972 resultados para CARCINOGENESIS
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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
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Head and neck tumors are a major health concern worldwide, due to their high incidence and mortality rates, particularly in developing countries. In Brazil, this type of cancer is commonly diagnosed and studies suggested that it may be the leading cause of mortality in the country. The increase in life expectancy worldwide, as well as environmental and behavioral factors, are related to carcinogenesis. Therefore, an understanding of basic epidemiology and statistical methods is critical, in order to promote early diagnosis and cancer prevention. Cancer patients with an indication for prosthesis were selected from the medical records of the Oral Oncology Center, School of Dentistry, São Paulo State University (UNESP), Araçatuba, between 1991 and 2010. The following variables were recorded: gender, age, type and location of the lesion, radiation dose and dental prosthesis. The majority of the patients were male (74.15%) and >60 years of age (53.37%). Tumors were most commonly located in the floor of the mouth (11.1%) and squamous cell carcinoma was the most prevalent type (72.8%). This study provides the profiles of patients who attended the Oral Oncology Center and the results may aid in the creation of cancer prevention programs.
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Considering that downregulation of HLA expression could represent a potential mechanism for breast carcinogenesis and metastasis, the aim of the present study was to use immunohistochemical methods to analyze the expression of HLA-Ia, HLA-DR, HLA-DQ, HLA-E, and HLA-G in invasive ductal carcinoma (IDC) of the breast and to relate this HLA profile to anatomopathological parameters. Fifty-two IDC from breast biopsies were stratified according to histological differentiation (well, moderately, and poorly differentiated) and to the presence of metastases in axillary lymph nodes. The expression of HLA molecules was assessed by immunohistochemistry, using a computer-assisted system. Overall, 31 (59.6%) out of the 52 IDC breast biopsies exhibited high expression of HLA-G, but only 14 (26.9%) showed high expression of HLA-E. A large number (41, 78.8%) of the biopsies showed low expression of HLA-Ia, while 45 (86.5%) showed high expression of HLA-DQ and 36 (69.2%) underexpressed HLA-DR. Moreover, 24 (41.2%) of 52 biopsies had both low HLA-Ia expression and high HLA-G expression, while 11 (21.2%) had low HLA-Ia expression and high HLA-E expression. These results suggest that, by different mechanisms, the downregulation of HLA-Ia, HLA-E, and HLA-DR and the upregulation of HLA-G and HLA-DQ are associated with immune response evasion and breast cancer aggressiveness.
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Chronic and excessive alcohol consumption is an established risk for hepatic inflammation and carcinogenesis. Luteolin is one of the most common flavonoids present in plants and has potential beneficial effects against cancer. In this study, we examined the effect and potential mechanisms of luteolin supplementation in a carcinogen initiated alcohol-promoted pre-neoplastic liver lesion mouse model. C57BL/6 mice were injected with diethylnitrosamine (DEN) [i.p. 25 mg/kg of body weight (BW)] at 14 days of age. At 8 weeks of age mice were group pair-fed with Lieber-DeCarli liquid control diet or alcoholic diet [ethanol (EtOH) diet, 27% total energy from ethanol] and supplemented with a dose of 30 mg luteolin/kg BW per day for 21 days. DEN-injected mice fed EtOH diet displayed a significant induction of pre-neoplastic lesions, a marker associated with presence of steatosis and inflammation. Dietary luteolin significantly reduced the severity and incidence of hepatic inflammatory foci and steatosis in DEN-injected mice fed EtOH diet, as well the presence of preneoplastic lesions. There was no difference on hepatic protein levels of sirtuin 1 (SIRT1) among all groups; however, luteolin supplementation significantly reversed alcohol-reduced SIRT1 activity assessed by the ratio of acetylated and total forkhead box protein O1 (FoXO1) and SIRT1 target proliferator-activated receptor gamma, coactivator 1 alpha (PGC1α). Dietary intake of luteolin prevents alcohol promoted pre-neoplastic lesions, potentially mediated by SIRT1 signaling pathway.
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In the present study, it was evaluated the susceptibility of prostatic lesions in male adult rats exposed to Di-N-butyl-phthalate during fetal and lactational periods and submitted to MNU plus testosterone carcinogenesis protocol. Pregnant females were distributed into four experimental groups: CN (negative control); CMNU (MNU control); TDBP100 (100 mg/kg of DBP); TDBP500 (500 mg/kg of DBP). Females from the TDBP groups received DBP, by gavage, from gestation day 15 (GD15) to postnatal day 21 (DPN21), while C animals received the vehicle (corn oil). CMNU, TDBP100, and TDBP500 groups received a single intraperitoneal injection of MNU (50 mg/kg) on the sixth postnatal week. After that, testosterone cypionate was administered subcutaneously two times a week (2 mg/kg) for 24 weeks. The animals were euthanized on PND220. Distal segment fragments of the ventral (VP) and dorsolateral prostate (DLP) were fixed and processed for histopathological analysis. Protein extracts from ventral prostate were obtained, and western blotting was performed to AR, ERα, MAPK (ERK1/2), and pan-AKT. Stereological analysis showed an increase in the epithelial compartment in TDBP100 and TDBP500 compared to CN. In general, there was increase in the incidence of inflammation and metaplasia/dysplasia in the DBP-treated groups, mainly in DLP, compared to CN and CMNU. Proliferation index was significant higher in TDBP500 and PIN (prostatic intraepithelial neoplasia) was more frequent in this group compared to CMNU. Western blot assays showed an increase in the expressions of AR and MAPK (ERK1/2) in the TDBP100 compared to CN, and ERα and AKT expressions were higher in the TDBP500 group compared do CN. These results showed that different doses of DBP during prostate organogenesis in Wistar rats could increase the incidence of premalignant lesions in initiated rats inducing distinct biological responses in the adulthood. © 2015 Wiley Periodicals, Inc. Environ Toxicol, 2015.
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Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)
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Introduction: much studies regarding risk factors associated with oral cancer. Factors such as smoking and alcohol and solar radiation are well established, but others, such as bacterial influence in the development or progression of a tumor still remain unexplained. Interest in the possible relationship between bacteria and different stages of cancer development has increased since the classification of H. pylori by the WHO as a definite carcinogen. Subsequently, links between infection and the onset of cancer in various sites in the body were discovered. Review of literature: this literature review attempts to show the influence of poor oral hygiene, with consequent bacterial accumulation as a possible important risk factor for the initiation and development of mouth cancer, and correlate the possible mechanisms by which bacteria can initiate or promote carcinogenesis. Conclusion: there is much evidence that bacteria in the oral cavity and periodontopathic are present in tumor tissue, however, still can not affirm that these bacteria initiate or promote carcinogenesis.
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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
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Introduction: much studies regarding risk factors associated with oral cancer. Factors such as smoking and alcohol and solar radiation are well established, but others, such as bacterial influence in the development or progression of a tumor still remain unexplained. Interest in the possible relationship between bacteria and different stages of cancer development has increased since the classification of H. pylori by the WHO as a definite carcinogen. Subsequently, links between infection and the onset of cancer in various sites in the body were discovered. Review of literature: this literature review attempts to show the influence of poor oral hygiene, with consequent bacterial accumulation as a possible important risk factor for the initiation and development of mouth cancer, and correlate the possible mechanisms by which bacteria can initiate or promote carcinogenesis. Conclusion: there is much evidence that bacteria in the oral cavity and periodontopathic are present in tumor tissue, however, still can not affirm that these bacteria initiate or promote carcinogenesis.
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Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
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Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
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Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)
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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
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Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)