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RESEARCH COMMUNICATION
University of California at San Francisco Comprehensive Cancer Center, San Francisco, California 94143, USA
Pten heterozygous (Pten+/-) mice develop increased papilloma numbers and show decreased carcinoma latency time in comparison with controls after skin treatment with dimethyl benzanthracene (DMBA) and tetradecanoyl-phorbol acetate (TPA). H-ras mutation is normally a hallmark of DMBA-TPA-induced skin tumors, but 70% of carcinomas from Pten+/- mice do not exhibit this mutation, and in all cases have lost the wild-type Pten allele. Tumors that retain the Pten wild-type allele also have H-ras mutations, indicating that activation of H-ras and complete loss of Pten are mutually exclusive events in skin carcinomas. Mitogen-activated protein kinase (MAPK) is consistently activated in the tumors with H-ras mutations, but is strongly down-regulated in Pten-/- tumors, suggesting that this pathway is dispensable for skin carcinoma formation. These data have important implications in designing individual therapeutic strategies for the treatment of cancer.
[Keywords: Pten; ras; Akt; skin; papilloma; carcinoma]
Received April 21, 2004; revised version accepted June 2, 2004.
1 These authors contributed equally to this work.
2 Corresponding author. E-MAIL abalmain{at}cc.ucsf.edu; FAX (415) 502-6779.
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