Scientists Find Gene That May Be Key to Onset of Deadly Skin CancerThursday, August 16, 2001 Posted Friday, August 17, 2001 by ctustis
BY TROY GOODMAN THE SALT LAKE TRIBUNE

Scientists analyzing various kinds of moles say they have pinpointed a
key gene heralding the transformation of a blemish from non-threatening
into melanoma, the deadliest type of skin cancer. The research by a Johns
Hopkins University team holds promise in the development of early
diagnostic markers for the rapidly-spreading disease, Utah cancer experts
said. Early treatment of melanoma is crucial for survival since less than
10 percent of people with a developed stage of the disease live beyond
five years. "Telling the difference between precancerous moles and
early-stage melanoma can be very difficult," said Rhoda Alani, an
oncology and genetics professor at Johns Hopkins in Baltimore and author
of the study. "If it's melanoma, you want to catch it very early and
treat it aggressively by removing as much tissue as possible to cure the
disease." Alani, along with a three-person research team, found that
melanomas contain a regulatory gene known as Id1, which acts like a DNA
accelerator to fuel cancer cells into uncontrollable growth. The presence
of Id1 in suspect moles could help doctors spot early melanoma and then
treat it while it's still at a curable stage, Alani said. The research
appears in the latest issue of Cancer Research, a journal of the American
Association for Cancer Research. It was based on 21 samples of skin
lesions, all in varying forms of non-malignancy or malignancy. The
findings caught the interest of Salt Lake City-based Huntsman Cancer
Institute where hundreds of melanoma patients -- all victims of Utah's
sun-drenched high-altitude atmospheric conditions -- are studied every
year for their skin cancer. Sancy Leachman, director of Huntsman's
familial melanomal research clinic, said the latest study holds promise.
The findings build on earlier research conducted at the University of
Utah and Salt Lake City biomed company Myriad Genetics during the early
1990s. Back then, Leachman said, the U. and Myriad were key players in a
skin cancer breakthrough that identified biological changes in another
gene, called p16, that led to melanoma formation. Today, those findings
are part of a widely held belief that "about 40 percent of the familial
melanoma is because of the p16 gene," Leachman said. But familial
melanoma, the results of an inherited predisposition to getting the
disease, isn't the only explanation. Sun overexposure, fair complexions
and occupational exposure (to coal tar, pitch, creosote, radium, for
example) also play a part, she said. This year alone, melanoma will
strike more than half a million Americans and kill some 7,800, according
to the research association. So the Cancer Research study on Id1, a gene
that regulates p16 action, sheds light on the genetic "pathway" cells
cross when they go from normal to cancerous, Leachman said. But knowing
more about that pathway could be less important than further research on
p16's direct role in melanoma formation. "It might be more important to
focus on p16 itself," she said of the Cancer Research findings. Still,
hopes for better genetic tests that could spot early skin cancer growths
were on the minds of the Johns Hopkins researchers when they wrote the
latest study. "Marker studies for Id1 in melanocytic lesions of uncertain
malignant potential may play a critical role . . . and may help determine
the appropriate treatment and prognosis of melanocytic lesions," the
authors wrote.

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