The scope of this project is limited to describing visual characteristics corresponding to various types of pigmented lesions in common, acquired melanocytic nevi and in patients with the rare genetic disease xeroderma pigmentosum. Under the auspices of clinical protocol 06-C-0060 (Thomas J. Hornyak, M.D., Ph.D., Principal Investigator), patients are recruited to the Dermatology Clinic for study and tissue acquisition of melanocytic nevi. Selected lesions are imaged with digital epiluminescent microscopy using a device, the digital dermatoscope, that permits evaluation of these lesions under illuminated magnification. Certain structures correlated with benign or malignant pigmented lesions can be observed with this technique. We collect images of lesions over time and analyze them for changes and for the presence of novel structures that can be correlated with specific types or arrangements of cells histopathologically. Also, in collaboration with Drs. Kenneth Kraemer and John DiGiovanna of the Dermatology Branch, we have obtained digital dermatoscopic images of biopsied pigmented skin lesions on approximately 20 patients with xeroderma pigmentosum. These patients have been seen at the NIH Clinical Center under the auspices of Dr. Kraemer's clinical protocol focused upon xeroderma pigmentosum. Currently the greater than twenty lesions whose information has been obtained from these patients are being analyzed, using standard dermatoscopic criteria, for features that may permit whether they can be classified clinically as malignant or benign. In addition, dermatoscopic evaluation of selected pigmented lesions on family members of those affected with xeroderma pigmentosum is sometimes performed.

National Institute of Health (NIH)
National Cancer Institute (NCI)
Investigator-Initiated Intramural Research Projects (ZIA)
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National Cancer Institute Division of Basic Sciences
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Fan, Tao; Jiang, Shunlin; Chung, Nancy et al. (2011) EZH2-dependent suppression of a cellular senescence phenotype in melanoma cells by inhibition of p21/CDKN1A expression. Mol Cancer Res 9:418-29
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