[Gestagen treatment of endometrial carcinoma--theoretical and practical application].
Since Kistner in 1959 took up the gestagen therapy for endometrial hyperplasia and endometrial carcinoma with a view to inhibiting cellular proliferation, many clinical reports on that therapy have been published. It has been clarified by cell-biological studies that progesterone inhibit the DNA synthesis of endometrial cells followed by the discontinuance of cell division. At dichophase , prior to the onset of the S-stage in cell division cycle, under conjugation of progesterone with a certain specific type of protein (hormone receptor) the cells are induced toward the development of secretory function, i.e. toward differentiation, resulting in no synthesis of DNA. On the basis of the consideration mentioned above, when hormone treatment will be applied to endometrial carcinoma it is required that those cancer cells have the gene activated by administered hormone or have specific type of protein produced by hormone dependent gene in cytoplasm. When cancer cells have still retained the traits of the normal epithelial cells of endometrium, they were believed still possess the character to show the specific reaction to progesterone. However, not all the cancer cells can be considered to have a uniform character (the degree of differentiation), so gestagen therapy cannot be interpreted to be able completely to bring about the fundamental cure of endometrial carcinoma.
D002455:Cell Division; D004273:DNA, Neoplasm / Q000096:biosynthesis; D004967:Estrogens / Q000502:physiology; D005260:Female; D006801:Humans; D008938:Mitosis; D011374:Progesterone / Q000502:physiology; D011372:Progestins / Q000627:therapeutic use*; D012334:RNA, Neoplasm / Q000096:biosynthesis; D011960:Receptors, Estrogen / Q000032:analysis; D014594:Uterine Neoplasms / Q000188:drug therapy* / Q000473:pathology
D004273:DNA, Neoplasm; D004967:Estrogens; D011372:Progestins; D012334:RNA, Neoplasm; D011960:Receptors, Estrogen; D011374:Progesterone