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)

Cancer is a disease predominantly seen in the older age group. The most frequent forms are in males: lung, prostatic, stomach, colonic and bladder cancer. In females: breast, colonic, stomach cancer, lymphoma, leukaemia and rectal cancer. In view of the expected demographic figures a dramatic increase in the incidence of cancer is expected. The malignancies seen in the elderly respond generally poor to chemotherapy. Most cytotoxic drugs are excreted by the kidneys. Especially the renal clearance of anticancer drugs will therefore be compromised in the elderly, this should be considered when giving cytostatics. Mucositis, bone marrow toxicity, pulmonary and neurotoxicity are quite often enhanced in the older patient group. The indications for chemotherapy are limited. Chemotherapy should not be withheld from patients with advanced breast cancer and certain haematological malignancies. Further clinical research focussed on the elderly is warranted. Drugs with a mild spectrum of side effects deserve priority. Hormonal treatment is an important modality in breast, prostatic and endometrial carcinoma. The burden for the patients is limited and the advantages are well documented.
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PMID:[Drug treatment of cancer in elderly patients]. 221 38

Alkylating agents have caused acute nonlymphocytic leukemia (ANLL), probably bladder cancer, and possibly other solid tumors. Phenacetin also has enhanced risk of bladder cancer, and probably also carcinoma of the renal pelvis. Topical nitrogen mustard, potassium arsenite, tar ointments, and methoxsalene have been related to development of nonmelanotic skin cancers. Immunosuppression by azathioprine, usually with prednisone, has enhanced risks of non-Hodgkin's lymphomas, hepatobiliary cancers, and various mesenchymal tumors. Liver cancers have been reported in users of androgenic anabolic steroids, and both hepatic cell adenomas and carcinomas have been associated with use of combined oral contraceptives. These contraceptives reduce risks of endometrial and ovarian carcinomas. Estrogens increase risk of endometrial cancer. Exposure to diethylstilbestrol in utero can result in clear cell carcinomas of the vagina and cervix, and possibly testicular carcinomas.
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PMID:Steroid hormones and medications that alter cancer risks. 304 37

Several examples of the use of vital statistics in drug epidemiology are described. The death rates for asthma remained stable from about 1860-1960 in the UK, about 0.5/100,000. In 1961 the rates began to rise, and after 1967 they declined; in the 1970s the rates almost approached pre-epidemic levels. The rates were found to vary with the use of isoproterenol-containing nebulizers. Investigations into the relationship between thromboembolism pulmonary embolism, and myocardial infarction and oral contraceptive (OC) usage showed an increase in death rates beginning after the introduction of OCs in 1960-61 in women at risk. Subacute myelo-optic neuropathy was an unexplained disease until Japanese investigators linked its occurrence to ingestion of the halogenated hydroxyquinoline drugs used to treat nonspecific gastroenteritis; seasonal outbreaks of the disease were linked to seasonal gastroenteritis. Animal experiments conclusively linked the drug to the disease. A Swedish report implicated the antihypertensive drug methyldopa as a possible cause of cancer of the biliary ducts. Links between thalidomide and phocomelia, saccharin or cyclamates and bladder cancer, diethylstilbestrol and vaginal cancer, and estrogens and endometrial cancer are discussed. Drug-monitoring systems, the collection of vital statistics and observations by clinicians all contribute to understanding drug-induced disease. Changes in disease incidence or emergency of new syndromes in areas where certain drugs are heavily used should be compared to areas where they are seldom used.
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PMID:The use of vital and morbidity statistics for the detection of adverse drug reactions and for monitoring of drug safety. 716 6

Between 1985 and 1990, five cases of radiation-induced bladder cancer were treated at our center. The first primary neoplasm was uterine cervical cancer in three patients, uterine endometrial cancer in one patient, and Hodgkin's disease in one patient. Additional treatment for the primary neoplasm included panhysterectomy for the patient with endometrial cancer and cyclophosphamide-based combination chemotherapy for the patient with Hodgkin's disease. The mean age at development of bladder cancer was 60.4 years, and the average time interval between irradiation and development of bladder cancer was 14.6 years. All the bladder cancers were invasive. The treatment modalities included anterior pelvic exenteration in one patient, partial cystectomy in one patient, reirradiation in two patients, including the use of intraoperative electron therapy in one patient, and TUR plus endoscopic Nd:YAG laser treatment in one patient. Four patients are alive without disease at a mean follow-up period of 15 months from the diagnosis of bladder cancer.
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PMID:Second primary bladder cancer following pelvic irradiation for other malignancies. 837 8

