Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0006142 (breast cancer)
 160,383 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A sandwich enzyme immunoassay was set up to measure tumor associated antigen (antigen PA8-15) detected by monoclonal antibody PA8-15. The cut-off value was set at 55 U/ml. Tests on 437 sera samples from patients with malignant or benign diseases yielded the following positive percentages: esophageal cancer, 9.1%; gastric cancer, 23.1%; colorectal cancer, 44.8%; hepatoma, 32.6%; biliary tract cancer, 47.5%; pancreatic cancer, 84%; lung cancer, 30.8%; breast cancer, 16%; benign diseases, 13.2%. Positive antigen PA8-15 levels in patients with gastric, colorectal and pancreatic cancers, increased with the progression of clinical stage. When antigen PA8-15 was monitored in 11 various cancer cases before and after surgery, a decrease in PA8-15 value was revealed in all resected patients postoperatively, whereas a more than 100% increase in PA8-15 values was noted in non-resected patients. Compared with CEA and CA19-9, the highest positive PA8-15 rate was seen in pancreatic cancer patients. By combining the rates of positive sera obtained with each tumor marker, the overall percentage increased. These results suggest that measuring serum PA8-15 levels will aid in serological cancer diagnoses, particularly pancreatic cancer.
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PMID:Detection of tumor associated antigen, PA8-15, in sera from pancreatic and gastrointestinal carcinoma patients. 237 Jun 93

The relationship between marital status and cancer incidence was examined based on 49,191 incident cases aged 30 or over in 1980-1984 by using the data from Aichi Cancer Registry and census data. Although married and widowed people did not show increased incidence for any cancer site studied, single and divorced people showed statistically significantly increased or decreased risks for several sites of cancer. Single males showed an increased risk for esophageal cancer and a decreased risk for lung cancer. Divorced males showed increased risks for cancers of the mouth & pharynx, esophagus, liver, skin and brain. Single females showed increased risks for cancers of the esophagus, stomach, small intestine, liver, pancreas, lung, breast, corpus uteri, ovary & fallopian tube and other female genital organs and a decreased risk for cervical cancer. Divorced females showed increased risks for cancers of the larynx, breast, all parts of uterus and cervix uteri and a decreased risk for biliary tract cancer. The increased risk for breast cancer in single females was more pronounced in older age groups and the increased risks for several sites of cancer in divorced people were more pronounced in younger age groups. These findings may be partly explained by differences in reproductive factors and life style, especially smoking and drinking habits.
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PMID:An epidemiological study on marital status and cancer incidence. 250 Dec 46

In 1976, an accidental explosion in a plant near Seveso, Italy, caused the contamination of a populated area by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). The area was subdivided into three zones (A, B, and R) having decreasing mean levels of TCDD soil contamination. This study examines the mortality between 1976 and 1986 among the subjects, aged 20-74 years, who were resident in the area since the accident (n = 556 in zone A, n = 3,920 in zone B, n = 26,227 in zone R). Subjects' exposure was classified by residence. A referent cohort of 167,391 subjects who lived in the immediate surroundings was concurrently examined. Vital status ascertainment was successful for over 99% of the subjects. Increased mortality from cardiovascular causes was found; incident-related stressors were considered more relevant to increased mortality than was TCDD exposure. Mortality from several cancers was elevated. The increases in biliary cancer (females), brain cancer, and lymphatic and hemopoietic neoplasms (particularly leukemia in males) did not appear to result from chance, confounding, or information/comparison bias. However, no definite patterns related to exposure classification were apparent. Merely suggestive increases in soft tissue tumors and melanoma were also noted. Liver and breast cancer mortality tended to be below expectations. Interpretation is hampered by the short observation period, small number of deaths from certain causes, and poor exposure definition. Further research is in progress.
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PMID:Ten-year mortality study of the population involved in the Seveso incident in 1976. 272 56

The risk of developing a second primary cancer was evaluated in approximately 64,000 persons diagnosed with cancer of the digestive system in Connecticut during 1935-82. Significant excesses of all second cancers combined were observed following cancer of the esophagus (58 observed vs. 33 expected), small intestine (41 vs. 24), and colon (2,268 vs. 1,714). A slight excess of multiple primaries was observed following cancer of the liver and biliary tract (47 vs. 40). The observed number of second cancers was nearly equal to the expected number for persons initially diagnosed with cancers of the stomach (251 vs. 258), rectum (952 vs. 941), and pancreas (40 vs. 40). Persons with initial cancers of the small intestine, colon, and rectum also had excess second cancers arising primarily in the colon, which suggested the influence of common etiologic factors or possibly misclassified metastases in some. Shared dietary, socioeconomic, or hormonal factors may explain the excess of uterine and ovarian cancers among patients with colon cancer and the excess of breast cancer among patients with colon and rectal cancers. Oral and respiratory cancers occurred more frequently than expected in persons with an initial esophageal cancer, which is likely due to common risk factors of cigarette smoking or alcohol intake, or both. The elevations in cancer of the prostate among males with cancers of the esophagus, small intestine, colon, rectum, liver/biliary, and pancreas are probably artifacts associated with increased medical surveillance of cancer patients. The prostate cancer excesses were limited to the first year after diagnosis of the initial cancer or decreased over time for all but cancer of the colon and small intestines. Increased medical surveillance may also contribute to the excess renal and bladder cancers seen within 5 years of diagnosis of stomach cancer. Excesses were also seen for second pancreatic cancer among small intestine and liver/biliary cancer patients and second kidney and brain cancers among those with colon cancer. The deficits of stomach and rectal cancer among persons initially diagnosed with the same tumors, respectively, were anticipated because surgical removal of the organ is the primary form of treatment. Patients with rectal cancer also had deficits of stomach and pancreatic cancers. Future research should clarify the role of diet, alcohol, metabolic and endocrine factors, and host susceptibility on the risk of second neoplasms following cancer of the digestive system.
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PMID:Second cancer following cancer of the digestive system in Connecticut, 1935-82. 408 13

