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Query: UMLS:C0476089 (endometrial cancer)
 11,379 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Plasminogen activator activity (PAA) has been proposed as an indicator of aggressiveness of tumors and has been shown to be hormonally modulated. To test this hypotheses in human endometrial carcinoma, tumor explants were assayed for PAA secretion and the results correlated with histopathologic criteria of aggressiveness. The effect of medroxyprogesterone acetate (MPA) on PAA secretion was also investigated. Lower levels of PAA were found to be associated with tumors displaying aggressive tendencies. MPA generally decreased PAA secretion. No apparent correlation was found between estrogen or progesterone receptor concentrations and PAA levels.
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PMID:Plasminogen activator activity in human endometrial carcinoma. 316 Jun 38

The presence of estrogen-independent progesterone receptors (PR) was demonstrated in a subline of a human endometrial cancer cell line, Ishikawa cells. Scatchard plot analysis of cytoplasmic binding data in a subline (IK-90) revealed a high affinity binding site for promegestone (Kd, 1.0 nM) with maximum binding sites of 158 fmol/mg protein. Competition experiments showed a binding specificity similar to that of typical PR. By low-salt sucrose gradient centrifugation, radioactive 8S and 4S peaks were found. The addition of 1 microM progesterone in culture medium resulted in a rapid nuclear translocation of cytoplasmic PR. Accumulation of glycogen in cytoplasm of the cells in response to 0.1 microM promegestone was observed by periodic acid-Schiff staining. Addition of various concentrations (1 nM-1 microM) of promegestone reduced the cell growth in a dose-dependent manner. The growth inhibition by promegestone was totally prevented by the concomitant addition of equimolar RU 486, a progestin antagonist. The other steroids including tamoxifen, cortisol, and testosterone had no significant effects on the growth of the cells. The growth-inhibitory effect of progestin on cultured cancer cells from human endometrial adenocarcinomas obtained by hysterectomy was also investigated. Addition of medroxyprogesterone acetate (1 nM-1 microM) caused a marked decrease in [3H]thymidine incorporation in cultured cancer cells from tumors with PR. From the viewpoint obtained in the present studies using both IK-90 cells and endometrial cancer cells in primary culture, it can be concluded that progestins produce regression of endometrial cancer directly via the PR system.
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PMID:[Growth inhibition by progestins in human endometrial cancer cells with progesterone receptors]. 338 35

This review briefly outlines the pharmacology of natural and synthetic estrogens, and synthetic progestins, and summarizes their beneficial and adverse effects for contraceptive and menopausal therapy. Currently, oral contraceptives contain 30-50 mc synthetic estrogen, and 1-5 mg nor-progestin; menopausal therapy may be either 0.625-1.25 mg natural estrogen or estrogen plus 10 mg medroxyprogesterone acetate daily if the woman has her uterus. The biologic effects of estrogens are : decrease in lipoproteins, increased blood coagulation factors, increased blood pressure, decreased glucose tolerance. Progestins increase blood lipids and increase insulin and glucose. Oral contraceptives increase the risk of cardiovascular disease, particularly in smokers and in women over 35, in proportion to dose. These studies should be recapitulated in more detail with the newer low-dose pills. Orals have far more beneficial effects, besides providing an inexpensive, effective method contraception. The death rate of users of oral contraceptives is 3.7/100,000 (1.8 in nonsmokers and 6.5 in smokers), but the risk is 5.5 times higher in nonusers exposed to pregnancy and childbirth. The risk for users of barrier methods backed up by abortion is lower, but pills are cheaper and more acceptable. If woman did not take oral contraceptives, they would not be protected from cancer of the breast, ovary, endometrium, and ovarian and breast cysts. Menopausal therapy puts woman at increased risk of endometrial cancer only if the estrogen is taken alone, not if progestin is combined with the estrogen. There are no other adverse effects except decreased glucose tolerance and possible comprise of lipoproteins if a norprogestin of menopausal estrogens effectively treat hot flashes, depression, vaginal atrophy and bones loss.
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PMID:The adverse effects of hormonal therapy. 351 31

