality." Cells are said to have become immortal when they grow past the point at which senescence and death is supposed to kick in.
Explains Yaswen, "Our data suggest that simple over-expression of the ZNF217 gene product itself only allows cells to continue growing when they would otherwise stop. However, continued growth allows the cells to accumulate additional changes which may favor invasion and metastasis."
Collaborating with Yaswen on this study were Genevieve Nonet and Martha Stampfer of Berkeley Lab, and Joe Gray, Colin Collins, and Koei Chin of UCSF. Their results were published in the February 15, 2001, ...