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

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

Colony forming ability of solid tumor cells was studied in a tumor colony assay (human tumor stem cell assay). In 50 cases of solid tumors, cloning efficiencies of 5 X 10(5) cells plated were as follows: breast cancer 12/12 (100%), colon cancer 10/11 (91%), ovarian cancer 9/9 (100%), sarcomas 7/9 (78%), gastric cancer 3/6 (50%), endometrial cancer 2/2 and pancreatic cancer 1/1. An overall cloning efficiency was 88% (44/50) and this rate is higher than those reported in literatures. Ovarian cancer showed the highest plating efficiency of 0.07% (number of colonies/number of cells plated X 100%) in various solid tumors tested. Subsequently, plating efficiencies of colon and breast cancer were 0.03 and 0.01%, respectively. In the cases of sarcomas and gastric cancer, low plating efficiencies were seen (0.008%, 0.003%). The overall rate succeeded colony growth of solid tumors was somewhat higher in enzymatically treated tumor cells, that is, cloning efficiencies in mechanical and enzymatic methods were 85 and 90%, respectively. The enzymatic disaggregation is an advantageous method in gastric cancer and sarcomas. Various solid tumors can be formed colonies in soft agar and chemosensitivity test using in vitro colony assay is expected in solid tumors.
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PMID:[Colony formation of solid tumors in in vitro colony assay (human tumor stem cell assay)]. 676 97

The relationship between diabetes mellitus and cancer risk was investigated using data from an integrated series of case-control studies conducted in Northern Italy between 1983 and 1992. Cases were 9,991 patients with incident, histologically confirmed neoplasms below age 75, including 181 cancers of the oral cavity and pharynx, 316 of the oesophagus, 723 of the stomach, 828 of the colon, 498 of the rectum, 320 of the liver, 58 of the gall bladder, 362 of the pancreas, 242 of the larynx, 3,415 of the breast, 726 of the endometrium, 971 of the ovary, 125 of the prostate, 431 of the bladder, 187 of the kidney, 208 of the thyroid, 80 Hodgkin's lymphomas, 200 non-Hodgkin's lymphomas and 120 multiple myelomas. Controls were 7,834 subjects in hospital for acute, non-neoplastic, non-metabolic, non-hormone-related disorders. A history of diabetes was reported by 5.1% of male and 5.4% of female controls. Significantly elevated relative risks (RRs) among subjects with diabetes were observed for cancers of the liver [RR = 2.8, 95% confidence interval (CI) 2.0-3.9], pancreas (RR = 2.1, 95% CI 1.5-2.9) and endometrium (RR 3.4, 95% CI 2.7-4.3). After allowance for obesity and education as well as age and sex, the RRs were 3.0 for liver, 2.3 for pancreas, and 2.8 for endometrium. Diabetic subjects had no elevated risk for any of the other cancer sites considered. For liver and endometrial cancer the RRs remained elevated up to 10 years after diagnosis of diabetes (RR 2.6 and 2.0 respectively), while the RR for pancreatic cancer declined from 3.2 in the first 5 years after diagnosis of diabetes to 2.3 from 5 to 9 years and to 1.3 (95% CI 0.7-2.3) 10 or more years since diagnosis. This suggests that the relationship between diabetes mellitus and liver and endometrial cancer is probably real, while that with pancreatic cancer is compatible with diabetes being an early symptom of the disease, or at least of preneoplastic lesions.
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PMID:A case-control study of diabetes mellitus and cancer risk. 794 3

The sequences encoding the full-length epidermal growth factor receptor (EGFR) were cloned from a cDNA library prepared from T3M4 cells. A transition (G to A) was identified at codon 497 of EGFR cDNA, resulting in the substitution of a lysine for an arginine. The same substitution was identified by sequencing cDNA derived from 3 of 7 additional human pancreatic cancer cell lines, one endometrial cancer cell line, and one lung cancer cell line, but not in A431 cells. Variant EGFR was always co-expressed with wild-type EGFR. Both sequences were present in genomic DNA from two cell lines expressing the variant receptor and in DNA from normal (3 of 7 individuals) human lymphocytes. These findings indicate that there are two alleles in this region of the EGFR gene, and that expression of variant EGFR is a common occurrence in normal and cancerous cells.
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PMID:Cloning of a variant epidermal growth factor receptor. 846 82

