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  • 1
    ISSN: 1569-8041
    Keywords: AIDS ; bcl-6 ; genetic lesion ; lymphoma ; oncogene
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Background: Non-Hodgkin's lymphoma (NHL) represents a major complication of AIDS. Systemic AIDS-related NHLs (AIDS-NHLs) derive from B cells and are classified into four distinct groups, including small noncleaved-cell lymphoma (SNCCL), diffuse large-cell lymphoma (DLCL), anaplastic large-cell lymphoma (ALCL), and body-cavity-based lymphoma (BCBL). The molecular pathogenesis of AIDS-NHL is characterized by the association of specific genetic lesions with distinct AIDS-NHL categories. Genetic lesions of AIDS-NHL involve proto-oncogenes (c-myc, Ras), tumor suppressor loci (p53,6q), and viral infection (Epstein–Barr virus, human herpesvirus type8). Design: The aim of this work was to define the involvement of the bcl-6gene in AIDS-related lymphomagenesis by investigating the distribution ofbcl-6 structural alterations throughout the pathologic spectrum of AIDS-NHL. Both gross rearrangements and mutations in the 5′ non coding regions of the gene were investigated. Results: Gross rearrangements of bcl-6 are confined to a fraction of AIDS-DLCL cases among AIDS-NHLs. Conversely, mutations of the 5′noncoding regions of bcl-6 are detected in a large proportion of AIDS-SNCCLs, AIDS-DLCLs and AIDS-ALCLs independent of the concomitant presence of bcl-6 rearrangements. Conclusions: Mutations of the 5′ noncoding regions of bcl-6 represent the most frequent genetic lesion presently detectable among systemic AIDS-NHLs. The frequency of these mutations and their location in the proximity of bcl-6 regulatory regions suggest that they may play a rolein AIDS-related lymphomagenesis.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1569-8041
    Keywords: AIDS ; bcl-6 ; genetic lesion ; lymphoma ; oncogene
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Background: Non-Hodgkin's lymphoma (NHL) represents a major complicationof AIDS. Systemic AIDS-related NHLs (AIDS-NHLs) derive from B cells and areclassified into four distinct groups, including small noncleaved-celllymphoma (SNCCL), diffuse large-cell lymphoma (DLCL), anaplastic large-celllymphoma (ALCL), and body-cavity-based lymphoma (BCBL). The molecularpathogenesis of AIDS-NHL is characterized by the association of specificgenetic lesions with distinct AIDS-NHL categories. Genetic lesions ofAIDS-NHL involve proto-oncogenes (c-myc, Ras), tumor suppressor loci (p53,6q), and viral infection (Epstein–Barr virus, human herpesvirus type8). Design: The aim of this work was to define the involvement of the bcl-6gene in AIDS-related lymphomagenesis by investigating the distribution ofbcl-6 structural alterations throughout the pathologic spectrum of AIDS-NHL.Both gross rearrangements and mutations in the 5′ noncoding regions ofthe gene were investigated. Results: Gross rearrangements of bcl-6 are confined to a fraction ofAIDS-DLCL cases among AIDS-NHLs. Conversely, mutations of the 5′noncoding regions of bcl-6 are detected in a large proportion ofAIDS-SNCCLs, AIDS-DLCLs and AIDS-ALCLs independent of the concomitantpresence of bcl-6 rearrangements. Conclusions: Mutations of the 5′ noncoding regions of bcl-6 represent the most frequent genetic lesion presently detectable amongsystemic AIDS-NHLs. The frequency of these mutations and their location in theproximity of bcl-6 regulatory regions suggest that they may play a rolein AIDS-related lymphomagenesis.
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
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  • 3
    ISSN: 1573-0778
    Keywords: deletion 7q ; met oncogene ; myelofibrosis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine , Process Engineering, Biotechnology, Nutrition Technology
    Notes: Abstract The met oncogene is the normal counterpart of a chemically-induced transforming gene. The chromosomal localization of met is 7q21–31. In a patient with myelofibrosis and an interstitial deletion on 7q, we demonstrate that a Taq I polymorphism for the met oncogene is lost in the neoplastic cells, thus indicating that the deletion occuring in the long arm of chromosome 7 involves the met locus.
    Type of Medium: Electronic Resource
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