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Reactivation of Developmentally Expressed p63 Isoforms Predisposes to Tumor Development and Progression

Departments of ¹ Molecular and Cellular Biology, ² Molecular and Human Genetics and ³ Dermatology, Baylor College of Medicine, Houston, Texas; ⁴ Department of Otolaryngology, and ⁵ Departments of Dermatology and Cell and Developmental Biology, Oregon Health and Science University, Portland, Oregon

Requests for reprints: Dennis R. Roop, Department of Molecular and Cellular Biology, Baylor College of Medicine, One Baylor Plaza, Room T721, Houston, TX 77030. Phone: 713-798-4966; Fax: 713-798-3800; E-mail: roopd{at}bcm.tmc.edu.

Genes that are active during normal development are frequently reactivated during neoplastic transformation. We now report that developmentally expressed TAp63 isoforms are frequently reactivated in human squamous cell carcinomas. To determine the consequences of TAp63 reactivation, we induced TAp63 expression during chemically-induced skin carcinogenesis. Deregulated TAp63 expression dramatically accelerated tumor development and progression, frequently resulting in epithelial-mesenchymal transitions to spindle cell carcinomas and lung metastases. Consistent with this observation, we detected high levels of Twist and N-cadherin in tumors overexpressing TAp63. Thus, as observed for other developmental pathways, aberrant reactivation of TAp63 predisposes to tumor development and progression. (Cancer Res 2006; 66(8): 3981-6)

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