[Cell culture--its application in the study of hormone and endometrial carcinoma and feed-back to clinical medicine].
By statistical study on 135 patients with endometrial carcinoma, it is clarified that the most effective prognostic factor of the cancer is the histological grading. Well differentiated type is best prognostic and possesses hormone receptors. Application of cell culture is one of the most suitable choices in the study of hormone and human endometrial carcinoma. Present paper is to show usefulness of in vitro study by taking example of the above theme. 1) Binding ability of endometrial carcinoma cells to estrogen: Being explained by Gurpide et al. by using HEC-1 cells, the ability is under control of cGMP and cAMP ratio. 2) Responses to estrogen: DNA polymerase alfa of Ishikawa cells which possesses both estrogen and progesterone receptors (ER, PR) is stimulated first showing peak at 18 hours and alkaline phosphatase (ALP) is at 72 hours by E(2)10(-8)M, which is antagonized by OH-tamoxifen. PR level is also enhanced at its maximum after 3 day E2 treatment, and is analyzed by immunocytochemistry with PR mono-clonal antibody as well as biochemical assay. Gorski and Greene's theory that steroid receptor is localized in nuclei is confirmed in endometrial carcinoma. Growth of Ishikawa cells is apparently enhanced in the aspects of shortened cell cycle and unlimited saturation density. 3) Responses to progestogen: Nucleic acid syntheses of HEC-1 are immediately suppressed by progesterone (P) 2.5 microg or more. Electron microscopic findings show appearances of Golgi apparatus and lysosomal granules. Growth suppression is observed in the cell lines regardless of PR positivity. ALP activity of PR-negative HEC-50 cells
Kuramoto
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Department of Obstetrics and Gynecology, School of Medicine, Kitasato University, Kanagawa.
D000469:Alkaline Phosphatase / Q000378:metabolism; D000818:Animals; D002455:Cell Division / Q000187:drug effects; D004257:DNA Polymerase II / Q000378:metabolism; D004958:Estradiol / Q000378:metabolism* / Q000494:pharmacology; D004960:Estradiol Dehydrogenases / Q000378:metabolism; D005260:Female; D006003:Glycogen / Q000096:biosynthesis; D006006:Glycogen Synthase / Q000378:metabolism; D006801:Humans; D051379:Mice; D008819:Mice, Nude; D009368:Neoplasm Transplantation; D009696:Nucleic Acids / Q000096:biosynthesis; D011374:Progesterone / Q000378:metabolism* / Q000494:pharmacology; D045167:Progesterone Congeners / Q000494:pharmacology; D011379:Prognosis; D011960:Receptors, Estrogen / Q000378:metabolism; D011980:Receptors, Progesterone / Q000378:metabolism; D014407:Tumor Cells, Cultured / Q000187:drug effects; D014594:Uterine Neoplasms / Q000378:metabolism / Q000473:pathology*
D009696:Nucleic Acids; D045167:Progesterone Congeners; D011960:Receptors, Estrogen; D011980:Receptors, Progesterone; D011374:Progesterone; D004958:Estradiol; D006003:Glycogen; D004960:Estradiol Dehydrogenases; D006006:Glycogen Synthase; D004257:DNA Polymerase II; D000469:Alkaline Phosphatase