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)

Circulating carcinoembryonic antigen (CEA) and alpha fetoprotein (AFP) levels were measured by radioimmunoassay in 53 patients with carcinoma of the ovary, 16 patients with other malignant genital tumors, and 31 women with nonmalignant diseases of the genital tract. The serum CEA concentration was elevated (greater than 5 ng/ml) in 11 patients with ovarian cancer, 2 patients with endometrial cancer, 1 patient with carcinoma of the cervix, and 1 patient with a benign embryonal cystic teratoma. Elevated CEA levels were found only in patients with advanced malignant disease, while early stages were associated with normal CEA concentrations. AFP levels were normal in all but 1 patient. Both CEA and AFP levels were markedly raised in a case of advanced genital carcinoma arising probably from the ovary. Ascitic fluid of another patient with ovarian cancer contained a high concentration of CEA, giving an identical reaction in immunodiffusion with CEA from colon cancer. The present results indicate that while the increased expression of carcinofetal components takes place in some malignant tumors of the female genital tract, it is usually a late phenomenon.
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PMID:Carcinoembryonic antigen and alpha fetoprotein in malignant tumors of the female genital tract. 4 62

A review of 172 patients with squamous cell cancer of the vulva treated at the University of Michigan Medical Center from 1975-1989 was performed to compare the 1988 FIGO Staging System to the 1970 FIGO Staging System. The stage distribution according to the 1970 FIGO Staging System was stage I, 65; stage II, 44; stage III, 50; and stage IV, 13. The cumulative 5-year survival under the old system was stage I, 94%; stage II, 91%; stage III, 36%; and stage IV, 26%. The distribution changed under the 1988 FIGO system to stage I, 58; stage II, 36; stage III, 49; stage IVA, 16; and stage IVB, 13. The cumulative survival also changed to stage I, 94%; stage II, 89%; stage III, 71%; stage IVA, 19%; and stage IVB, 8%. The new FIGO stage distribution shifted for the worse due to the influence of positive lymph nodes found at the time of surgery. The survival was then analyzed for death from all causes. This was markedly decreased when compared to the cumulative corrected survival. This relates to the high number of other primary malignancies and the age of the patients. Among these 172 patients, other primary malignancies included squamous cell cancer of the cervix (11), squamous cell cancer of the vagina (2), endometrial cancer (3), squamous cell cancer of the lung (2), colon cancer (3), and others (6). An additional 5 patients died from myocardial infarction within 2 years of diagnosis. The new 1988 FIGO Staging System provides for better discrimination of survival between stages than the 1970 FIGO Staging System.
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PMID:A comparison of staging systems for squamous cell carcinoma of the vulva. 142 97

A mass screening has been performed for the early detection of colon cancer by evaluating Hemocult II slides of blood relatives of patients with endometrial cancer. Though the defect of this screening is that the subject of the investigation, which was undertaken in all parts of Japan, is restricted, one case of colon cancer, two cases of colon polyposis, two cases of hemorrhoids, and one case of colon diverticulum have been uncovered by this screening. The rate of discovery of colon cancer proved to be 0.45%, a rate that is higher than seen in usual screening method. It has been concluded that blood relatives of patients with endometrial cancer should be screened, since they represent a high risk group for developing colon cancer.
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PMID:[Mass screening for the early detection of colon cancer in patients with endometrial cancer]. 284 10

Disease-oriented phase II trials of doxifluridine were performed in advanced colorectal, breast, renal, endometrial, stomach, and ovarian carcinomas. The dose schedule recommended by the phase I trial (12.5 g/m2 by continuous iv infusion over 6 hours once a week for 3 weeks followed by a 1-week rest) was chosen first: the initial dose was later decreased to 10 g/m2 due to the fact that several neurotoxic effects were reported. A total of 207 patients were entered: 137 patients who received at least two courses of treatment were evaluable for response. Therapeutic activity was demonstrated in breast cancer [two complete responses (CR) and 13 partial responses (PR) among 42 patients], colon cancer (seven PRs among 35 patients), and rectal cancer (six PRs among 23 patients). Some therapeutic activity was detected in ovarian cancer (one CR among nine patients), endometrial cancer (one PR among five patients), and stomach cancer (one PR among five patients). No significant activity was noticed in renal cancer (one PR among 18 patients). Nonhematological toxicity was evaluated according to World Health Organization criteria. Nausea and vomiting were recorded in 50% of the patients (Grade 3-4 in 5%), diarrhea was recorded in 20% (Grade 3-4 in 5%), and cutaneous and allergic reactions were recorded in 10% (Grade 3-4 in 2%). Myelotoxicity during the first treatment course was mild; median wbc and platelet count nadirs (x 10(9) cells/L) were 4.1 (range, 0.1-11) and 194 (range, 20-482), respectively. Nevertheless, some cases of acute leukopenia and thrombopenia were reported. Consciousness alterations and neurologic symptoms were the major side effects (72 of 173 evaluable patients), since treatment had to be interrupted in 34 patients and four lethal neurotoxic effects occurred. At the same total dose of doxifluridine, the risk of neurotoxicity significantly increases with age and with the weekly dose and to the contrary it decreases with increasing bilirubin level. Although activity was demonstrated, this treatment cannot be recommended because of major neurotoxicity. Further pharmacological studies seem warranted to define the optimal dosage schedule and to obtain a better therapeutic index.
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PMID:Phase II clinical evaluation of doxifluridine. 294 45

