Reduced progression of endometrial hyperplasia with oral mTOR inhibition in the Pten heterozygote murine model

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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.


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.


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.


Oral mTOR inhibition decreases the progression of endometrial hyperplasia in the Pten heterozygote murine model through decreased cell proliferation and increased apoptosis.

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