Skip Navigation

JNCI Journal of the National Cancer Institute 2003 95(11):768-769; doi:10.1093/jnci/95.11.768
© 2003 by Oxford University Press
This Article
Right arrow Full Text Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrow Search for citing articles in:
ISI Web of Science (3)
Right arrow Request Permissions
Google Scholar
Right arrow Articles by Kraemer, K. H.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Kraemer, K. H.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Journal of the National Cancer Institute, Vol. 95, No. 11, 768-769, June 4, 2003
© 2003 Oxford University Press

EDITORIAL

NRAS Hypermutability in Familial Melanoma With CDKN2A Mutations—Cause and Effect?

Kenneth H. Kraemer

Correspondence to: Kenneth H. Kraemer, M.D., Basic Research Laboratory, Center for Cancer Research, National Cancer Institute, Bldg. 37, Rm. 4002 MSC 4258, Bethesda, MD 20892–4258 (e-mail: kraemerk@nih.gov).

The first 10% of the full text of this article appears below.

The frequency of cutaneous melanoma has been increasing worldwide for several decades. Approximately 8%–12% of melanomas occur in individuals with a history of cutaneous melanoma in a blood relative. Germline mutations in the CDKN2A tumor suppressor gene have been identified in approximately 20% of familial melanoma families, including many with dysplastic nevi (DN) (1). The CDKN2A region of chromosome 9p21 codes for p16 (INK4A), which functions in the retinoblastoma (Rb) protein cell-cycle control pathway, and also p14ARF, the product of an alternatively spliced transcript, which participates in the p53-mediated cell-cycle control pathway. Melanoma cell lines that do not express p16, or that express a mutant form of p16, do not show the normal G2 cell-cycle delay after UV exposure (2. . . [Full Text of this Article]


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
 Genes Dev.Home page
S. Carreira, J. Goodall, L. Denat, M. Rodriguez, P. Nuciforo, K. S. Hoek, A. Testori, L. Larue, and C. R. Goding
Mitf regulation of Dia1 controls melanoma proliferation and invasiveness
Genes & Dev., December 15, 2006; 20(24): 3426 - 3439.
[Abstract] [Full Text] [PDF]