標題: in their pigmented skin cells [打印本頁] 作者: xfigawdw 時間: 2016-3-25 04:40 標題: in their pigmented skin cells
Study May Help Explain Sunlight's Role In Melanoma Development
Now, for the first time, scientists have identified a specific molecular pathway within cells that becomes mutated by ultraviolet light exposure, thereby speeding up melanoma development.
New findings published in the Feb. Norman Sharpless, assistant professor of medicine and genetics at the University of North Carolina at Chapel Hill School of Medicine and a member of UNC's Lineberger Comprehensive Cancer Center.
"Who hasn't been sunburned?" he said. "This work suggests a rational method for risk stratification, for screening questionable skin moles atypical nevi Pandora New Zealand Charms for specific molecular lesions."
In the new study, Sharpless and colleagues at Harvard Nike High Heels New Zealand Medical School used mice deficient in an important tumor Supra Skytop White suppressor protein connected to the "anti cancer" cell signaling pathway Ray Ban Glasses Nz ARF p53. In addition to this Nike Online Store.html deficiency, Ralph Lauren Polo Shirts these mice were genetically designed to produce another protein, H Ras, in their pigmented skin cells, or melanocytes.
"Loss of ARF p53 and activation of Ras are two of three hallmark events detected in human melanomas. The third being loss in another 'anti cancer' cell signaling pathway, p16INK4a Rb," said Sharpless.
This mouse model allowed researchers to selectively test the effects Buy Ray Ban Lenses of ultraviolet light exposure on the p16INK4a Rb pathway.
The Rb pathway regulates cell growth. The retinoblastoma protein acts to hold cell proliferation in check. The regulatory capacity of Rb is moderated by CDK6 and the tumor suppressor protein, p16INK4a. The researchers found targeting of the Hollister Outlet Store Rb pathway, either by an increase in CDK6 expression or a loss of p16INK4a, in the melanomas that developed on mice treated with a single exposure of ultraviolet light essentially, a mouse sunburn. In mice genetically engineered to lack p16INK4a, however, ultraviolet light exposure did not increase melanoma formation.
"These data suggest that it is not so much this gene or that gene, but the pathway that is what UV light targets," Sharpless said.
"This is one of the better mouse models for any human tumor that I'm aware of," he added. "This finding is unique in that it identifies the Rb pathway as a target of UV's mutagenic action."
The next research step is to look at a collection of clinical samples to determine if exclusive lesions in the Rb pathway are linked to melanomas from patients with a detailed history of ultraviolet light exposure.
"Melanoma screening is a good idea, but it needs some molecular help to distinguish the really high risk patients from those at a lower risk for developing melanoma," Sharpless said. chief, visiting Ebola countries, urges respect for health rules.
