Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0476089 (endometrial cancer)
 11,379 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

Electrophoresis of cytosol prepared from normal and malignant tissue samples of uterine cervix and endometrium revealed interesting differences which may be relevant to the characteristic alterations in glucose metabolism associated with tumour development. Hexokinase II was detected in 30% of the cancer material from both sources, but in none of the samples of normal cervix. A duplet band of 6-phosphogluconate dehydrognease was seen in the majority of the cancer samples but in no sample of normal cervix; it appeared to be partly due to ageing of the sample, and is not phenotypically related to the malignant process. Analysis of genetic variance for phosphoglucomutase at the PGM1 locus revealed a highly significant excess of the PGM1-1 phenotype in patients with cancer of the endometrium, which may reflect susceptibility to endometrial cancer in patients with this phenotype. At the PGM2 locus, samples of malignant cervix were deficient in "Band f" compared with normal cervix samples, all of which showed this band. Conversely, gene products of the PGM3 locus were found in most samples of malignant cervix and a small minority of normal cervix samples. Compared with the isomorphic distribution of lactate dehydrogenase enzymes in normal uterine tissue, cancers showed a shift towards either a more anodal or a more cathodal pattern. The former may be associated with tumours enjoying a good oxygen supply, and the latter with tumours which, because of their depth or poor blood supply have to function under less aerobic conditions.
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PMID:Isoenzymes of hexokinase, 6-phosphogluconate dehydrogenase, phosphoglucomutase and lactate dehydrogenase in uterine cancer. 50 67

The concentration of carcino-embryogenic antigen in the serum of healthy women and of patients with different benign and malignant genital tumors was determined before and after treatment. The carcino-embryogenic antigen was elevated to more than 2.5 ng/ml in 11% of the healthy control patients. Patients with carcinoma of the breast had positive CEA tests in 60%. Patients with ovarian cancer had positive CEA tests in 57%, women with carcinoma of the uterine cervix had positive tests in 50% and women with endometrial carcinoma had increased CEA levels in the serum in 38% of the cases. Following treatment the CEA values decreased.
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PMID:[Carcino-embryogenic antigen (CEA) in patients with genital tumors (author's transl)]. 88 32

Report on 2309 vaginal hysterectomies. The leading indication for vaginal hysterectomy was benign disease of the uterus (54.4%). Utero-vaginal prolapse was the indication in approximately 32% of the patients. In 71.1% of the hysterectomies, the vaginal approach for removal of the uterus was selected in malignant and pre-malignant diseases. Of these cases 11.9% had carcinoma in situ and 2.7% had micro-invasive carcinoma of the cervix. 2.6% of these cases had carcinoma of the endometrium. In 69.9% of the cases the vaginal hysterectomy was combined with a colporrhaphy. Previous genital operations or laparotomies where no contra-indication to vaginal hysterectomy. Trauma to the urinary tract or the rectum occurred in 26 cases (1.02%). Post-operatively 3 urinary tract fistulas and 3 rectovaginal fistulas developed. The mortality was 0.51%. Among 272 cases of carcinoma in situ and 62 cases of micro-invasive carcinoma of the cervix treated by vaginal hysterectomy, one case developed a recurrent carcinoma in situ of the vaginal vault eight years after vaginal hysterectomy for carcinoma in situ. One patient treated for micro-invasive carcinoma of the cervix died four years following vaginal hysterectomy in another hospital of suspected pulmonary metastases. The diagnosis was not confirmed by autopsy. Simple total hysterectomy whenever possible by the vaginal approach is at present the maximal treatment in the University Department in Graz for carcinoma in situ and micro-invasive carcinoma of the uterine cervix.
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PMID:[Vaginal hysterectomy at the department of gynecology of the university of Graz from 1955 to 1970 (author's transl)]. 118 93

The effect of oral contraceptives on the development of cancer indirectly is explored with regard to cancer of the female genital tract and the breast. No correlation between oral contraception and squamous cell carcinomas of the vulva and vagina and tumors of the ovary is known. As yet no statistics are available on the incidence of carcinoma of the endometrium in women who took oral contraceptives during their reproductive life span. Because of the direct hormonal suppression of the endometrial growth by oral contraception, a protective effect against endometrial hyperplasia and endometrial cancer must be expected. For cancer of the female breast no protective and no enhancing cancer risk due to progestational agents can be postulated. The known fragmentary data suggest rather a protective effect. Regarding dysplasia and carcinoma in situ of the uterine cervix, large investigations with great numbers of patients are available. An increase of the risk of developing cancer of the cervix by using oral contraception cannot be shown with sufficient accuracy at our present state of knowledge by statistical means. Some observations suggest that oral contraception increases the relevant exogenous factors for carcinogenesis of the uterine cervix such as sexual behavior and hygiene.
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PMID:[Does oral contraception cause cancer? (author's transl)]. 126 87

Women who have no children are more prone to mammary cancer than those who have them. Abstinence from sexual relations is associated with enhanced risk of uterine fibrosis and endometrial cancer, but a much-reduced risk of cancer of the uterine cervix. In some strains of rats the incidence of mammary tumors, mostly fibroadenomas, is almost 100% in old age. In other strans of rats, chromophobe adenomas of the p ituitary gland have a high incidence with age, and other tumors are also frequent. Overfeeding of laboratory rats and mice may contribute to the risk of developing tumors. Since 1972, there have been reports of liver tumors in women taking oral contraceptives (OC'S). Theoretically, hormones may increase cancer risk because of their hormonal activity or because they may be intrinsically carcinogenic. It is thought that cancer risk because of hormonal activity can be meaningfully studied in humans only by epidemiological methods. The chemistry of OCs makes it unlikely that they could have intrinsic carcinogenicity. This has been shown by large-scale long-term tests on laboratory animals. However, this is not adequate assurance that these drugs do not influence cancer risk in humans. Studies of the mechanisms of toxicology are needed.
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PMID:Possible carcinogenic hazards of oral contraception. The interpretation of animal studies. 127 84

