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)

Since its discovery as a protein associated with the cytoplasmic region of E-cadherin, beta-catenin has been shown to perform two apparently unrelated functions: it has a crucial role in cell-cell adhesion in addition to a signaling role as a component of the Wnt/wg pathway. Wnt/wg signaling results in beta-catenin accumulation and transcriptional activation of specific target genes during development. It is now apparent that deregulation of beta-catenin signaling is an important event in the genesis of a number of malignancies, such as colon cancer, melanoma, hepatocellular carcinoma, ovarian cancer, endometrial cancer, medulloblastoma pilomatricomas, and prostate cancer. beta-catenin mutations appear to be a crucial step in the progression of a subset of these cancers, suggesting an important role in the control of cellular proliferation or cell death. The APC/beta-catenin pathway is highly regulated and includes players such as GSK3-beta, CBP, Groucho, Axin, Conductin, and TCF. c-MYC and cyclin D1 were recently identified as a key transcriptional targets of this pathway and additional targets are likely to emerge. Published 1999 John Wiley & Sons, Inc.
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PMID:beta-catenin signaling and cancer. 1058 Sep 87

About 13% of all colorectal cancer may be dominantly inherited. This amounts to about 300 new cases a year in Norway. Colorectal cancer can be cured by early diagnosis and treatment. Coloscopy with polypectomy may prevent infiltrating cancer. Affected families should be offered genetic evaluation, and family members subjected to regular colonoscopy. The genetic bases of five colorectal cancer syndromes, accounting for most cases of hereditary early onset colorectal cancer, have now been determined. These are familial adenomatous polyposis, colon-endometrial cancer (hereditary non-polyposis colon cancer), Cowden's syndrome, Peutz-Jegher's syndrome and juvenile polyposis. These account for at most 3% of all colorectal cancers. In this group, predictive genetic testing may be employed in families with known mutation. Demonstration of mutation carriers by predictive testing must be based on health service available to the persons at risk. With regard to prophylactic measures, experimental and epidemiological data suggest a preventive effect of aspirin and resistant starch. Empirical information on the effect of intervention is insufficient; multicentre studies are needed.
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PMID:[Hereditary colorectal cancer]. 1059 56

Hereditary non-polyposis colorectal cancer (HNPCC) is a relatively common autosomal dominantly inherited predisposition leading to a familial occurrence of cancer of the colon, rectum, endometrium and some other organs. Cancer mortality can be significantly reduced by appropriate intervention. The diagnosis of HNPCC is suspected on the basis of early onset and multiple foci of colorectal cancer (CRC), in many cases affecting the proximal part of the colon, and of endometrial cancer. It may be confirmed by molecular genetic analysis of the mismatch repair genes, especially hMLH1 and hMSH2. In spite of considerable progress in the understanding of hereditary colon cancer, many questions which are of basic importance for the identification and appropriate genetic counselling of gene carriers remain to be answered. HNPCC defined on clinical and genealogical grounds is by no means identical with the presence of mutated mismatch-repair genes. This impedes the identification of persons/families at increased cancer risk. Mutations of other, mainly as yet unidentified genes may lead to a similar phenotype. Not only heterogeneity of the predispositions underlying CRC, but also penetrance and expressivity of the identifiable mutations of the MMR-genes, have been explored only superficially. The process of carcinogenesis in the colon can follow different routes depending on the genetic background of the patients. Its investigation will open up new possibilities of cancer prevention. In addition, genetic counselling must be developed into a more "evidence"-based medical undertaking. These gaps in the understanding of hereditary CRC and in the care of persons at risk can only be overcome through structured collaboration between family doctors, medical specialists such as gastroenterologists, oncologists and surgeons, medical geneticists and basic researchers.
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PMID:[Identification and genetic counseling of people with HNPCC (hereditary nonpolyposis colorectal cancer): old and new research goals]. 1063 51

A patient who had triple cancer (colon cancer, endometrial cancer, and ovarian cancer) in HNPCC kindred is reported. Her family history revealed the occurrence of colon cancer in her paternal aunt and in two cousins, fulfilling the minimum HNPCC criteria. Microsatellite instability analysis revealed replication error (RER)+ in all cancer lesions at 2 microsatellite loci (D1S191, BAT 40). SSCP analysis suggested germline mutation in exon 2 of the hMSH2 gene. This case showed the importance of complete family-history investigations to identify HNPCC patients. In the near future, definitive diagnosis of HNPCC will be possible on the basis of DNA studies.
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PMID:Microsatellite instability and hMSH2 gene mutation in a triple cancer (colon cancer, endometrial cancer, ovarian cancer) patient in hereditary non-polyposis colorectal cancer (HNPCC) kindred. 1068 Mar 34

