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[Cancer Research 62, 3200-3206, June 1, 2002]
© 2002 American Association for Cancer Research

Molecular Biology and Genetics

Cyclin D1 Is a Candidate Oncogene in Cutaneous Melanoma1

Edward R. Sauter, Un-Cheol Yeo, Andrea von Stemm, Weizhu Zhu, Samuel Litwin, David S. Tichansky, Giuseppa Pistritto, Mark Nesbit, Dan Pinkel, Meenhard Herlyn and Boris C. Bastian2

Departments of Dermatology and Pathology, University of California, San Francisco [U-C. Y., A. v. S., B. C. B.] and University of California San Francisco Comprehensive Cancer Center [D. P., B. C. B.], San Francisco, California 94143; The Wistar Institute, Philadelphia, Pennsylvania 19104 [E. R. S., D. S. T., G. P., M. N., M. H.]; Department of Surgery, Thomas Jefferson University, Philadelphia, Pennsylvania 19107 [E. R. S., W. Z.]; and Division of Population Science, Fox Chase Cancer Center, Philadelphia, Pennsylvania 19111 [S. L.]

The retinoblastoma pathway has been implicated in melanoma; however, previous studies of oneof the key components of this pathway, cyclin D1 (CD1), failed to find amplification of this gene in a large series of melanomas. We have recently shown that a particular subtype of melanoma, acral melanoma (AM), has frequent amplification of the CD1 locus. This suggested that CD1 might be important in AM and that it may also be important in other melanoma types, even though its copy number may not be altered. We compared CD1 gene copy number and protein expression in 137 invasive primary cutaneous melanomas (71 superficial spreading melanomas, 17 nodular melanomas, 19 lentigo maligna melanomas, 18 AMs, and 12 unclassifiable melanomas) using fluorescence in situ hybridization and immunohistochemistry. We found frequent amplification of CD1 in AM (44.4%) and occasional amplification in lentigo maligna melanoma (10.5%) and superficial spreading melanoma (5.6%). CD1 protein was overexpressed in all cases with amplifications and in an additional 20% of cases without amplification. We tested the importance of CD1 in cell growth in melanoma by using adenovirus-mediated antisense treatment targeted to CD1 in two melanoma cell lines, one with and the other without CD1 amplification and overexpression. Antisense mediated down-regulation of CD1 induced apoptosis in vitro and led to significant tumor shrinkage of melanoma xenografts in severe combined immunodeficient mice. However, it did not alter the growth of normal melanocytes. Together, these results suggest that CD1 may be an oncogene in melanoma and that targeting its expression may be therapeutically beneficial.




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Copyright © 2002 by the American Association for Cancer Research.