Rat endometrial hyperplasia (A) has increased glandular crowding, increased glandular size, increased glandular complexity, and increased epithelial nuclear.

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Presentation transcript:

Rat endometrial hyperplasia (A) has increased glandular crowding, increased glandular size, increased glandular complexity, and increased epithelial nuclear atypia compared with normal rat endometrial epithelium (D). Rat endometrial hyperplasia (A) has increased glandular crowding, increased glandular size, increased glandular complexity, and increased epithelial nuclear atypia compared with normal rat endometrial epithelium (D). Similar to humans, rat endometrial hyperplasia has high immunohistochemical expression of phosphorylated (S235) S6 (B) compared with normal endometrium (E). Similar to humans, rat endometrial hyperplasia has absent immunohistochemical expression of phosphorylated (S636/639) IRS-1 (C), whereas expression is retained in normal endometrium (F). The majority (94%) of normal endometrial epithelium do not express phospho-(S235) S6 (E) and retain negative feedback to IRS-1 (F). Very few (6%) of normal-appearing glands [indicated by the arrow (↓)] express phospho-(S235) S6 (H) and retain phospho-(S636/639) (I), suggesting that these glands are “preneoplastic.” Data shown in H and I suggest that activation of mTOR signaling precedes the loss of negative feedback to IRS-1 in the progression to endometrial hyperplasia. Original magnification, ×200. Adrienne S. McCampbell et al. Cancer Prev Res 2010;3:290-300 ©2010 by American Association for Cancer Research