In this study, the nuclear DNA and cellular protein in endometrial cancer cells were simultaneously determined by combined DNA-protein cytofluorometry (Olympus MMSP-RF) using a double staining method. Thirty-one cases of endometrial adenocarcinoma treated preoperatively with medroxyprogesterone-acetate were investigated for cytomorphological responses with special reference to DNA and protein content. The result of this study showed increases in DNA and protein over the normal range in all the cases of endometrial carcinoma. Gestagen produced a marked histological effect in 9 cases of well differentiated carcinoma and 2 cases of moderately differentiated carcinoma out of the 31 cases. On the other hand, no effect was found in cases of poorly differentiated carcinoma. Gestagen treatment induced changes in DNA and protein content according to morphological changes in cases of marked histological response. The population of over 4C or 4P cells on the DNA-protein histogram before gestagen treatment was 45.1% in cases of marked morphological response and 69.2% in cases of no response. This finding suggests a correlation between the effectiveness of gestagen treatment and the DNA-protein histogram. Estimation of such a cell population before gestagen administration is considered useful in gestagen therapy for endometrial adenocarcinoma.
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PMID:[Simultaneous cytofluorometric studies on DNA and protein in endometrial adenocarcinoma--with reference to gestagen treatment]. 372 54

A 2-years-old nulliparous cross-bred bitch had persistent vulval discharge following treatments that included a combined ethinyloestradiol/methyltestosterone preparation and megoestrol acetate. The uterus, removed at ovarohysterectomy, contained a large polypoid intraluminal mass with the histological features of endometrial carcinoma. The bitch has remained well for thirty-one months after surgery. The possibility is considered that the lesion is drug-related but no firm conclusion can be drawn about the precise nature and pathogenesis of this unusual lesion.
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PMID:Endometrial carcinoma in a young dog. 373 75

An attempt was made to elucidate the relationship between the progestational activities and antitumor effects of various steroid hormones in vitro and in vivo. The established cell line (Ishikawa cells) of a human endometrial adenocarcinoma bearing estrogen and progesterone receptors was used in this study. Sixteen kinds of steroid hormones including progesterone, medroxyprogesterone acetate (MPA) and danazol were used in vitro. Each hormone was administered at 20 micrograms/ml continuously from the 4th day of culture and the growth curve was evaluated. The effects of progesterone, MPA and danazol at a dosage of 24 mg/kg/day for 53 days on the tumor induced in athymic nude mice with Ishikawa cells were also evaluated. Three kinds of hormones, progesterone, 16 alpha-methylprogesterone and danazol revealed cytocidal effects on the cells in vitro. There was no relationship between the progestational activity and cytocidal effect of each steroid hormone. On the other hand, no significant tumor regression was observed in vivo, but progesterone and danazol showed a tendency to suppress the growth of the tumor. These results suggest that the cytotoxic properties of progesterone may play a more important role than progestational action the cytocidal effect in vitro. It has been known that MPA had antitumor effects on DMBA-induced mammary cancer in rat and human endometrial cancer. However, MPA did not show a significant antitumor effect either in vitro or against the transplanted tumor in this study. Therefore, it was suggested that the antitumor effect of MPA is not direct action on the tumor cells, but indirect action through the interstitial cells of the target organ.
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PMID:[Mechanisms of the antitumor action of gestagens on endometrial cancer]. 380 31

Fifty consecutive patients with recurrent and metastatic endometrial carcinoma were treated with melphalan, 5-fluorouracil, and medroxyprogesterone acetate with or without tamoxifen as first-line chemotherapy. The objective response rate was 48%, with 20% complete responses. The estimated median progression-free survival time was only five months (0.5 to 65 months) with estimated two- and five-year progression-free survival rates of 16 and 13%, respectively. The estimated median progression-free survival time was 24 months for complete responders; the progression-free survival times were significantly longer than the survival times (median = four months) for all other patients (P = .0002). Whether or not the addition of cytotoxic chemotherapy to progesterone hormonal therapy for metastatic endometrial carcinoma lengthens survival time is still open to question.
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PMID:Melphalan, 5-fluorouracil, and medroxyprogesterone acetate in metastatic endometrial carcinoma. 394 37

