p53 is a cell cycle checkpoint control protein that assesses DNA damage and acts as a transcription factor regulating genes, which control cell growth, DNA repair, and apoptosis. p53 mutations have been found in a wide variety of different cancers including flow cytometric assessment of p53 protein expression using anti-p53 monoclonal antibodies. We studied p53 protein expression by flow cytometry (

It has been suggested that alterations of cell cycle genes probably contribute to the pathogenesis of endemic Burkitt's lymphoma (BL) in addition to c-MYC translocation. Mutations disrupting the normal nuclear localization signal of the retinoblastoma-related gene Rb2/ p130 have been documented in BL cell lines and primary tumors from endemic areas. The aim of this study was to investigate the involvement of Rb2/p130 gene in the pathogenesis of sporadic BL in Brazil. DNA samples from 26 pediatric BL tumors and two healthy blood donors were screened by PCR amplification followed by single strand conformation polymorphism analysis of exons 19 and 20 (B domain) and exons 21 and 22 (C-terminus), where most of the point mutations in the Rb2/p130 gene were identified. No abnormal band shifts were present in the samples analyzed. We concluded that mutations in exons 19-22 of the Rb2/p130 are unlikely to be involved directly in the pathogenesis of sporadic Brazilian BL.

Alterations involving the short arm of chromosome 17 (17p) during the progression of chronic myeloid leukemia (CML) have been described. This chromosomal region contains the tumor suppressor gene TP53 that may be an important factor in the evolution of this disease. In this study, we used flow cytometry and western blotting to assess p53 protein expression and single stranded conformational polymorphism to examine TP53 gene alterations in three patients with CML who showed alterations in 17p. Only the case with del(17)(p11) had p53 expression positive by flow cytometry and an abnormal migration pattern by SSCP analysis. The importance of the correlation between the results obtained with these techniques, as well as the clinical course of the patients, are discussed.

p53 protein induces cell cycle arrest, DNA repair, or apoptosis of damaged cells. Loss of wild-type p53 (wt-p53) function was shown to be associated with upregulation of survivin and resistance to therapy. Here we investigated the effects of DNA-damage agents in inducing apoptosis and cell cycle arrest, and modulation of survivin levels in two Burkitt's lymphoma (BL) cell lines with different p53 mutations. Our results showed that BL cell lines have variable response to DNA-damaging agents that cannot be correlated exclusively with p53 mutation or survivin expression suggesting that p53-independent transactivation may play a role in apoptosis induced by DNA-damaging agents.

IntroduçãoInicialmente descrito na África, o linfoma de Burkitt (LB) foi depois identificado em outras regiões.1 O tumor tem origem numa célula derivada do centro germinativo (CG) que perde a regulação da proliferação em virtude da ativação do proto-oncogene c-myc 2 e superexpressão da proteína C-MYC. A perda da regulação dessa proteína resulta na ativação e repressão de pelo menos nove genes regulados por ela, entre os quais ciclina D1, p27, o gene da enzima lactatodesidrogenase A, p19ARF, p53, Bax, Fas e Fas ligante entre outros. 3,4,5 A classificação mais recente da Organização Mundial da Saúde (OMS) para as neoplasias linfóides identifica duas variantes morfológicas do LB: o LB clássico e o LB atípico ou Burkitt-like, uma variante cujo infiltrado tumoral apresenta diferenciação plasmocitóide, ou características intermediári-as entre o linfoma difuso de grandes células e o LB. Esses tumores têm alta taxa de proliferação e expressam marcadores típicos de células do CG, como BCL-6 e CD10.6 Um padrão Revisão / Review