Familial adenomatous polyposis has been associated with several extraintestinal cancers, but the relative and absolute risks of these malignancies have not been determined. Extraintestinal cancers reportedly associated with adenomatous polyposis (thyroid gland, adrenal gland, pancreas, and biliary tract) were identified in polyposis patients and their at risk relatives in The Johns Hopkins Registry. The incidence rates of identified tumours were then compared with the general population through person year analysis with adjustment for population. For comparison, the incidence rates of the two most common cancers not associated with polyposis (breast cancer in women and lung cancer) were also calculated. There was an increased relative risk of thyroid cancer (relative risk 7.6; 95% confidence limits (CL) 2.5-17.7) and pancreatic adenocarcinoma (relative risk 4.46; 95% CL 1.2-11.4) in polyposis patients and at risk relatives. The absolute risk was 26.8 and 21.4 cases/100,000 person years, respectively. No cases of adrenal or biliary cancer were found in this cohort. There was no increased relative risk of lung cancer (95% CL 0.04-1.4) or breast cancer (95% CL 0.04-1.4) over the general population. The relative risks of thyroid and pancreatic cancer are increased in familial adenomatous polyposis, but the absolute lifetime risk is low. Screening for pancreatic cancer may not be worthwhile with currently available methods, but careful physical examination of the thyroid gland is warranted along with consideration for ultrasonography.
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PMID:Increased risk of thyroid and pancreatic carcinoma in familial adenomatous polyposis. 824 8

C. Heidelberger et al left great gifts to us. Approximately 50 years have elapsed since their discovery of 5-FU in 1957 before eventually elucidating the mechanisms by which the drug exerts its pharmacological actions and provokes its adverse reactions. Namely, 5-FU is a typical antimetabolite with strong time dependency, and continuous venous infusion(CVI) is considered to be its optimal regimen. The following facts may be mentioned to explain why such a long period of time has been spent to reach this level of research: 1) 5-FU, when administered to the living individual, is mostly inactivated by hepatic catabolic enzymes without delay and is then excreted in the urine, thus making it difficult to precisely analyze the relationship of blood 5-FU concentrations with concentration persistence, anticancer activity, and adverse reactions; and 2) unlike other anticancer agents, an antimetabolite 5-FU separately generates metabolites which show anticancer activity and adverse reactions, as well as metabolites which show adverse reactions only. For the last 30 years, we paid attention especially to 5-FU among chemotherapeutic agents for cancer and have sought for a long-lasting therapeutic modality which maintains quality of life of the patient and patient compliance by considering the balancing between its effects and adverse reactions. Consequently, we concretized an innovative therapeutic drug, TS-1 (S-1). We have a long history of research before developing S-1, which is represented by a series of investigations consisting in the developments of Futrafur (FT)--an oral anticancer agent of a 5-FU derivative (prodrug)-in 1970 subsequent to the above discovery of 5-FU, of UFT(FT: Ura=1 : 4) in 1976, and of S-1 in 1999. To date, we took the initiative in the world to devise S-1, the first self-rescuing concept(SRC)-based anticancer agent with dual actions, i.e., enhancement of pharmacological actions of 5-FU and reduction of its adverse reactions, by making use of the biochemical and enzymological properties of 5-FU and by combining FT, which is gradually converted to 5-FU in the body, with a 5-FU's effect-enhancing substance and a 5-FU's adverse reaction-reducing substance. S-1 is an oral anticancer agent in capsule, in which the following 2 modulators for 5-FU are combined to FT: one is CDHP(5-chloro-2,4-dihydroxypyridine) which increases blood concentrations and enhances pharmacological actions of 5-FU by potently inhibiting the degradation of 5-FU; and another is Oxo(potassium oxonate) which is localized in the mucosa of the gastrointestinal (GI) tract after oral administration and reduces GI toxicities provoked by 5-FU. S-1 is an oral anticancer agent in which these 3 components, FT, CDHP, and Oxo, are combined at a molar ratio of 1 : 0.4 : 1. Our conception to develop an SRC-based therapeutic drug and the preclinical concepts validated by numerous basic studies were demonstrated also in the clinical trials. In January 1999, S-1 was approved for the treatment of advanced and recurrent gastric cancers through the priority review system. From 2001 to 2005, S-1 was approved for the treatment of head and neck cancer, colon cancer, non-small cell lung cancer, and breast cancer. S-1 has been applied to acquire its expanded indications for the treatment of pancreatic cancer and biliary tract cancer. We are confident that the combined regimen of S-1 with other anticancer agents and with other therapeutic modalities will contribute to the routine medical practice of cancer treatment in the future.
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PMID:[Timeline from discovery of 5-FU to development of an oral anticancer agent S-1 and its drug concept]. 1689 67