This work is devoted to research on the selective screening possibilities of hormonodependent tumours of the female reproductive system organs (endometrial cancer, ovarian cancer, breast cancer). After morbidity analysis using case-control study elucidation of risk factors affecting cancer of the uterine cervix, endometrium, ovary and breast were carried out on of female population the Ashkhabad (311 cancer patients and 14872 healthy women). Using established risk factors and mathematical methods optimized computer programmes were developed processing individual risk and models forming risk groups or hormonedependent tumours which were used in practice. As a result in the risk group were found 0.9% subclinical states and hormonedependent tumours (control -0.16%). The research accomplished has shown the practical importance of hormonedependent selective screening and necessity of elucidating new disease-epidemiological and laboratory risk factors in cancer of the reproductive system's organs.
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PMID:Selective screening on hormonedependent tumours of women's reproductive system organs. 138 65

The correlation between histological ovarian metastasis and histologic cell type, clinical stage, depth of invasion, lymph node metastasis, and menstrual activity were analyzed in 566 patients who underwent surgery for uterine cancer at the hospital of Niigata University between January, 1971 and May, 1990. Ovarian metastasis was studied in 456 patients with stage Ib or more advanced cervical cancer and 110 patients with stage Ia or more advanced endometrial cancer. The following results were obtained: 1. The incidence of ovarian metastasis of cervical cancer by histologic cell type was 18.6% (8/43) for adenocarcinoma, 6.7% (1/15) for mixed type adenocarcinoma and squamous cell carcinoma, and 0% (0/398) for squamous cell carcinoma. The metastasis rate in patients with endometrial carcinoma was 10.8% (10/93) for adenocarcinoma, but there was no metastasis of 2 squamous cell carcinoma, 13 mixed type of adenocarcinoma and squamous cell carcinoma or 2 undifferentiated carcinoma. 2. The incidence of metastasis of cervical adenocarcinoma by stage was 5.3% (1/19) for stage Ib and 29.2% (7/24) for stage II. The metastasis rate of mixed type of adenocarcinoma and squamous cell carcinoma was 0% (0/6) for stage Ib and 11.1% (1/9) for stage II. The incidence of metastasis of endometrial carcinoma was 2.1% (1/47) for stage Ia, 15.0% (3/20) for stage Ib, 15.0% (6/40) for stage II and 0% (0/3) for stage III. 3. All the patients with ovarian metastases of uterine cervical cancer had invasion to a depth of more than 2/3 of the uterine cervix, while the incidence of ovarian metastasis of endometrial carcinoma was increased with deep invasion of the uterine muscular layer, and metastasis was present even in shallow invasion.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[The study of ovarian metastasis in uterine cancer]. 160 54

We have constructed deletion maps of chromosome 3p for cancers of the female genital tract (uterine endometrium, uterine cervix and ovary). The tumours were tested for loss of heterozygosity using CA-repeat polymorphisms. The high degree of informativeness of these markers allowed the construction of detailed deletion maps from a relatively small number of samples. A common region of deletion was identified at chromosome 3p13-21.1 in endometrial cancer and at 3p13-14.3 in cervical cancer; 5 out of 13 (38%) endometrial cancers and six out of eight (75%) cervical cancers showed loss of heterozygosity at these regions. In ovarian cancer a separate common region of deletion was identified at 3p21.1-22; two out of four (50%) ovarian cancers had alleles deleted at this region. These data suggest the presence of a tumour-suppressor gene(s) for endometrial and cervical cancer at 3p13-21.3 and a separate gene at 3p21.1-22 that is involved in the carcinogenesis of ovarian cancer.
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PMID:Deletion mapping of chromosome 3p in female genital tract malignancies using microsatellite polymorphisms. 163 Aug 22

A series of 47 human carcinoma cell lines and their cultured cells were examined for human papillomavirus (HPV) genomes with the use of an HPV detection kit (DNA-RNA hybridization, mixed HPV DNA probe of types 6, 11, 16, 18, 31, 33 and 35). Four of 8 cases of mild dysplasia, 3 of 9 cases of severe dysplasia, 3 of 7 cases of carcinoma in situ, 3 of 15 cases of uterine carcinoma and 5 of 6 cases of condyloma acuminatum were shown to contain the HPV DNA genome in primary cultured cells, while HPV was not detected in the third-passage cells except for the three cases of large cell, nonkeratinizing squamous cell carcinoma. HPV was also not detected in such normal tissues as uterine cervical squamous epithelium, uterine cervical columnar epithelium and endometrium. The presence of HPV DNA genomes was detected consistently in the passages of three lines (SKG-II, HKMUS and HKTUS; large cell nonkeratinizing squamous cell carcinomas of the uterine cervix) with the use of the Southern Blot method (DNA-DNA hybridization, mixed HPV probe of types 6, 11, 16 and 18). HPV type 16 DNA was detected in HKTUS, and HPV type 18 DNA was found in SKG-II and HKMUS. The other 44 cell lines, including ovarian carcinoma, endometrial carcinoma, sarcoma, gastric cancer, pancreatic cancer and rectal cancer, were negative for the HPV-6, HPV-11, HPV-16, HPV-18, HPV-31, HPV-33 and HPV-35 genomes under stringent hybridization conditions.
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PMID:Presence of human papillomavirus genome in human tumor cell lines and cultured cells. 166 88


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