867 resultados para Malignant transformation


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Objective: The objective of this study was to compare the expression of proteins p53, MDM2, and SUMO-1 in oral lichen planus (OLP) lesions, epithelial dysplasia, and squamous cell carcinoma. Materials and Methods: The sample consisted of the following five groups of cheek mucosa lesions: normal mucosa (NM), inflammatory fibrous hyperplasia (IFH), lichen planus, epithelial dysplasia, and squamous cell carcinoma. The tissue samples were stained with hematoxylin-eosin and submitted to immunohistochemistry using anti-p53, anti-MDM2, and anti-SUMO-1 antibodies. Results: The results of this study demonstrated similar expression of p53 and MDM2 between OLP, oral epithelial dysplasia and, to a lesser extent, between OLP and oral squamous cell carcinoma (OSCC). However, for SUMO-1 a similar expression was observed in OLP, NM, and IFH. Conclusions: The results demonstrated overexpression of important proteins (p53 and MDM2) related to regulatory mechanisms of apoptosis in OLP, suggesting that there is a favorable environment for malignant transformation. The expression of SUMO-1 in OLP was similar to NM and IFH, suggesting that alterations of this protein occur at later stages of carcinogenesis, because important overexpression occurred in oral epithelial dysplasia and OSCC. © 2013 John Wiley & Sons A/S.

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Background: Sex steroid exposure during early human development may influence disease susceptibility. Digit ratio (2D:4D) is a putative marker for prenatal hormone exposure and sensitivity, as well as the action of genes closely related to carcinogenesis. Digit ratio could act as a possible marker for cancer predisposition. Aims: The aim of this study is to investigate the possible correlations between right hand, left hand and right minus left (R. - L) 2D:4D and gastric cancer (GCA) in men and women and assess the correlations with tumor staging and histological diagnosis. Methods: Digital images of the right and left hand palms of patients diagnosed with GCA (n = 57, 42 males, 15 females) and age and sex-matched controls (n = 59, 41 males, 18 females) were obtained. Means for 2D:4D were compared. Data were analyzed by repeated-measures one-way ANOVA and Student's t-test for finger measurements and group comparisons and Pearson's and Spearman's tests for correlations with tumor staging (α = 0.05). Results: GCA group presented significantly higher left 2D:4D, but significantly lower R. - L in comparison to healthy controls, particularly so for males. Digit ratio did not correlate to clinical staging or TNM staging. However, low R. - L was significantly related to adenocarcinomas. Conclusions: Early developmental conditions, including prenatal testosterone seem to play a role on the malignant transformation of gastric lesions. The 2D:4D pattern found for gastric cancer parallels that earlier described for breast cancer. The findings suggest that 2D:4D could add to the list of etiological factors and be a putative marker for the screening of patients' susceptibility to develop gastric cancer. © 2012 Elsevier Ltd.

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Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)

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Pós-graduação em Pesquisa e Desenvolvimento (Biotecnologia Médica) - FMB

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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)

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Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)

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Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)

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Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)

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Pós-graduação em Pesquisa e Desenvolvimento (Biotecnologia Médica) - FMB

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A significant proportion (up to 62) of oral squamous cell carcinomas (OSCCs) may arise from oral potential malignant lesions (OPMLs), such as leukoplakia. Patient outcomes may thus be improved through detection of lesions at a risk for malignant transformation, by identifying and categorizing genetic changes in sequential, progressive OPMLs. We conducted array comparative genomic hybridization analysis of 25 sequential, progressive OPMLs and same-site OSCCs from five patients. Recurrent DNA copy number gains were identified on 1p in 20/25 cases (80) with minimal, high-level amplification regions on 1p35 and 1p36. Other regions of gains were frequently observed: 11q13.4 (68), 9q34.13 (64), 21q22.3 (60), 6p21 and 6q25 (56) and 10q24, 19q13.2, 22q12, 5q31.2, 7p13, 10q24 and 14q22 (48). DNA losses were observed in 20 of samples and mainly detected on 5q31.2 (35), 16p13.2 (30), 9q33.1 and 9q33.29 (25) and 17q11.2, 3p26.2, 18q21.1, 4q34.1 and 8p23.2 (20). Such copy number alterations (CNAs) were mapped in all grades of dysplasia that progressed, and their corresponding OSCCs, in 70 of patients, indicating that these CNAs may be associated with disease progression. Amplified genes mapping within recurrent CNAs (KHDRBS1, PARP1, RAB1A, HBEGF, PAIP2, BTBD7) were selected for validation, by quantitative real-time PCR, in an independent set of 32 progressive leukoplakia, 32 OSSCs and 21 non-progressive leukoplakia samples. Amplification of BTBD7, KHDRBS1, PARP1 and RAB1A was exclusively detected in progressive leukoplakia and corresponding OSCC. BTBD7, KHDRBS1, PARP1 and RAB1A may be associated with OSCC progression. Proteinprotein interaction networks were created to identify possible pathways associated with OSCC progression.

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Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)

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The aim of this study was to relate the clinical case of a patient with oral lichen planus (OLP) and a history of epidermoid carcinoma associated with metallic restorations. The etiology of OLP is a mucocutaneous disease, which is poorly understood. Studies point to the potential of malignant transformation of OLP and its association with metallic restorations. The metallic restorations were replaced by crowns with a ceramic covering associated and osseointegrated implants in the edentulous areas. About 1 year later, it was observed a bilateral regression of the tongue lesions. The replacement of metallic restorations can contribute to improvement of OLP.

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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)