The large subunit of human ribonucleotide reductase, RRM1, is involved in the regulation of cell proliferation, cell migration, tumour and metastasis development, and the synthesis of deoxyribonucleotides for DNA synthesis. It is also a cellular target for the chemotherapeutic agent, gemcitabine. RRM1 has been studied in a large number of patients with different types of cancer, such as non-small-cell lung cancer, pancreatic cancer, breast cancer, and biliary tract cancer, to establish its prognostic or predictive value when patients were treated with gemcitabine, and mRNA expression and genetic variants as determined by genotyping have in some cases been associated with clinical outcome of patients with cancer. Here, we review preclinical and clinical studies of RRM1 assessment and discuss the further steps in the development of this clinically pertinent biomarker.
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PMID:The ribonucleotide reductase large subunit (RRM1) as a predictive factor in patients with cancer. 2116 2

Dichloromethane (methylene chloride) is a widely used chlorinated solvent. We review the available epidemiology studies (five cohort studies, 13 case-control studies, including seven of hematopoietic cancers), focusing on specific cancer sites. There was little indication of an increased risk of lung cancer in the cohort studies (standardized mortality ratios ranging from 0.46 to 1.21). These cohorts are relatively small, and variable effects (e.g., point estimates ranging from 0.5 to 2.0) were seen for the rarer forms of cancers such as brain cancer and specific hematopoietic cancers. Three large population-based case-control studies of incident non-Hodgkin lymphoma in Europe and the United States observed odds ratios between 1.5 and 2.2 with dichloromethane exposure (ever exposed or highest category of exposure), with higher risk seen in specific subsets of disease. More limited indications of associations with brain cancer, breast cancer, and liver and biliary cancer were also seen in this collection of studies. Existing cohort studies, given their size and uneven exposure information, are unlikely to resolve questions of cancer risks and dichloromethane exposure. More promising approaches are population-based case-control studies of incident disease, and the combination of data from such studies, with robust exposure assessments that include detailed occupational information and exposure assignment based on industry-wide surveys or direct exposure measurements.
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PMID:Insights from epidemiology into dichloromethane and cancer risk. 2190 13

MicroRNAs (miRNAs) are involved in the development of most cancers. However, few studies have been conducted to determine their relationship to biliary tract cancer (BTC). Farnesoid X receptor (FXR) has been reported to be a tumor suppressor for hepatocellular carcinoma and breast cancer; but few studies have focused on its correlation with BTC. In this study, we identified miR-421 as a potential regulator of FXR expression. We found that their expression amount was inversely correlated as FXR was aberrantly down-regulated in both primary tumor specimens and cell lines; while miR-421 was significantly up-regulated. Ectopic expression of miR-421 significantly decreased FXR protein concentration in BTC cells and promoted cell proliferation, colony formation and migration in vitro. Furthermore, a decrease in miR-421 expression induced G(0)/G(1) cell cycle arrest. In conclusion, our study identified microRNA-421 functions as an oncomiR in BTC by targeting FXR. This finding may provide a novel therapeutic strategy for treatment of biliary tract cancer.
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PMID:MicroRNA-421 functions as an oncogenic miRNA in biliary tract cancer through down-regulating farnesoid X receptor expression. 2214 19

Cyclin-dependent kinase 10 (CDK10) is a member of the Cdc2 family of kinases, and has been demonstrated to be an important determinant of resistance to endocrine therapy for breast cancer. To investigate the expression and possible function of CDK10 in biliary tract cancer (BTC), we systematically examined CDK10 in tissues and cell lines. We found that expression of CDK10 was downregulated in both biliary tract tumors and cell lines. Remarkably, the expression of CDK10 correlated with clinical characteristics. Overexpression or knockdown of CDK10, respectively, inhibited or promoted cell proliferation, colony formation and migration. This suggests that CDK10 functions as a tumor suppressor gene in BTC. Overexpression of CDK10 caused malignant cells to become sensitive to chemotherapy and other hostile environments, suggesting that CDK10 functions to regulate survivability of BTC cells. We investigated the expression of six genes to resolve the mechanism. c-RAF was negatively regulated by CDK10 in both cells and specimens. Our results indicate that CDK10 plays a crucial role in the growth and survivability of biliary tract cancer, and offers a potential therapeutic target for this fatal disease.
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PMID:CDK10 functions as a tumor suppressor gene and regulates survivability of biliary tract cancer cells. 2220 42


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