Proliferação celular nos linfomas caninos / Cell proliferation in canine lymphoma

O estudo dos linfomas caninos além de abordar a classificação morfológica e imunofenotípica necessita ser ampliado para que se tenha a avaliação da cinética celular. Esta verificação só pode ser feita com segurança quando são avaliados os parâmetros que indicam a taxa de proliferação celular. No homem, estes fatores têm influência no prognóstico e no tratamento dos limfomas. Os 40 linfomas utilizados neste trabalho foram classificados de acordo com a classificação de Kiel e a imunofenotipagem utilizou CD3 (linfócitos T) e CD79a (linfócitos B). A proliferação celular foi avaliada pelos métodos de contagem dos AgNORs e Ki-67 (MIB-1) De acordo com a classificação de Kiel os linfomas de alto grau foram os mais freqüentes, a imunofenotipagem mostrou a mesma freqüência de linfomas T e B. Quando avaliada a proliferação celular houve diferença significativa entre os linfomas de alto e baixo grau tanto pelo método do AgNOR como do KI-67.(MIB-1), porém não foram estatisticamente entre os imunofenótipos Entre as neoplasias de alto grau de malignidade a média de número de NORs por núcleo de célula neoplásica foi de 1,37 ± 0,32, e nos casos de baixo grau de 0,98 ± 0,36, de acordo com o KI-67 a média do percentual de células positivas foi de 43,19% ± 19,01, e 14,09% ± 11,74 nos casos de alto e baixo grau, respectivamente.

Lymphoma studies deals with morphological classification and immunophenotypic features and they have to be amplified for cellular kinetics evaluation. This evaluation can only be safely made, when the proliferative index are evaluated. In men the proliferation index have, most of the time, important influence in the neoplasia prognosis and treatment In this work it was used 40 canine lymphomas that were classified according to Kiel methods and immunophenotype was achieved with CD3 (T lymphocyte) and CD79a (B lymphocyte). Cellular proliferation was evaluated by AgNORs and Ki-67 (MIB-1) According to Kiel classification system, high grade lymphomas were more frequent and T and B lymphoma showed the same frequency.When cellular proliferation was evaluated, there was a significant difference between high grade and low grade lymphomas by AgNOR and Ki-67 (MIB-1) methods, but did not differ when comparing immunophenotype. Among high grade malignancy lymphomas the NORs medium number per cell nucleoli was 1.37± 0.32 and in low grade was 0.98± 0.36, concerning Ki-67 the positive cellular percentual was 43.19% ± 19.01, e 14.09% ± 11.74 in high and low grade, respectively

No mutations found in exons of TP53, H-RAS and K-RAS genes in liver of male Wistar rats submitted to a medium-term chemical carcinogenesis assay

The standart protocol to evaluate the carcionogenic potencial of chemicals is the long-term bioassay in rodents, not performed in developing countries due to its high cost and complex operational procedures. Our laboratory has established an alternative an alternative medium-term bioassay in Wistar rats, also DMBDD assay, based on the paradigm iniation/promotion of chemical carcinogenesis. This method was accepted by the Brazilian Environment Agency (IBAMA) as an official source of evidence of carcinogenity. The aim of this study was to evaluate alterations in exons 5 to 8 of the tumor suppressor gene TP53 and exons 1 and 2 of oncogenes K-RAS and H-RAS in preneoplastic hepatic lesions observed in DMBDD assay. The characterization of these alterations may contribute to the recognition of patterns of damage in critical genes, as well as to suggest mechanisms of action of the compounds tested in the protocol. Sixty male wistar rats were separeted into3 groups? the first was treated with no chemicals; the second received five initiaing agents and the third received initiation followed by phenobarbital. Liver DNA samples (obtained from formalin-fixed and parafin-fixed and paraffin-embedded tissues after histological analysis) were evaluated by the non-isotopic PCR-SSCP technique. No changes in any analyzed exons were detected by the PCR-SSCP banding pattern in all experimental groups. This suggests that liver in exons 5 to 8 of TP53 and exons 1 and 2 of H-RAS are not among the early molecular alterations occuring in the hepatic carcinogenesis process by the DMBDD protocol in male Wistar rats