One might call it a tale of two melanocytes. Given the same genetic mutation, why does one melanocyte shut down growth and become a relatively benign mole, while another rages out of control and develops into deadly melanoma"
In trying to tease out the answer to this simple question, Howard Hughes Medical Institute (HHMI) researchers have uncovered a protein that stops the growth of melanoma, a cancer that develops from pigment-producing cells in the skin called melanocytes. HHMI investigator Michael Green and colleagues at the University of Massachusetts Medical School reported their identification of the genetic underpinnings of a new way to thwart one of the deadliest forms of cancer in the February 8, 2008, issue of the journal Cell.
Green and his colleagues began by designing experiments that would help them determine what separates melanomas from ordinary moles at the genetic level. Moles, also known as nevi, and melanoma often result from the same genetic mutation, and the biological pathway that differentiates the two had been a mystery. The new study uncovers a relatively unknown protein that regulates the melanocytes decision to ward off cancer by either entering a programmed hibernation or committing suicide.
According to the American Cancer Society, 60,000 people in the United States developed melanoma in 2007, and more than 8,000 died of the disease. Melanoma is caused by the uncontrolled proliferation of melanocytes, whose pigment, melanin, protects the skin against the suns ultraviolet rays. Nevi, which are benign, are also caused by abnormal growth and differentiation of melanocytes.
While nevi are, by definition, non-cancerous, more than half the time the same mutation is at fault in melanoma and nevi: a single amino acid change in a protein called BRAF. BRAF is part of a signaling system that is important for cell growth and proliferation. The BRAF mutation found in nevi and melanoma increases the activity of the BRAF protein,
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| Contact: Jim Keeley keeleyj@hhmi.org 301-215-8858 Howard Hughes Medical Institute Source:Eurekalert |