Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:Q86TM3 (cage)
 29,987 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Finding at least 2-3 ppm and occasionally as much as 10-20 ppm of vinyl chloride monomer in a wide range of foodstuffs has prompted concern for a possible human health hazard. The recognition of vinyl chloride as a carcinogen to humans in April 1974, following the discovery of angiosarcoma as the cause of death in at least 25 workers who had been engaged in the manufacture of polyvinyl chloride, enhanced this concern with respect to the presence of vinyl chloride monomer in foods. To assess the hazard presented by the oral ingestion of vinyl chloride monomer, rats that had been surgically prepared with an indwelling jugular cannula were dosed by intragastric intubation with aqueous solutions containing up to 2.0 mg/ml vinyl chloride. Time-concentration curves were obtained from sequential samples of blood. The uptake of vinyl chloride by this route was found to be extremely rapid; peak concentrations were achieved less than 10 min after administration of the dose. Elimination from the blood compartment appeared to be biexponential. Studies with the same animal model in a single restraint cage that allowed a "head only" exposure to concentrations of vinyl chloride up to 7,000 ppm in the gas phase have shown a similar rapid uptake followed by a plateau blood concentration during several hours of exposure. On removal from the vinyl chloride atmosphere, blood levels fell rapidly to barely detectable concentrations after 2 hr. The precise kinetic coefficients that describe the distribution and elimination rates of vinyl chloride from the blood compartment were also determined from the blood concentration data after the administration of an intravenous dose of aqueous or vegetable oil solution.
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PMID:Pharmacodynamics and uptake of vinyl chloride monomer administered by various routes to rats. 124 84

Blood transfusions are a lifesaving but transient therapy used to correct deficiencies of blood cells and coagulation factors that occur in cancer patients. Anemia can occur in cancer patients as a result of hemolysis, blood loss, or bone marrow failure. The blood component most commonly recommended for the treatment of anemia is packed red blood cells. Coagulation disorders are common with hemangiosarcoma and diffuse hepatic tumors. Fresh frozen plasma is used as a source for replacement coagulation factors for the treatment of disseminated intravascular coagulation or other cancer-associated coagulopathies. Although thrombocytopenia and neutropenia can be the result of bone-marrow failure from tumor infiltration, chemotherapy, or radiation therapy, these platelets and neutrophils are rarely transfused to veterinary cancer patients. Pretransufsion testing consists of blood typing in cats, and cross matching in dogs and cats if the dog has previously been transfused. Cancer patients receiving transfusions should be monitored on a continual basis during and immediately following the transfusion to enable early identification of an adverse event, allowing the transfusion to be discontinued.
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PMID:Transfusion issues in the cancer patient. 1283 Oct 78

Pleural angiosarcoma is an extremely rare disease. Although the clinical course could be indolent, the prognosis is very poor once the tumour spreads. Herein, a 69-year old male with a history of thyroid goitre was noted for 5 years before the symptoms of right chest pain and body weight loss developed. His serial chest roenterogram revealed loculated pleural effusion which rapidly progressed to be multiple pleural haematomas. After several sono-guided aspiration/biopsies with undiagnosed pleural haematomas, an exploratory thoracotomy confirmed the diagnosis of pleural angiosarcoma. Whole body image studies did not find other suspicious primary sites except for a thyroid tumour with eccentric calcification extending into the thoracic cage. Aspiration cytology of the thyroid tumour was shown to be morphologically consistent with angiosarcoma. This case reminds clinicians that pleural metastatic angiosarcomas presenting as haematomas have a high risk of massive and refractory haemothorax.
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PMID:Pleural angiosarcoma mimicking pleural haematoma. 2383 36

Canine hemangiosarcoma is a highly aggressive vascular neoplasm associated with extensive clinical and anatomical heterogeneity and a grave prognosis. Comprehensive molecular characterization of hemangiosarcoma may identify novel therapeutic targets and advanced clinical management strategies, but there are no published reports of tumor-associated genome instability and disrupted gene dosage in this cancer. We performed genome-wide microarray-based somatic DNA copy number profiling of 75 primary intra-abdominal hemangiosarcomas from five popular dog breeds that are highly predisposed to this disease. The cohort exhibited limited global genomic instability, compared to other canine sarcomas studied to date, and DNA copy number aberrations (CNAs) were predominantly of low amplitude. Recurrent imbalances of several key cancer-associated genes were evident; however, the global penetrance of any single CNA was low and no distinct hallmark aberrations were evident. Copy number gains of dog chromosomes 13, 24, and 31, and loss of chromosome 16, were the most recurrent CNAs involving large chromosome regions, but their relative distribution within and between cases suggests they most likely represent passenger aberrations. CNAs involving CDKN2A, VEGFA, and the SKI oncogene were identified as potential driver aberrations of hemangiosarcoma development, highlighting potential targets for therapeutic modulation. CNA profiles were broadly conserved between the five breeds, although subregional variation was evident, including a near twofold lower incidence of VEGFA gain in Golden Retrievers versus other breeds (22 versus 40 %). These observations support prior transcriptional studies suggesting that the clinical heterogeneity of this cancer may reflect the existence of multiple, molecularly distinct subtypes of canine hemangiosarcoma.
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PMID:Genomic profiling reveals extensive heterogeneity in somatic DNA copy number aberrations of canine hemangiosarcoma. 2459 18

MicroRNAs (miRNAs) are emerging as critical regulators for the development and progression of various cancers, including angiosarcoma. Accumulating evidence suggests that miRNA-340 (miR-340) is an important cancer-associated miRNA. However, little is known about the role of miR-340 in angiosarcoma. In this study, we aimed to investigate the potential biological functions of miR-340 and its potential target gene in angiosarcoma. Our results showed that miR-340 expression was significantly decreased in angiosarcoma compared with normal controls. The overexpression of miR-340 inhibited the growth and invasion of angiosarcoma cells, while the inhibition of miR-340 showed the opposite effect. Bioinformatics analysis predicted that Sirtuin 7 (SIRT7) was a potential target gene of miR-340. The binding relationship between miR-340 and the SIRT7 3'-untranslated region was verified by dual-luciferase reporter assay. Moreover, our results showed that miR-340 negatively regulated SIRT7 expression in angiosarcoma cells and an inverse correlation between miR-340 and SIRT7 expression was shown in clinical angiosarcoma tissues. We found that silencing SIRT7 significantly inhibited the proliferation and invasion of angiosarcoma cells. Notably, the overexpression of SIRT7 promoted the proliferation and invasion of angiosarcoma cells and also partially reversed the antitumor effect of miR-340 on angiosarcoma cell proliferation and invasion. Taken together, our results demonstrate that miR-340 inhibits the growth and invasion of angiosarcoma cells by targeting SIRT7. Our study provides evidence that the miR-340/SIRT7 axis may play an important role in the molecular pathogenesis of angiosarcoma and suggests that miR-340 and SIRT7 may be used as potential and novel therapeutic targets for the treatment of angiosarcoma.
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PMID:MicroRNA-340 inhibits the growth and invasion of angiosarcoma cells by targeting SIRT7. 2971 Jun 64