Studies on development and proliferation of endometrial cancer from sex steroid receptor and oncogenes

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In the tissues of female reproductive organs and corresponding benign and malignant tumors and circumstances, cellular profiferation and function are basically regulated by sex steroids, which imply the expressions (mRNA) of cellular oncogenes and steroid receptors, corresponding to mutations.(1) Synthesis of cellular SHBG/CBG (mRNA) in the uterine endometrium is primarily regulated by estrogen/progesterone. However abandance of SHBG gives the supply of estrogen to the endometriotic tissues.(2) Monocyte/macrophage in the ascites with pelvic endometriosis is activated, while expression of fms (M-CSF receptor) oncogene is stimulated by estrogen/progesterone, resulting in activation of tyrosine kinase, and anti-estrogenic compound inhites it.(3) Expressions of Ha-ras, c-myc, fos and jun oncogenes (mRNA) are induced by estrogen in the normal uterus but altered in corresponding benign and malignant tumors due to the difference of estrogen/progesterone effectiveness.(4) The cellular carcinogenesis and proliferation in endometrial cancer are partly related to estrogen action, which involves the pointmutations in the estrogen receptor domains and delations ofextracellular domains of erbB-1 and erbB-2 products, and overexpression of progesterone B type (proliferation) instead of A type (inhibition).Accumulation o those abnormalities of gene expressions might be related to the cancer events.