Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:2.7.7.7 (DNA polymerase)
 17,007 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Proliferative cell indices (PCI) in 20 cases of endometrial adenocarcinoma were obtained by staining DNA polymerase alpha. The PCI ranged from 11.1 to 42.1, averaging 24.7 +/- 8.7. Four cases of stage III all exhibited fairly large PCI (30.4-32.9). In contrast, in 16 cases of stage I the values were spread over a wide range. In 13 cases with histological grade (HG) 1 of stage I, larger PCI were obtained in the nuclear grade (NG) 2 group; the mean PCI values of HG 1-NG 1 and HG 1-NG 2 were 16.5 +/- 4.6 and 25.6 +/- 5.2, respectively. Because of the good correlation between PCI and HG or NG, PCI may be useful as an additional prognostic factor in endometrial adenocarcinoma, especially in stage I cases.
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PMID:Proliferative cell index in endometrial adenocarcinoma of different nuclear grades. 247 Jul 14

The responsiveness and action mechanisms of steroid hormones and epidermal growth factor on human endometrial carcinoma cells are analyzed by using in vitro culture system. 1) The Ishikawa cells, derived from a well differentiated endometrial adenocarcinoma and possess ER and PR, are shown to respond to estrogens by increasing a variety of parameters, viz cell proliferation, PR levels, ALP and DNA polymerase activities. 2) ER and PR of those cells are localized in the nuclei by immunocytochemical staining using the monoclonal antibodies against to ER and PR, confirming the correctness of Gorski and Greene's one step theory involving the action mechanisms of steroid hormones. 3) Progestins reduced the ER level and stimulate E2DH activities and glycogen content, which are completely abolished by anti-progestin (RU486), suggesting that PR of those cells should be functional. 4) These responses to steroid hormones of Ishikawa cells are synergistically enhanced or appeared earlier by addition of EGF. 5) The main metabolite of E2 incubated with Ishikawa cells is E2-3-sulfate instead of E1, indicate that the higher estrogenic status may be persisted in endometrial cancer tissues.
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PMID:[Responsiveness and mechanisms of action of steroid hormones in human endometrial adenocarcinoma cells]. 251 14

Endometrial hyperplasia (EH) was found to coexist in 13 of 21 patients (cystic glandular hyperplasia, 13; adenomatous hyperplasia, 9) with endometrial adenocarcinoma (EC), but in only 44 of 940 patients with other than EC. In this study, blood type (A, B, H), c-myc translation products, estrogen receptor and DNA polymerase alpha were examined on endometrium of proliferative phase (EPP), EH and EC. Patient blood type products were shown in EH surrounding EC, and yet they were detected in only small portion or none of EC itself. H products were detected in EC of other than O type. c-myc translation products were shown in only a small portion of cancer cells. EPP had many ER positive cells and a few proliferating cells as they were shown by staining with anti-DNA polymerase alpha monoclonal antibody. EC can be divided into two types, one has few ER positive cells and many proliferating cells, other many ER positive cells and a few proliferating cells. In EH, the numbers of ER positive cells and DNA polymerase alpha positive cells were between those of EPP and EC. In a patient with atypical hyperplasia, high dose Medroxyprogesterone acetate (MPA) therapy induced that stratification and papillary growth of gland lining epithelia disappeared, and that cytoplasmic enlargement and vacuolation appeared. These findings were important histopathological changes in high dose MPA administration to EH and EC.
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PMID:[Diagnosis and treatment of endometrial hyperplasia]. 252 3

The effects of estradiol on DNA polymerase alpha activity were investigated in an estrogen-responsive human endometrial cancer cell line (Ishikawa) derived from a well differentiated endometrial adenocarcinoma. These cells are known to respond to estradiol by increasing progesterone receptor levels, alkaline phosphatase activity, and cell density. Four- to 5-fold increases in DNA polymerase alpha activity occurred when estradiol was added to cultures of Ishikawa cells in medium containing charcoal-treated fetal bovine serum. Maximal stimulation was achieved at 18 h during incubations with 10(-8) M estradiol, but significant effects also were found with 10(-9) and 10(-6) M. These effects were almost completely counteracted by a 100-fold excess of 4-hydroxytamoxifen. At 10(-6) M, the antiestrogen had no influence on the basal levels of DNA polymerase alpha. Medroxyprogesterone acetate (10(-6) M) was ineffective as either an enhancer of enzymatic activity or an antiestrogen when tested in combination with 10(-8) M estradiol, even in the presence of appreciable levels of specific progesterone binders. The responsiveness of the Ishikawa cells to estrogen contrasts with the lack of effects of estradiol on DNA polymerase alpha activity in another human endometrial adenocarcinoma cell line (HEC-50).
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PMID:Effects of estradiol on deoxyribonucleic acid polymerase alpha activity in the Ishikawa human endometrial adenocarcinoma cell line. 294 47

Nucleo-cytoplasmic distribution of estrogen receptors and DNA polymerase alpha activity in human endometrial adenocarcinoma cells (HEC-50 line) was evaluated after separation of nuclei following either homogenization or enucleation with cytochalasin B. About 30% of the estrogen receptor was found in the nuclear fraction after homogenization whereas 86% was found in the karyoplasts after enucleation. The total amounts of estrogen receptor per cell after homogenization and enucleation were not significantly different (14,000-17,000 binding sites/cell). Receptor measurements were carried out using the hydroxylapatite method after labeling with [3H]estradiol (5 nM [3H]E2 +/- 500 nM E2) at 30 degrees C for 3 h. About 20% of the DNA polymerase alpha activity was found in the nuclear fraction after homogenization, whereas 96% was found in the karyoplasts after enucleation. The average total activity (0.84 Units/10(6) cells) in homogenized cells was about 1/8 of the activity in karyoplasts. These results indicate that estrogen receptor and DNA polymerase alpha activity reside in the nucleus in intact HEC-50 cells. DNA polymerase alpha is translocated to the cytoplasmic fraction and inactivated after homogenization.
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PMID:Enucleation of human endometrial cells: nucleo-cytoplasmic distribution of DNA polymerase alpha and estrogen receptor. 370 33

Estradiol (E2) stimulates the proliferation of human endometrial adenocarcinoma cells of the Ishikawa line, which had been previously shown to respond to estrogen by increasing their levels of progesterone receptor and the specific activities of DNA polymerase alpha and alkaline phosphatase. Although E2 (10(-8) M) did not increase rates of proliferation during the initial logarithmic growth period of the cultures under the chosen experimental conditions (MEM with 15% charcoal-treated fetal bovine serum renewed every 2-3 days), it sustained cell proliferation after about day 10, when parallel control cultures had reached plateau cell densities. Cell proliferation in control cultures at plateau levels was resumed when the hormone was added. Growth rates of cultures containing E2 from the time of seeding and the proportion of quiescent cells, estimated by using a simple cell kinetic model, decreased steadily with time. Ornithine decarboxylase and DNA polymerase alpha activities, as well as estrogen receptor levels, also decreased with time in culture. Ishikawa cells formed colonies in soft agar; colony formation efficiencies were higher as the number of cells seeded was increased from 10,000 to 100,000 cells/6 cm dish, were not influenced by the addition of E2 to the medium (10(-9) to 10(-5) M) and were markedly reduced by difluoromethylornithine (10(-2) M), an effect that was counteracted by putrescine (25 X 10(-6) M).
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PMID:Effects of estradiol on proliferation of endometrial adenocarcinoma cells (Ishikawa line). 380 63