Gene amplifications are common in many different tumor types and may confer diagnostic, prognostic, or therapeutic information for patient management. Tedious experiments are often required to determine which tumor types have amplifications of a specific oncogene. To facilitate rapid screening for molecular alterations in many different malignancies, a tissue microarray consisting of samples from 17 different tumor types was generated. Altogether, 397 individual tumors were arrayed in a single paraffin block. To determine whether results from the literature can be reproduced on minute tissue samples (diameter, 0.6 mm), amplification of three extensively studied oncogenes (CCND1, CMYC, and ERBB2) was analyzed in three fluorescence in situ hybridization experiments from consecutive sections cut from the tissue microarray. Amplification of CCND1 was found in breast, lung, head and neck, and bladder cancer, as well as in melanoma. ERBB2 was amplified in bladder, breast, colon, stomach, testis, and lung cancer. CMYC was amplified in breast, colon, kidney, lung, ovary, bladder, head and neck, and endometrial cancer. These results confirm and even extend existing data in the literature on such amplifications. In summary, we applied three fluorescence in situ hybridization experiments to analyze amplifications of three oncogenes in three x 397 tumors within a week. This demonstrates the power of using minute arrayed tissue specimens for tumor screening.
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PMID:Tissue microarrays for gene amplification surveys in many different tumor types. 1047 73

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

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

Cyclin E amplification and overexpression have recently been described in several tumour types. However, many tumour entities have never been examined for cyclin E alterations. Numerous and time-consuming experiments were previously required to determine the significance of potential oncogenes across different tumour types. To overcome this problem, tissue microarrays (TMAs) consisting of 3670 primary tumours from 128 different tumour types, 709 metastases, and 354 normal tissues were generated. Cyclin E alterations were then analysed by fluorescence in situ hybridization (FISH) and immunohistochemistry (IHC). Cyclin E gene amplification was observed in 15 different tumour types and subtypes, ie rhabdomyosarcoma, urinary bladder cancer (three subtypes), ovarian cancer (two subtypes), malignant fibrous histiocytoma, adenocarcinoma of the small intestine, medullary breast cancer, gall bladder adenocarcinoma, phaeochromocytoma, gastric adenocarcinoma, squamous cell carcinoma of the uterine cervix, colonic adenocarcinoma, and endometrial carcinoma. Cyclin E protein accumulation was found in 48 different tumour types. The use of TMA technology has enabled us to expand considerably our knowledge of cyclin E alterations in human tumours. The occurrence of amplification and overexpression in many different tumour types suggests that cyclin E plays an important role in tumour biology.
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PMID:Cyclin E overexpression and amplification in human tumours. 1284 34

We report a case of primary non-Hodgkin lymphoma of the breast as third metachronous neoplasm in the same patient. Primary non-Hodgkin lymphoma of the breast occurred about 2 years after endometrial cancer and 1 year after bladder cancer. The patient underwent quadrantectomy with level I-II axillary lymph nodes dissection plus rituximab-cyclophosphamide, doxorubicin, vincristine, prednisone chemotherapy. Patient's health status gradually got worse and 11 months after surgery the patient died.
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PMID:Primary non-Hodgkin lymphoma of the breast as third malignancy in one patient. 1901 3

The genes TSC1 and TSC2, encoding hamartin and tuberin, respectively, have been shown to be involved in the development of the autosomal dominantly inherited tumor syndrome tuberous sclerosis (TSC). However, inactivation of these genes has also been demonstrated to be associated with sporadic bladder cancer, ovarian and gall bladder carcinoma, non-small-cell carcinoma of the lung, breast cancer, pancreatic cancer, astrocytoma, xanthoastrocytoma, ependymomas, oral squamous cell carcinoma and endometrial cancer. The hamartin/tuberin protein complex plays a central role in the regulation of the mammalian target of rapamycin (mTOR) signalling network. A wide variety of components of the mTOR cascade have been demonstrated to be involved in many different human cancers. Mutations in several mTOR pathway component genes are known to cause specific monogenic human genetic diseases and this signalling cascade has been shown to be of relevance for Alzheimer's disease, type 2 diabetes, obesity and hypertrophy. Consequently, e.g. clinical trials for the treatment with rapamycin, a negative regulator of mTOR, of hamartomas in TSC have already been initiated. Now the first evidence is provided for an involvement of the TSC genes in acute leukemia.
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PMID:New insights into the role of the tuberous sclerosis genes in leukemia. 1925 Jun 71


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