Aromatase Overexpression Results in Gynecomastia and Leydig Tumors in Male Transgenic Mice

Overexpression of ARO in male transgenic mice results in increased MG epithelial growth as early as 3 mo of age with well-organized ductal structures and lobulo-alveolar growth. We did not observe further progression of hyperplastic and dysplastic changes in the ARO transgenic mice with age (31). In addition, our data demonstrated that the Overexpression of ARO plays a significant role in the formation of Leydig cell tumors, and that these cells are targets for estrogenic action and are involved in E-mediated tumorigenesis (32). The presence of ERs in human testicular Leydig cell tumors indicate that these cells are the source of E in both rodents and human testis (33-36). Our studies show that the level of ER expression and ARO are higher in the testicular tissue of these mice compared to that of non-transgenic mice, and that the serum E2 levels are significantly higher in transgenic mice vs non-transgenic littermates. Therefore, we suggest that an enhanced ER phenotype of Leydig cells and increased peripheral aromatization may contribute to Leydig cell tumorigenesis. The studies described above demonstrate that tissue Es play a direct role inducing gynecomastia and testicular cancer in male ARO transgenic mice and are consistent with recent observations with ARO knock out mice (37).

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