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

1. It has become evident that the estrogen secreting tumors of the ovary are associated with endometrial carcinoma, but this association is most easily observed in the postmenopausal patient where the incidence of carcinoma has been reported at 10.3% (1. 02) to 24% (83). 2. The most consistent association of endometrial carcinoma is with polycystic ovarian disease, where 19 (34), 21 (152), and 25% (150) of young women with endometrial carcinoma had Stein-Leventhal syndrome (67). 3. A very significant discovery became known in 1967 when the peripheral aromatization of delta4 androstenedione to estrone was reported by Kase (94) and MacDonald (111,112). Since that time we have learned that endometrial carcinoma patients have an increased peripheral conversion (139) (0.1% compared to 0.027%), which is similar to that found in obese and aging patients, by Hemsell, et al (77). This can be 2 to 4 times greater than the young adult or the patient without cancer. Estrone produced peripherally in normal postmenopausal women can amount to 40-60 microng/day and rise as high as 120-180 microng/day in the endometrial neoplasia group (39). Similarly patients with polycystic ovary disease, hyperthecosis and lipoid cell tumors of the ovary demonstrate androgen excess with extraglandular conversion to estrone (2). 4. It has become apparent that the principal estrogen in the postmenopausal patient is estrone and that the estrone-estradiol ratio in the serum is higher in postmenopausal women with corpus cancer than similar patients without cancer (135). Clearly, we must find the effect of this estrone excess at the nuclear "acceptor" level; and does this imbalance create a hormonal environment conducive to the development of endometrial carcinoma when age (an extremely important factor) and an oncogenic agent are added? 5. With the lack of ovarian estrogen there is a relative excess of adrenal testosterone, dihydrotestosterone and delta4 androstenedione, the available precursors of extraglandular estrone (1). 6. With the passage of time it appears that endometrial carcinoma is associated with hypothalamic "hyperactivity" (31) which exhibits immunologic-biologic dissociation of LH as previously observed in persistent trophoblastic disease when measuring hCG. The significance of this is still unknown. In a like fashion a significant number of the at risk polycystic ovary disease patients have an increased LH secretion. 7. Patient susceptibility is required as seen in animal experiments where prolonged administration of stilbestrol is used and still only rabbits and mice developed a malignant change. 8. Long term exogenous estrogen appears to have caused malignant changes in the endometrium, but it was universally given over a prolonged period (4 or more years). The recent retrospective studies demonstrate an association of oral estrogen therapy with endometrial cancer, but prospective studies investigating dose and duration of all estrogen preparations need to be undertaken. 9...
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PMID:Estrogen and endometrial carcinoma. 32 64

Samples of human endometrial carcinomas and cervical adenocarcinomas were screened for the presence of single site DNA mutations at codon 12 of the K-ras gene using dot blot hybridization of DNA amplified by the polymerase chain reaction (PCR). Of 21 cases of endometrial carcinoma, point mutations were observed in three cases (14.3%). Mutation from GGT to GTT was seen in one case, and mutation to GAT was observed in two cases. Of seven cases of cervical adenocarcinoma, point mutations were noted in two cases (28.6%). Mutation from GGT to GTT and double mutation to GAT and GCT were in one case each. However, no correlation was found between the presence of point mutation and age, clinical stage, or depth of muscular invasion. With respect to prognosis, of five patients with point mutation, one with cervical carcinoma died, and of 23 patients without mutation, one with endometrial carcinoma died.
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PMID:Analysis of point mutations at codon 12 of K-ras in human endometrial carcinoma and cervical adenocarcinoma by dot blot hybridization and polymerase chain reaction. 181 93

This paper considers the debate over the risks of developing cancer from using various contraceptive methods. Claiming that the debate provokes unfair publicity and misinterpretation, various risks of cancer due to the oral pill, long-acting contraceptives, and IUDs are discussed. The oral pill is examined in the context of its potential relationship in causing breast cancer, endometrial cancer, ovarian cancer, cervical cancer, vaginal and fallopian tube neoplasms, and trophoblastic disease. Long-acting contraceptives are discussed in the context of genital tract neoplasia, while IUDs are examined in regard to gynecologic malignancies. The paper finds that no conclusive evidence exists indicating that IUDs cause gynecological cancers. Low-dose oral contraceptive pills are currently being used, and no clear evidence exists that they cause or increase the chance of developing cancer in the genital tract and the breast. Oral contraceptives do, however, have beneficial effects in preventing endometrial and ovarian cancer. The low-dose combined oral contraceptive should be considered safe where cancer, cardiovascular, and thrombotic risks are concerned.
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PMID:Fertility control and the risk of gynecological malignancies. 184 23

