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• W2009823089 abstract "GENERAL CONCEPTS EVER SINCE the initial observations made by Boveri, unquestionable evidence has been accumulated that human neoplasms derive from damage to the cell DNA [ 11. As in human turnout-s in general, genetic lesions of non-Hodgkin’s lymphomas (NHL) involve proto-oncogenes, tumour suppressor genes, and-to a lesser extent-viral infection of the neoplastic clone [2]. Structural lesions of proto-oncogenes convert them into activated pathological variants, the oncogenes, which constitutively promote cell growth. Conversely, bi-allelic inactivation of tumour suppressor genes, occurring most commonly through deletion of one allele and mutation of the other, deprives these genetic loci of their normal ability to suppress cell growth. At present, all known NHL genetic lesions, thought to be primary events in NHL pathogenesis, lead to proto-oncogene activation through chromosomal translocation [2]. In the most common instance, these translocations involve the protooncogene on one chromosome and an antigen receptor locus (namely, the immunoglobulin heavy or light chain loci in Bcell NHL and the T cell receptor loci in T-cell NHL) on the partner chromosome [2]. The functional consequence of this type of translocation lies in the deregulated expression of the proto-oncogene. More rarely, NHL chromosomal translocations may cause the fusion of the proto-oncogene with another gene, causing the formation of a fusion transcript which is translated into a fusion protein displaying novel biochemical properties compared to the wild-type proteins [2]. With one exception, all the proto-oncogenes involved in NHL code for transcription factors or anti-apoptotic genes. Among tumour suppressor genes, only the TP53 gene is currently known to be altered in NHL, although several other chromosomal loci are thought to harbour novel tumour suppressor loci relevant to NHL pathogenesis [2]. Finally, viral infection of NHL cellis is virtually restricted to the case of Epstein-Barr virus (EBV), human T-cell lymphotropic virus-1 (HTLV-I) and human herpes virus-8 (HHV-8)." @default.
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• W2009823089 date "1996-08-01" @default.
• W2009823089 modified "2023-09-23" @default.
• W2009823089 title "Diagnostic and prognostic implications of genetic lesions in non-Hodgkin's lymphoma" @default.
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• W2009823089 doi "https://doi.org/10.1016/0959-8049(96)00183-9" @default.
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