Cell-autonomous activation of the PI3-kinase pathway via biallelic loss of PTEN or activation of AKT in adult uterine epithelia in this model was sufficient to initiate endometrial carcinoma. Regenerated endometrial glands responded to pharmacologic variations in hormonal milieu similar to the native endometrium. To address this question, we established a malleable in vivo endometrial regeneration system from dissociated murine uterine epithelium and stroma. Consequently, the biologic outcome of selectively activating the PI3-kinase pathway in the endometrial epithelium remains unknown. Currently reported PTEN knockout mouse models initiate type I endometrial cancer concomitant with loss of PTEN in both uterine epithelium and stroma. In the majority of these tumors, PTEN expression is lost in the epithelium but maintained in tumor stroma. Epithelial-specific activation of the PI3-kinase pathway is the most common genetic alteration in type I endometrial cancer.
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