The molecular genetics of human endometrial carcinoma have yet to be defined to any significant extent. Cell lines from 11 endometrial carcinomas were examined for alterations in proto-oncogenes that might predictably be present, based on existing data from the better-characterized human carcinomas of the uterine cervix, ovary, and breast. Codons 12, 13, and 61 of the Ha-ras, Ki-ras, and N-ras genes were examined for possible point mutations, and the c-erbB2/neu, c-myc, and epidermal growth factor receptor (EGFR) genes were examined for amplification or overexpression. Ras mutations were found in seven of 11 (64%) tumors, including three in codon 61 of Ha-ras (CAG----CAT) and four in codon 12 of Ki-ras (GGT----GAT in two and GGT----GTT in two). No evidence was found for amplification or overexpression of the c-erbB2 or EGFR genes in any tumor. One tumor contained amplified c-myc sequences and exhibited relative overexpression of c-myc. These data suggest that the amplification or overexpression of several proto-oncogenes frequently observed in other human gynecologic and breast tumors are not prevalent in endometrial carcinoma and that ras gene mutations are relatively common in this tumor type.
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PMID:Analysis of oncogene alterations in human endometrial carcinoma: prevalence of ras mutations. 206 24

The role of cellular oncogenes in the development of epithelial tumors of the human female reproductive tract has not previously been extensively studied. DNAs isolated from ten human uterine, 13 ovarian, and four cervical neoplasms and from three cell lines derived from endometrial adenocarcinoma were investigated by dot blot hybridization after polymerase chain reaction amplification of ras gene sequences and in some cases by NIH 3T3 transfection. Transforming activity was found in two of nine endometrial adenocarcinomas, but none of seven ovarian carcinomas and none of four cervical carcinomas showed transforming activity. K-ras sequences with a GGT----GAT mutation in codon 12 were demonstrated in both transformants derived from endometrial carcinoma. K-ras codon 12 mutations were similarly detected in six of 13 endometrial carcinomas (one GAT and GCT, one GTT and GCT, two GAT, two GTT) and two of 13 ovarian tumors (GAT and GCT, GAT), both mucinous adenocarcinomas. Point mutation of K-ras in codon 12 is thus comparably frequent in uterine endometrial carcinomas and in colorectal carcinomas and may have similar significance as an event that contributes to progression of these tumors. Cervical carcinomas and ovarian tumors in general, with the possible exception of mucinous adenocarcinoma of the ovary, do not appear to have this characteristic.
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PMID:K-ras activation in neoplasms of the human female reproductive tract. 220 77

Color and pulsed Doppler ultrasound examinations were done on 11 normal volunteers (NU) and 286 patients that consisted of cervical carcinoma (CC), leiomyoma and/or adenomyosis (M), endometrial carcinoma (EC), trophoblastic disease (TD), benign ovarian tumor (BO), Krukenberg tumor (KT) and ovarian carcinoma (OC). The vascularity was based on the resistance index (RI) and maximum blood flow velocity (Vmax). In uterine disease, there was significant difference (p less than 0.01) among each group, except but one correspondence between NU and CC with RI, and there was significant difference (p less than 0.001) between NU and M, CC and M with Vmax. In ovarian disease, there was significant difference among each group with RI, and there was no significant difference among each group with Vmax. Therefore, Doppler ultrasound is a useful diagnostic tool for assessing gynecologic tumor vascularity.
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PMID:[Doppler ultrasonic assessment with hemodynamics of gynecologic tumor]. 223 Apr 41

