| First Author | Milam MR | Year | 2007 |
| Journal | Am J Obstet Gynecol | Volume | 196 |
| Issue | 3 | Pages | 247.e1-5 |
| PubMed ID | 17346540 | Mgi Jnum | J:122611 |
| Mgi Id | MGI:3714878 | Doi | 10.1016/j.ajog.2006.10.872 |
| Citation | Milam MR, et al. (2007) Reduced progression of endometrial hyperplasia with oral mTOR inhibition in the Pten heterozygote murine model. Am J Obstet Gynecol 196(3):247.e1-5 |
| abstractText | OBJECTIVE: Phosphatase and tensin homolog (PTEN) mutations are associated with human endometrial cancers, and PTEN heterozygote(+/-) mice have a high rate of endometrial neoplasia. The objective of this study was to evaluate an oral mTOR inhibitor (mTOR-I) on the reduction of endometrial hyperplasia in an animal model. STUDY DESIGN: Three groups of 10 female mice were treated from age 20-26 weeks: group A, Pten wild type with mTOR-I; group B, Pten+/- with placebo; and group C, Pten +/- with mTOR-I. Rates of hyperplasia and markers of proliferation and apoptosis were evaluated. RESULTS: Higher grade hyperplasia occurred in a significantly greater percentage of the untreated Pten+/- group B (80%; 8/10) compared with groups A (0%; 0/10) and C (20%; 2/10; P < .02). The treated Pten+/- mTOR-I group C also demonstrated significantly increased apoptosis (P < .002) and decreased proliferation index (P < .02) compared with the untreated group B. CONCLUSION: Oral mTOR inhibition decreases the progression of endometrial hyperplasia in the Pten heterozygote murine model through decreased cell proliferation and increased apoptosis. |