Hereditary non-polyposis colorectal cancer (HNPCC) is an autosomal dominant condition predisposing to cancers of the colorectum and endometrium. Endometrial cancer is the most commonly occurring extracolonic cancer in HNPCC. Estimates of the cumulative incidence of endometrial cancer in women with mutations in the HNPCC genes range from 22-43%. In order to determine how frequently double primary cancers of the colorectum and endometrium are the result of a hereditary factor, we conducted a registry based study in Ontario and Quebec, Canada. We obtained pedigrees on 80 women diagnosed with double primary cancers of the colorectum and endometrium at less than 70 years of age. Family histories of cancer were obtained for all first degree relatives of these women and cancer rates were compared with age standardised provincial incidence rates in order to estimate the relative risks. There was a total of 82 cancers observed in relatives below the age of 55, compared with 31.2 expected, giving a relative risk of 2.6 (95% confidence interval (CI) 2.1-3.3). The relative risk for colorectal cancer below 55 was 16.1 (95% CI 11.6-21.8). This risk decreased with increasing age of onset of cancers in probands. For probands with both colorectal and endometrial cancer diagnosed under the age of 55, the relative risk of colorectal cancer in relatives below the age of 55 was 30.5 (95% CI 18.8-46.6). Similar patterns were observed for endometrial and pancreatic cancer. There were non-significant increases in rates of cancer of the oesophagus, stomach, small intestine, and bladder. There was no increased risk of breast cancer. The risk of lung cancer was decreased, especially in older relatives. Our findings indicate the presence of a significant genetic component of cancer in women with double primary cancers of the colorectum and endometrium.
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PMID:Genetic implications of double primary cancers of the colorectum and endometrium. 986 92

In conclusion, obesity has been associated with increased risk for a number of different types of cancer. The evidence has been most consistent for endometrial cancer, breast cancer in postmenopausal women, and renal cell cancer. More variable results have been reported for colorectal, prostate and pancreatic cancer. Possible mechanisms by which obesity may influence cancer risk include alteration in hormonal patterns, including sex hormones and insulin, and factors such as the distribution of body fat and changes in adiposity at different ages. The increasing prevalence of obesity in many parts of the world emphasizes the importance of learning more about the relationship between obesity and cancer and the mechanisms involved in their interaction.
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PMID:Obesity as a risk factor for certain types of cancer. 987 Aug 99

Hereditary nonpolyposis colorectal cancer (Lynch syndrome) is an autosomal dominant disease caused by mutations in the mismatch repair genes in particular in MLH1, MSH2 and MSH6. The disease is characterized by the development of colorectal, endometrial cancer and several other cancers. There is evidence that the clinical expression of the disease varies from one country to another. This variation might affect not only the application of criteria proposed to identify families but also clinical risk factors reported to predict the outcome of genetic testing. Data on site of the cancer, age at diagnosis and pathology were collected from 155 families with suspected HNPCC known at the Korean and Dutch HNPCC registries. DGGE, SSCP and DNA-sequencing were performed to identify MSH2, MLH1 and MSH6 mutations. A total of 33 Korean and 42 Dutch families met the clinical criteria for HNPCC. Germline mutations in the MMR-genes were found in 23 Korean and 24 Dutch families. In families that met the Amsterdam criteria, and also in those associated with MLH1 mutations, more cancers of the stomach and pancreas were observed in the Korean families than in the Dutch HNPCC families; in relative terms, the incidence of cancers of the endometrium in the Korean families was lower. Multivariate analysis showed that an early age at diagnosis, and the occurrence of pancreatic cancer were independent predictive factors of germline mutations in MLH1, MSH2 and MSH6 in the Korean subset of families.
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PMID:Gene-environment interaction in hereditary nonpolyposis colorectal cancer with implications for diagnosis and genetic testing. 1040 64