Lynch syndrome is a peculiar disease, accounting for 5% of the total burden of colon cancer. Characteristics of this disease are autosomal dominant transmission, early onset, and frequent right colon localization. Diagnostic criteria, aimed to collaborative studies, are based on these features (so called Amsterdam criteria). Lynch syndrome has specific biomolecular features (microsatellite instability); mismatch repair genes have been identified as responsible of this syndrome. Lynch syndrome causes high risk for extracolonic malignancies, particularly for endometrial cancer, supposed to be related to mutation of hMSH2 gene. Another feature of Lynch syndrome tumours is better survival with respect to sporadic counterpart. Genetic test allows identifying the state of mutation carriers and selects the patients to submit to screening. Endoscopic screening has been demonstrated to reduce incidence of colorectal malignancies in this syndrome.
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PMID:[The Lynch syndrome]. 1068 68

The benefits of oestrogen replacement therapy (ERT) in preventing vasomotor symptoms, cardiovascular disease, osteoporosis, and colon cancer are well documented. Other potential benefits i.e. dementia and macular degeneration are being investigated. Although oestrogen is said to be contraindicated in women previously treated for breast and endometrial cancer, there is no data to support this admonition. Preliminary data would suggest ERT can be used safely in women who have had these cancers. Prospective randomised studies are currently on going in the United States and Europe addressing ERT in previously treated breast and endometrial cancer. Informed consent, patients' desires, and benefit-risk considerations are all part of information the woman needs to make a decision concerning ERT.
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PMID:HRT and women who have had breast or endometrial cancer. 1069 60

A new method of survival analysis, denoted period analysis, has recently been developed, which has been shown to provide more up-to-date estimates of long-term survival rates than traditional methods of survival analysis. We applied period analysis to data from the nationwide Finnish cancer registry to provide up-to-date estimates of 5-, 10-, 15- and 20-year relative survival rates (RSR) achieved by the end of the 20th century. For most forms of cancer, period estimates of long-term survival are much higher than corresponding traditional survival estimates which suggests that for these cancers there has been ongoing major progress in survival rates in recent years which so far has remained undisclosed by traditional methods of survival analysis. For example, period analysis reveals that 10 year RSR have come close to (or even exceed) 80% for cancer of the corpus uteri and melanoma, 75% for breast cancer, 70% for bladder cancer, 65% for cancer of the cervix uteri, and 55% for cancer of the colon and prostate. Period analysis further reveals that 20 year RSR have now come close to (or even exceed) 75% for endometrial cancer and melanoma, 60% for breast cancer and cervical cancer, 55% for colon cancer and bladder cancer, and 40%-50% for cancer of the rectum, the ovaries, kidneys and nervous system.
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PMID:Long-term cancer patient survival achieved by the end of the 20th century: most up-to-date estimates from the nationwide Finnish cancer registry. 1148 67

The advantages and disadvantages of hormone replacement therapy (HRT) have been debated nearly as long as the treatment has been in use, especially the relationship between HRT and risk of cancer development. It is hoped that recently published studies will shed more light on this complex issue. Several large population studies suggest that there may be a small but increased risk of developing breast cancer in HRT users, especially in estrogen and progesterone users. This risk appears most pronounced after 5 years of HRT use. Endometrial cancer, which has long been associated with unopposed estrogen use, can be successfully prevented with the addition of progestins to the HRT regimen, provided it is given for at least 10 days each month. Estrogen replacement therapy has also been shown to significantly reduce the risk for colon cancer but not rectal cancers. Finally, a large prospective study has linked HRT with an increase in ovarian cancer mortality.
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PMID:Hormone replacement therapy and cancer risk. 1155 17