Progestogens should be added to estrogen replacement therapy, not only to prevent endometrial cancer in women with a uterus, but also to reduce the risk of breast cancer in some women. Smoking should be discouraged to reduce the risk for both lung cancer and heart disease. Recommendations should be made to increase fiber intake to lessen the risk for carcinoma of the colon. Reducing fat intake also decreases risk for colon cancer, as well as carcinoma of the breast. Postmenopausal bleeding must be investigated for early diagnosis of endometrial cancer and, when endometrial hyperplasia is the finding, it should be treated with progestogens to prevent adenocarcinoma. The progestogen challenge test is recommended for all women with a uterus, and if bleeding occurs, the progestogen should be continued for 13 days each month. Use of mammograms and other diagnostic modalities should be increased to make the earliest possible diagnosis of breast cancer.
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PMID:Cancer in the older woman: diagnosis and prevention. 304 28

HNPCC is an autosomal dominantly inherited disorder with proclivity to early onset colorectal cancer in the absence of multiple polyps of the colon. There is a predilection for proximal colonic location (70 per cent) and an excess of synchronous and metachronous colorectal cancers. HNPCC is subdivided into Lynch syndrome I, which is restricted to site-specific colon cancer susceptibility, and Lynch syndrome II, which shows all of the features of Lynch syndrome I, but in addition, patients are at inordinately increased risk for carcinoma of the endometrium, ovary, and other anatomic sites. The frequency of HNPCC is conservatively estimated to be 4 to 6 per cent of the total colorectal cancer burden. Because of the fact that the family history is underreported almost uniformly in medical practice, we believe that the true frequency of this disease may be much greater. Heterogeneity may be extant with respect to tumor association, in that in certain Lynch syndrome II kindreds, carcinoma of the pancreas, kidney, breast, and other anatomic sites may predominate. Knowledge of the natural history of HNPCC predicates surveillance and management strategies. Thus, because of the early onset of and proximal predilection for colorectal cancer, we recommend initiation of colonscopy at age 25 and annually thereafter. We also recommend guaiac testing of the stool at least twice a year. In the case of Lynch syndrome II, in addition to colonscopy, we recommend intensive surveillance for the endometrium, including aspiration biopsies. Other targeted organs, depending on the tumor spectrum in the family, should be given priority attention. Because of an excess of synchronous and metachronous colorectal cancer in HNPCC, subtotal colectomy with ileorectal anastomosis is the treatment of choice for initial colorectal cancer. In women presenting with initial colorectal cancer who have completed their families, consideration should be given to prophylactic hysterectomy and bilateral salpingo-oophorectomy at the time of surgery for colorectal cancer. Needed are biomarkers of acceptable sensitivity and specificity for the genotype, because HNPCC lacks premonitory physical signs. We believe that increased knowledge about colorectal cancer etiology and carcinogenesis can be attained through the study of families prone to the Lynch syndromes.
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PMID:Hereditary nonpolyposis colorectal cancer--Lynch syndromes I and II. 306 37

Lynch syndrome II is characterized by an autosomal dominantly inherited susceptibility to early onset colon cancer with proximal predominance, an excess of synchronous and metachronous colonic cancer, carcinoma of the endometrium, ovary, and multiple primary cancer excess. Knowledge of the full tumor spectrum in this disorder(s) remains elusive. Cancers that are uncommon in this disease, but present in three extended Lynch syndrome II families, included brain tumors, carcinoma of the bile duct, duodenum, the urological system, and breasts. Long-term followup of these families (as long as two decades) provided the opportunity to trace in depth this tumor spectrum. Full scrutiny of cancer of all anatomic sites in the absence of biomarkers of high sensitivity and specificity to the cancer-prone genotype will be necessary to comprehend more clearly whether these (or other) cancer sites are integral to this disorder, whether common environmental exposures are involved and, finally, whether chance can explain these cancer associations.
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PMID:Tumor variation in three extended Lynch syndrome II kindreds. 338 6

Hereditary nonpolyposis colorectal cancer (HNPCC) is comprised of the following: the cancer family syndrome (CFS), or Lynch syndrome II, which shows early-onset proximal colonic cancer predominance and other associated extracolonic adenocarcinomas, particularly endometrial carcinoma; and hereditary site-specific colon cancer (HSSCC), or Lynch syndrome I, which shows all of the same characteristics, except for extracolonic cancer. Nine families with CFS and two with HSSCC provided the resource that was tested for biomarkers (see companion article). All families were meticulously evaluated for genealogy and cancer verification. Biologic specimens were obtained during field visits to areas of closest geographic proximity to the families. Cancer education and recommendations for surveillance/management were provided to patients and their physicians. Additionally, 40 families (about 3000 individuals) with either CFS or HSSCC have been ascertained. Syndrome cancers were restricted to direct-line relatives as opposed to nonbloodline relatives, arguing against involvement of environmental factors. One documented clinical feature was a predilection for proximal versus distal colonic cancer in both CFS and HSSCC kindreds. This has important clinical significance in that it clarifies the need for instituting effective surveillance earlier to detect the predominantly proximal colonic cancers.
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PMID:Hereditary nonpolyposis colorectal cancer (Lynch syndromes I and II). I. Clinical description of resource. 401 85

Although only a small proportion of common cancers show familial aggregation, studying such families can elucidate the roles of shared environment and genes in the development of neoplasia. We report an analysis of nine colon cancer pedigrees using new nonparametric objective methods to measure familial aggregation as a means of determining the existence of heterogeneity in the data. Each family was selected through a proband with nonpolyposis colon cancer who had a first-degree relative with documented colon cancer. To assess the aggregation of different cancers in these families we employ a method which evaluates both excess number of cases as well as distribution by risk in family members. We find that eight of the nine families exhibit significant aggregation of colon cancer: endometrial cancer aggregates in three families, breast in none, kidney in one, and all sites in eight. In this way, we show that two families fit the criteria for Cancer Family Syndrome, and that one is not a high-risk cancer family.
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PMID:Aggregation of colon cancer in family data. 654 32

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


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