Cancer-associated retinopathy (CAR) is an ocular manifestation of a paraneoplastic syndrome whereby immunological reactions to retinal antigens aberrantly expressed in tumor cells lead to the degeneration of retinal photoreceptor cells. In our previous study (H. Ohguro et al., Invest. Ophthalmol. Vis. Sci., 40: 82-89, 1999), recoverin, a retina-specific calcium-binding protein, and heat shock cognate protein 70 (hsc 70) were identified as autoantigens recognized by sera from patients with CAR. Therefore, we suggested that autoimmune reactions against both recoverin and hsc 70 might be involved in the pathogenesis of CAR. To elucidate the initial step of the molecular pathology of CAR, we examined the expression of recoverin and hsc 70 by reverse transcription-PCR and Western blot using cell lines of several kinds of cancers, including lung small cell carcinoma, lung adenocarcinoma, gastric cancer, pancreatic cancer, breast cancer, uterine cervical cancer, endometrial cancer, and leukemia. Recoverin was expressed in 21 of the 31 cancer cell lines. The expression levels of hsc 70 were significantly higher in cancer cell lines than in noncancerous cell lines. However, no difference in the expression levels of hsc 70 was observed between recoverin-positive and -negative cell lines. Immunofluorescence labeling by the affinity-purified recoverin antibody revealed the immunoreactivity to recoverin as a granular pattern within the cancer cells. Lung adenocarcinoma A549 cells, which did not express recoverin, exhibited a significant reduction in cell proliferation upon transfection with human recoverin cDNA. Taken together, our present data suggest that the retina-specific calcium-binding protein recoverin is expressed in more than 50% of a variety of cancer cells and may play a significant role in the cell proliferation of these tumor cells.
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PMID:Aberrant expression of photoreceptor-specific calcium-binding protein (recoverin) in cancer cell lines. 1076 80

Disruption of the DNA mismatch repair (MMR) system has been found to play an important role in sporadic human cancers of several organs such as colorectum, stomach, endometrium, and pancreas. In cancers of the former three organs, disruption of the MMR system is mainly caused by hypermethylation of the hMLH1 gene. We investigated the expression of the hMLH1 and hMSH2 proteins immunohistochemically in pancreatic and endometrial cancers with high frequency microsatellite instability (MSI-H). Loss of expression of hMLH1 was found in none of seven pancreatic cancer, whereas eight (57%) of 14 endometrial cancer showed loss of expression of hMLH1. On the other hand, one (14%) of seven pancreatic cancers and two (14%) of 14 endometrial cancers showed loss of hMSH2 expression. We further analyzed the methylation status at the promoter region of the hMLH1 and hMSH2 genes and found hypermethylation of hMLH1 at the promoter region in the great majority of endometrial cancers with loss of expression. However, no pancreatic cancer showed hypermethylation. We then further analyzed 22 pancreatic cancer cell lines and obtained similar results. These results suggested that MSI-H in pancreatic cancer is probably caused by different mechanisms from those of other sporadic cancers with MSI-H.
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PMID:Not hMSH2 but hMLH1 is frequently silenced by hypermethylation in endometrial cancer but rarely silenced in pancreatic cancer with microsatellite instability. 1093 95

Familial risk of pancreatic cancer has been mainly assessed through case-control studies based on reported but not medically verified cancers in family members. We used the nationwide Swedish Family-Cancer Database on 10.2 million individuals and 21,000 pancreatic cancers to calculate standardized incidence ratios (SIRs) and 95% confidence intervals (CIs) for pancreatic cancer in 0- to 66-year-old offspring of parents with pancreatic or other specified tumors. Additionally, SIRs for second primary pancreatic cancers were analyzed after any first neoplasm. SIRs for pancreatic cancer (1.68, 95% CI 1.16-2.35) and pancreatic adenocarcinoma (1.73, 95% CI 1.13-2.54) were increased when a parent presented with pancreatic cancer. The risk was not dependent on diagnostic age of offspring or parents. Pancreatic cancer was associated with parental lung, rectal or endometrial cancer and with melanoma. SIRs for pancreatic cancer were 10.01 and 7.96 among offspring who were diagnosed before age 50 years when parents were diagnosed with squamous cell and adenocarcinoma of the lung, respectively, before age 60 years. The population-attributable proportion of familial pancreatic cancer was 1.1%. Risks for second pancreatic cancers were increased in men and women after small intestinal, colon and bladder cancer. The degree of familial clustering for pancreatic cancer and its population-attributable proportion were lower than the data cited in the literature. Clustering of pancreatic cancer with sites presenting in hereditary nonpolyposis colorectal cancer was noted. The strong association of pancreatic and lung cancers is puzzling, and it remains unclear to what extent this represents familial sharing of smoking habits.
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PMID:Familial and second primary pancreatic cancers: a nationwide epidemiologic study from Sweden. 1247 70


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