Sex steroids are not known to damage DNA directly. They can stimulate or inhibit cell proliferation, and thus can modulate tumor developmental progression. Sex steroid-related tumors in women are represented by breast cancer and endometrial cancer, and a possible relationship exists between sex steroids and both ovarian and colon cancer. Among current ERT users or those who stopped use 1-4 years previously, the relative risk of having breast cancer diagnosed increases by a factor of 1.023 for each year of hormone use. This increase is comparable with the effect on breast cancer of delaying menopause, and seems to be largely limited to lean women. The breast cancers diagnosed during ERT are more likely to contain ER and are less aggressive. Some reports indicate no increase in breast cancer mortality in HRT users. Recent data suggest that an estrogen-progestin regimen may increase breast cancer risk beyond that associated with estrogen alone. However, the effect of progestogens on the breast awaits further clarification. ERT/HRT is generally considered to be contraindicated in breast cancer patients, as no firm data are yet available from randomized clinical trials. Despite the potential risks, ERT/HRT could be considered for breast cancer patients suffering from menopausal symptoms resistant to alternative treatments, after completely informed consent is given, particularly in women with ER--(hormone-resistant) cancers. Unopposed estrogen therapy is known to increase endometrial cancer risk, and is appropriate only for hysterectomized women. To negate the excess risk of endometrial hyperstimulation, an adequate progestin dose must be given in a continuous combined regimen or for an appropriate number of days in sequential regimens (10 days or more for some progestogens or 12 days or more for other progestogens). An appropriate combination of estrogen and progestin does not appear to increase, and may even decrease, the risk of endometrial cancer. HRT is generally considered to be contraindicated in endometrial cancer patients. Despite the potential risks, HRT could be considered for patients suffering from menopausal symptoms resistant to alternative treatments, after completely informed consent is given. Available data suggest a reduced risk of colorectal adenoma and colon cancer in current users of HRT, but definitive studies are still needed. There is no contraindication to HRT prescription in colon cancer survivors. Consistent epidemiological data describe a decreased incidence of ovarian cancer with oral contraceptive use during the reproductive years. Studies on HRT and risk of epithelial ovarian cancer have produced conflicting results but most data seem to exclude a strong association. While no data contraindicate HRT use in epithelial ovarian cancer survivors, current studies do not allow us to exclude the possibility that estrogens alone could stimulate ovarian cancer growth in a small fraction of patients. Additional studies are required. It is important to consider that not all estrogens and progestins are used with the same dosage, route of administration (oral, transdermal and for estradiol intranasal) and, mostly, different estrogens do not show the same bioavailability and tissue effects. The available data do not allow to discriminate for all these variables and therefore it is inappropriate to consider jointly all forms of hormonal therapy. This issue is considered as an important area for future evaluation and research. The International Menopause Society is in the process of drawing up specific recommendations for further research in the field of HRT and cancer.
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PMID:Controversial issues in climacteric medicine II. Hormone replacement therapy and cancer. International Menopause Society Expert Workshop. 9-12 June 2001, Opera del Duomo, Pisa, Italy. 1158 39

Hereditary nonpolyposis colorectal cancer (HNPCC) is associated with highly penetrant germline mutations in mismatch repair genes. Due to a high lifetime risk in gene carriers for synchronous and for metachronous colorectal cancer and endometrial cancer in women, prophylactic and extended surgery are considered as options for gene carriers. A 54-year-old patient with a history of metachronous rectal cancer and a family history fulfilling the Amsterdam criteria presented with carcinoma of the cecum and highly dysplastic adenomas of the splenic flexure and descending colon. As a result of these findings, medical history and molecular diagnosis, the decision was made to perform colectomy and prophylactic hysterectomy with oophorectomy; histological examination of the specimen showed three synchronous colon carcinomas. The 31-year-old son carrying the pathogenic mutation refused to be included in the HNPCC surveillance program. One year later he presented with symptoms of bowel obstruction, and a carcinoma of the descending colon was diagnosed. Intraoperatively, in addition to the colon cancer, a small bowel cancer and peritoneal carcinomatosis were found. In another family fulfilling the Amsterdam criteria without known germline mutation a woman presented with synchronous cancer of the ascending colon and the lower rectum at the age of 49 years. Proctocolectomy and prophylactic hysterectomy were performed, which revealed an additional colon cancer and endometrial cancer. We discuss approaches for individual decision making for surgery in HNPCC patients. Is a subtotal colectomy indicated in the case of first colon cancer in HNPCC patients, or if the first tumor occurs in the lower rectum, should a proctocolectomy or a restorative proctocolectomy be considered? The aim of prospective clinical studies should be to assess acceptability, survival rates, mortality, and the quality of life in HNPCC patients who have undergone surveillance and standard oncological resections versus extended or prophylactic surgery.
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PMID:Combined molecular and clinical approach for decision making for surgery in HNPCC patients: a report on three cases in two families. 1176 Sep 4


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