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Vet Pathol 41:278-282 (2004)
© 2004 American College of Veterinary Pathologists
BRIEF COMMUNICATIONS AND CASE REPORTS

The Roles of Smad2 and Smad3 in the Development of Chemically Induced Skin Tumors in Mice

S. H. Tannehill-Gregg, D. F. Kusewitt, T. J. Rosol and M. Weinstein

Abstract

Transforming growth factor-ß (TGF-ß) plays a complex role in skin carcinogenesis, acting as a suppressor early in tumor development but later as a promoter. Smad proteins are important intracellular mediators of TGF-ß signaling. To determine the effect of disrupting Smad genes and TGF-ß signaling on chemically induced skin carcinogenesis in mice, transgenic mice heterozygous for Smad2 or Smad3 deletions and wild-type controls were treated with topical dimethylbenzanthracene for 7 months. Tumor multiplicity, type, and degree of differentiation were assessed by histopathology and immunohistochemistry. Smad3± mice developed significantly fewer tumors than the wild-type group (P < 0.05). This indicated a possible oncogenic function for Smad3 in skin carcinogenesis. Smad2± mice formed less-differentiated tumors than their wild-type counterparts, supporting a tumor suppressor role for Smad2. There was a significant difference (P < 0.05) in tumor type between Smad2± and Smad3± groups, suggesting that Smad2 and Smad3 may regulate different targets.

Key words: Dimethylbenzanthracene; keratinocytes; mice; papilloma; squamous cell carcinoma; transforming growth factor beta.

Request reprints from Dr. M. Weinstein, Department of Molecular Genetics, Division of Human Cancer Genetics, The Ohio State University, 484 West 12th Avenue, Columbus, OH 43210 (USA). weinstein.41{at}osu.edu.




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