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

A long experience in the treatment of endometrial cancer shows that the therapeutic measures vary considerably with regard to the extention of the tumor, the age of the patient and her general condition. This circumstances and particularly the critical study of the therapeutical results give the limits, within a certain kind of operation can reasonably be recommended. The intercurrent deaths are an important factor in the statistical evaluation of therapeutical success. As long as the tumor is limited to the body of the uterus, the corrected 5-year recoveries are about 90%. Considering all the circumstances, it becomes obvious, that in this stage, the simple abdominal hysterectomy with removal of the adnexa is still the operation of choice. Beside the histological degree of differentiation, the depth of the muscular invasion is the most important prognostic factor which might lead to additional measures. Postoperative radiation therapy of the vagina reduces considerably the incidence possibility of vaginal apex recurrence. In stage II radical hysterectomy must be considered, although we are aware of the fact, that a simple hysterectomy and bilateral salpingo-oophorectomy combined with radiation treatment may yield just as good results. In the clinical stage III laparotomy ought to be used more frequently. Also in case of operative intervention additional radiotherapy is mostly useful.
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PMID:[Aminoacid-p-nitroanilides splitting activities in the mature human placenta (author's transl)]. 1 5

A proportion of cancers in endocrine target tissues can show the presence of specific receptors for either steroid or polypetide hormones. Manipulation of the controlling hormones does not guarantee regression. A third of cancers in endocrine target organs (breast, uterine endometrium, and prostate) show a 50% reduction in size of lesions after hormonal therapy. If regression resulting from an aggressive form of therapy lasts a short while and the tumor reactivates by the time the unpleasant effects of the therapy wear off, the treatment is not palliative. Endocrine therapy in prostatic cancer is palliative but there is no evidence that is increases survival. 11 different progestational agents in endometrial cancer therapy in the past 25 years resulted in a 30-35% response. Response must be maintained by continual treatment and may last from 12 months to 7-8 years. In breast cancer, tumors with a significant level of estrogen receptor (ER+) have about a 60% chance of regression vs. tumors without estrogen receptors (ER-), 10%. Advanced cancers of the thyroid of the papillary or follicular type regress when the patient is treated by thyroxine, .3 mg daily. Leukemia and lymphoma are frequently treated, with varying degrees of success with corticosteroid therapy, which may also predispose the patient to intercurrent infection. Renal cancer has been often treated by medroxyprogesterone acetate or testosterone propionate, with little success.
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PMID:Endocrine therapy in cancer. 8 86

Dr Thom and her colleagues (Sept. 1, p. 455) are incorrect when they state that the U.S. case-control studies of endometrial cancer and oestrogen use "are open to criticism on grounds of selection of patients, poor medical supervision, inappropriate hormone therapy, and lack of clarification of the pathology by the addition of progestagens." It is not the studies which are open to criticism on the grounds stated but the way in which oestrogen therapy had been administered before the publication of these studies. A case-control study compares the frequency of exposure to a suspect carcinogen (oestrogens, in the example of endometrial carcinoma) to that of a control group. Since it was not at all a common practice to prescribe oestrogen with a progestagen when these studies were done, few histories of this combined regimen were found in either the cases or controls. But it is a great mistake to conclude that the absence of data on the risk of combined oestrogen and progestagen therapy means that there is no risk attached to combined therapy. The case-control studies that have thus far been reported shed no light on this risk because the regimen was too rarely used for these studies to have picked up a risk if indeed it was present. Thom et al. suggest that treatment with progestagen is effective in preventing or reversing endometrial hyperplasia. It is not yet well established that hyperplasia is a precursor to neoplasia. Thom et al. may be correct in believing that the combined regimen is safe but we must be perfectly clear about the meaning of the results of our case-control study, the largest reported to date. Our results do not put the combined regimen beyond suspicion but rather point up the need for continued monitoring of this regimen for cancer risk until the issue can be settled one way or the other. Meanwhile, the unfortunate experience with widely prescribed unopposed oestrogens should serve as a warning that any recommendations about prolonged use of these substances should be made with considerable caution.
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PMID:Oestrogen-replacement therapy. 9 Aug 98

A test is described for the evaluation of hormone sensitivity of endometrial cancer in vivo. The concentrations of progesterone and estradiol receptors, and the activities of ornithine-decarboxylase and 17 beta-hydroxysteroid oxido-reductase enzymes have been measured in the tumor, before and after administration of the anti-estrogen tamoxifen. The responses observed, in particular the increase of progesterone receptor, could allow a more rational approach to hormonal therapy of endometrial cancer.
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PMID:[Response to an antiestrogen as a criterion for hormonal sensitivity of endometrial cancer]. 11 15

The serum levels of follicle stimulating hormone (FSH), luteinizing hormone (LH) and, prolactin (PRL) were measured before and after gonadotrophin releasing hormone (GnRH) and thyrotrophin releasing hormone (TRH) stimulation in 17 patients with endometrial cancer, in 15 patients with uterine fibroids, in 11 patients with ovarian cystadenomas or cancer and in 14 age-matched controls. The women with fibroids had a low FSH level and a diminished FSH response to GnRH but an excessive PRL response to TRH while the other patient groups did not differ from the controls. The results indicate no relation between pituitary function and endometrial or ovarian tumor.
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PMID:Pituitary gonadotrophins and prolactin in patients with endometrial cancer, fibroids or ovarian tumours. 11 72

