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Heal thyself: Systems biology model reveals how cells avoid becoming cancerous

Researchers at the University of California, San Diego and three other institutions have described for the first time a web of inter-related responses that cells use to avoid becoming diseased or cancerous after being exposed to a powerful chemical mutagen. The group led by UCSD bioengineering professor Trey Ideker describe in the May 19 issue of Science an elaborate system of gene control that is triggered by chemical damage to DNA.

"This research sheds light on the complexity of DNA repair, and offers an example of how the cellular process stimulates other pathways," said David Schwartz, director of the National Institute of Environmental Health Sciences (NIEHS), one of the agencies which funded the study. "This new knowledge has great potential for the development of new therapeutic agents to combat a broad spectrum of diseases, including cancer, neurodegenerative diseases, and premature aging."

Researchers involved in the study agreed that their findings could eventually be used to develop drugs to boost DNA repair in response to environmental toxins and possibly treat inherited degenerative diseases such as xeroderma pigmentosum, a disease in which the body's ability to repair DNA damage caused by ultraviolet light is disabled, ataxia telangiectasia, a progressive, neurodegenerative childhood disease, Werner syndrome, a premature aging disorder, and others.

"DNA damage is a basic physiological process that is important to coping with environmental toxins and a number of congenital diseases," said Ideker, the senior author of the paper. "Over the past several decades, scientists have discovered many parts of the DNA-damage-repair machinery, but what has been missing until now is a 'systems biology' approach that explains how all the parts function together to enable a cell to repair its DNA while under routine assault."

UCSD post-doctoral fellow Christopher T. Workman, Ph.D. candidate Craig Mak, and technicians Scott McCuine and
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Source:University of California - San Diego


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