The hypothesis that 17 beta-estradiol or tamoxifen (TAM) can potentiate clinical response of endometrial cancer treated with progestin was tested in an ovariectomized nude mouse system, using a sex steroid receptor-positive and a receptor-negative human endometrial carcinoma. Animals were divided into three groups: control; 17 beta-estradiol-treated; and TAM-treated. When tumors of a group reached about 1 cm in diameter, subgroups were given either 0.9% NaCl solution (saline) or medroxyprogesterone acetate (MPA). The receptor-negative tumor grew rapidly in all three groups, and several animals were dead before or during progestin treatment. The growth rate of receptor-containing carcinoma was significantly increased in TAM-treated mice compared to controls (p less than 0.02) but significantly less than that in 17 beta-estradiol-treated animals (p less than 0.01). Endometrial carcinoma in 17 beta-estradiol-saline-treated animals continued to grow rapidly, and all animals were dead by 11 weeks. The growth of tumors in the 17 beta-estradiol-progestin group was suppressed at 11 weeks, and some of these animals lived 20 weeks. Administration of progestin to TAM-exposed animals resulted in a remarkable regression of the tumor compared to TAM-saline-treated group. The growth rate of tumors in control animals (no implants) was unaffected by progestin treatment. We conclude that, in this nude mouse model, treatment with TAM and MPA is superior to MPA alone, or 17 beta-estradiol plus MPA for sex steroid receptor-positive endometrial carcinoma.
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PMID:Hormonal therapy of human endometrial adenocarcinoma in a nude mouse model. 396 28

Spinal cord or cauda equina compression secondary to epidural metastasis rarely develops in patients with endometrial carcinoma and the early signs and symptoms of compression can therefore be inadvertently overlooked. A 78-year-old patient who developed bone metastasis with destruction of the fifth lumbar vertebral body and blockage of the cauda equina at L-4, L-5 as the only sites of metastasis is reported. This occurred 2 years after initial treatment of a stage IB, well-differentiated, grade I, adenosquamous carcinoma of the endometrium. The patient remains alive, with good neurological function and free of metastatic disease, 2 1/2 years following vertebrectomy, radiation therapy, and adjuvant Provera (medroxyprogesterone acetate) therapy. This patient represents the only case of metastatic endometrial cancer with cauda equina compression in the literature in whom long-term disease-free follow-up has been noted.
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PMID:Cauda equina compression secondary to metastatic carcinoma of the uterine corpus: preservation of neurologic function and long-term survival following surgical decompression and radiation therapy. 397 89

Progestational agents induced an objective response in 11.2% of 155 patients with advanced primary or recurrent endometrial carcinoma. Response rates decreased with decreasing tumor differentiation from 40% with Broders grade 1 lesions to 17.5, 2.4, and 0%, respectively, with grades 2, 3, and 4. 17 alpha-Hydroxyprogesterone caproate (Delalutin), 6,17 alpha-dimethyl-6-dehydroprogesterone (Colprone), and 6-methyl-6-dehydroprogesterone acetate (Megace) were the progestogens used; there was no significant advantage for any one agent. Overall, survival after initiation of hormone therapy was 40% at one year, 19% at two years, and 8% at five years. Survival was highly dependent on the degree of tissue differentiation (P less than .001) and was influenced significantly by the estimated tumor volume at the start of therapy (P less than .01) and by the time interval from primary treatment to the beginning of hormone therapy (P less than .01).
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PMID:Effects of progestational agents in treatment of endometrial carcinoma. 401 Oct 61


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