A so-called "endometrial" adenocarcinoma of the prostate has been studied by light and electron microscopy, and by histochemical techniques. The previously proposed utricular origin and estrogen dependence of such tumors is questioned. Strong acid phosphatase staining, and the ultrastructural demonstration of multivacuolated, lipid, and lysosome-containing tumor cells, suggest a prostatic ductal origin for this type of carcinoma despite the histologic similarity to carcinoma of the endometrium.
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PMID:"Endometrial" adenocarcinoma of the prostate: a distinctive tumor of probable prostatic duct origin. 13 Sep 69

Sera from cancer patients and healthy individuals, obtained from two independent sources, were examined for their abilities to react with herpes simplex virus-associated tumor antigens, AG-4 and NVA-TAA (nonvirion antigen-tumor-associated antigen). Both antigens were prepared by infection of HEp-2 cells with herpes simplex virus type 2, and all antigen-antibody interactions were measured by the micro-complement fixation test. Of sera from 16 patients with cancer of the uterine cervix, 81% (P less than 0.01) reacted with NVA-TAA, whereas 78% (P less than 0.001) of 18 sera examined reacted with AG-4. These values differed significantly from those for normal sera, of which 14% reacted with NVA-TAA and 13% with AG-4. Of sera for 8 patients with squamous cell carcinoma of head and neck or vulva, 75% (P less than 0.02) reacted with NVA-TAA, whereas 63% (P less than 0.05) reacted with AG-4. As a group, other cancers (including adenocarcinoma of lung, breast, ovary, and cervix; liposarcoma; sarcoma; melanoma; and carcinoma of the endometrium) did not differ significantly from controls in reactive patterns with AG-4 or NVA-TAA. These studies partly supported the reported preferential reactivity of AG-4 and NVA-TAA with sera of patients with squamous cell carcinoma, especially of the uterine cervix.
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PMID:Comparative diagnostic aspects of herpes simplex virus tumor-associated antigens. 18 98

Six patients who took oral contraceptive agents for 5 to 18 years developed endometrial neoplasia. Endometrial adenocarcinoma occurred in 4 of these patients and severe adenomatous hyperplasia occured in 2. Five of the 6 patients took sequential agents; 1 patient used a combined agent. An additional patient who took Premarin and Provera sequentially developed adenocarcinoma of the endometrium. Eighteen cases of endometrial adenocarcinoma and 7 cases of adenomatous hyperplasia in patients with long-term sequential oral contraceptive use have previously been reported by others. Progestogens may not be completely protective against the endometrial cancer-causing potential of the estrogens, especially in the sequential regimens.
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PMID:Endometrial carcinoma and oral contraceptive agents. 19 73

Feminizing ovarian tumors and polycystic ovarian disease may cause endometrial cancer by abnormal, unopposed endogenous estrogenic stimulation. We reviewed the clinical course of 72 endometrial cancer patients with a concomitant feminizing ovarian tumor or polycystic ovarian disease and compared tumor characteristics and treatment results with those exhibited by 523 patients treated for endometrial cancer alone. With functioning ovarian tumor and with polycystic ovaries, the cancer tended to be more often low-grade, low-stage, and superficial than did endometrial cancer alone. The high 5-year and 10-year survival rates observed in our functioning ovarian tumor-polycystic ovary patients support the conclusion that endometrial carcinoma with a coexistent endogenous estrogenic stimulus has a more favorable prognosis (P less than 0.01) than endometrial carcinoma alone.
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PMID:Endometrial cancer associated with feminizing ovarian tumor and polycystic ovarian disease. 19 78

At the Wilford Hall U.S. Air Force Base Medical Center, Texas, about 4000 postmenopausal women received estrogen replacement therapy during 1975. Of these, 2700 took estrogens only and 1240 were given a progestogen along with estrogen. Hysterectomy had been done previously on 1700 patients (42%), leaving 2300 with intact uteri and a risk of endometrial cancer. Adenocarcinoma of the endometrium was diagnosed in 7 patients. Of these, 6 had received estrogen therapy. There was 1 endometrial malignancy in a patient also receiving a progestogen. Among 510 untreated postmenopausal women with intact uteri, 1 adenocarcinoma of the endometrium was found. Type and dosage of estrogen were unrelated to endometrial malignancy. In addition to the 7 endometrial cancers from the clinic, 22 cases were diagnosed elsewhere and referred for treatment, 11 of these had received no hormones. 10 were taking estrogens and 1 was receiving Oracon for birth control. The incidence of endometrial malignancy in the U.S. is reported to be 21/100,000 women/year. There is a 3-fold to 9-fold increased risk of endometrial cancer associated with obesity alone. The probability that untreated postmenopausal women with intact uteri will develop carcinoma of the endometrium is 1/1000/year. With estrogen users, it is reported to be increased -7.6/1000 women/year. In the author's clinic during 1975, the incidence among those receiving only estrogen was 4.7/1000. Among those also receiving a progestogen the incidence was .8/1000. Unopposed estrogens apparently have a role in the etiology of endometria hyperplasia and neoplasia through incomplete shedding of the endometrium. Progesterone produces more complete sloughing of the endometrium and also converts all degrees of hyperplasia into secretory endometrium. Nulliparity, infertility, and anovulation are predisoposing factors to endometrial carcinoma. Progestogens are palliative therapy for endometrial cancer.
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PMID:Estrogens, progestogens and endometrial cancer. 19 79


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