Real-time two-dimensional and pulsed-wave Doppler ultrasonic examinations were performed on 8 normal volunteers and 97 patients with various gynecologic disorders; the objective was to assess uterine and tumor vascularities. Each arterial blood flow velocity wave-form was classified into two types. The resistance indices of normal and abnormal flows were greater than .7 and less than .7, respectively. In normal volunteers, abnormal flows were nil. In 8 of 44 patients with benign tumors (18.2%), abnormal flows were evident and all proved to be cases of leiomyoma or adenomyosis. Doppler signals were not detected in 18 of 36 patients with cervical carcinoma (50%) and abnormal flows were noted in only 6 (16.7%). In all cases of endometrial carcinoma, ovarian carcinoma, and trophoblastic disease, typically abnormal flows were noted. Moreover, in most subjects a decrease in blood flows was observed after chemotherapy by anticancer drugs or irradiation. Therefore, Doppler ultrasound is a pertinent and noninvasive tool that can be used repeatedly for assessing the tumor vascularity in gynecologic disorders.
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PMID:Doppler ultrasound assessment of tumor vascularity in gynecologic disorders. 266 56

A significance of contrast enhancement (CE) in CT (computed tomography) of gynecologic pelvic cavity has not yet been established despite of its application so far made for systemic CT scanner exploited in 1974. CT findings and tissue attenuation values (CT number) prior to I.V. injection was compared with those after infusion of contrast medium and observed the changes imaged on CT through contrast enhancement randomly carried out with 300 patients in need of CT diagnosis of intrapelvic lesion, and CE availability was assessed in terms of disorders. The results obtained are as follow; 1) CT was available, when CE was given, for 50% or more of the patients with endometrial cancer, trophoblastic disease, malignant ovarian tumor, and endometrial cyst. 2) CE availability was of significance in 40.7% of 30 subjects, in particular, being rated for 56.6% in adnexal diseases. 3) CE-induced changes in attenuation values of normal uterine body ranged from 44.2 +/- 6.6 to 87.5 +/- 8.9 Hounsfield units by which an increased CT number was indicated as being the high. 4) Tissue CT number and the CE-induced increase in cervical cancer were comparable to those in normal uterine body, while low in endometrial cancer and malignant ovarian tumor, allowing those tumors to discriminate from myometrium. 5) No increased attenuation values were seen in fluidal substances. 6) A significant information for diagnosis can be obtained through CE-induced increase in tissue CT number being a favorable aid for opacification.
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PMID:[Evaluation of contrast enhancement in gynecologic pelvic computed tomography (author's transl)]. 733 70

Several provocative studies in gynecologic cancer were recently presented. Long-term follow-up of ovarian cancer patients has confirmed the clinical impression of a low survival. Novel classes of active chemotherapeutics are the second-generation topoisomerase I inhibitors, irinotecan (CPT-11) and topotecan, and the taxanes, Taxol (Bristol-Meyers, Wallingford, CT) and Taxotere (Rhone-Poulenc Rorer, Antony, France). Dose intensity remains an intriguing issue. Biologic agents, including monoclonal antibodies, are being developed for palliation of ascites. In cervical cancer, use of retinoids and interferons has opened up a new avenue of investigation. Use of the World Health Organization sophisticated scoring criteria has improved the primary treatment of trophoblastic disease. Advances in salvage therapy have been noted. Progress in the treatment of advanced endometrial cancer and uterine sarcomas is beginning.
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PMID:Systemic therapy for gynecologic cancer. 810 75

One hundred sixty-eight patients treated at Hacettepe Hospital between 1969-1993 with metastatic ovarian tumors constituted 21.5% of all malignant ovarian neoplasms. Primary tumors were endometrial (51), breast (27), colorectal (18), and stomach cancer (17), lymphoma (14), sarcoma of the uterus (13), undetermined (11), tumors of the appendix (6) and ileum (4), carcinoma of the cervix (4), and gestational trophoblastic neoplasia (3). Overall 5-year and median survivals were 20.0% and 26.8% months, respectively. While worse prognoses were seen in gastric cancer and undetermined tumors followed by colorectal cancer, best survival figures were observed in endometrial cancer patients. A trend toward a better survival was seen with the advancement of the operation from bilateral salpingooophorectomy, and/or biopsy to total abdominal hysterectomy, bilateral salpingooophorectomy, total omentectomy, pelvic and paraaortic lymphadenectomy with debulking. Multivariate analysis identified the primary site, grade, laterality of involvement, type of surgery and adjuvant therapy status as significant prognostic parameters. Maximal surgical effort followed by adjuvant therapy might at least have some short term survival benefit in certain types metastatic to the ovaries.
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PMID:Malignant tumors metastatic to the ovaries. 855 38


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