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  • 1
    ISSN: 1432-0584
    Keywords: Microsatellite instability ; Genomic instability ; Chronic lymphocytic leukemia ; Richter's syndrome ; Lymphoma
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Microsatellite instability (MSI) represents one specific pattern of genomic instability and is one of the genetic lesions most frequently detected in human neoplasia. Although MSI has been found to be associated with a wide variety of solid cancers, its involvement in lymphoid malignancies is virtually unexplored. In this study, we have investigated the presence of MSI in chronic lymphoproliferative disorders by comparing the pattern of nine microsatellite repeats (two tetranucleotides, two trinucleotides, and five dinucleotides) on autologous germline and tumor DNA of 23 patients, including 17 with B-cell chronic lymphocytic leukemia/small lymphocytic lymphoma (B-CLL/SLL), four with hairy cell leukemia, one with lymphoplasmacytoid lymphoma, and one with T-cell chronic lymphocytic leukemia. All samples at diagnosis displayed a germline pattern of the microsatellites examined, thus suggesting that MSI is not involved in the pathogenesis of these lymphoproliferations. Also, no microsatellite alterations were observed in consecutive samples of B-CLL/SLL obtained from the same patient at various stages of the disease both before and after chemotherapy. Conversely, alterations in 3/9 microsatellite repeats were detected in one case of Richter's syndrome which had evolved from a pre-existent B-CLL/SLL phase. Overall, the low frequency of MSI among chronic lymphoproliferative disorders adds further weight to the common view that the mechanisms and patterns of genomic instability in lymphoid neoplasia differ markedly from those commonly observed in solid cancers.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1432-0584
    Keywords: Key words Microsatellite instability ; Genomic instability ; Chronic lymphocytic leukemia ; Richter's syndrome ; Lymphoma
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  Microsatellite instability (MSI) represents one specific pattern of genomic instability and is one of the genetic lesions most frequently detected in human neoplasia. Although MSI has been found to be associated with a wide variety of solid cancers, its involvement in lymphoid malignancies is virtually unexplored. In this study, we have investigated the presence of MSI in chronic lymphoproliferative disorders by comparing the pattern of nine microsatellite repeats (two tetranucleotides, two trinucleotides, and five dinucleotides) on autologous germline and tumor DNA of 23 patients, including 17 with B-cell chronic lymphocytic leukemia/small lymphocytic lymphoma (B-CLL/SLL), four with hairy cell leukemia, one with lymphoplasmacytoid lymphoma, and one with T-cell chronic lymphocytic leukemia. All samples at diagnosis displayed a germline pattern of the microsatellites examined, thus suggesting that MSI is not involved in the pathogenesis of these lymphoproliferations. Also, no microsatellite alterations were observed in consecutive samples of B-CLL/SLL obtained from the same patient at various stages of the disease both before and after chemotherapy. Conversely, alterations in 3/9 microsatellite repeats were detected in one case of Richter's syndrome which had evolved from a pre-existent B-CLL/SLL phase. Overall, the low frequency of MSI among chronic lymphoproliferative disorders adds further weight to the common view that the mechanisms and patterns of genomic instability in lymphoid neoplasia differ markedly from those commonly observed in solid cancers.
    Type of Medium: Electronic Resource
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  • 3
    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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  • 4
    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
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  • 5
    ISSN: 1569-8041
    Keywords: B-DLCL ; clinical correlations ; genetic lesions ; outcome
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Background: B-diffuse large-cell lymphomas (DLCL) have been associated with some molecular lesions, but the role of such lesions as prognostic markers is still controversial. This report concerns an investigation of the frequency and clinical correlation of bcl-6, bcl-2, c-myc rearrangements and 6(q) deletions in B-DLCL. Patients and methods: The presence of these genetic lesions was analyzed in samples of lymph nodes or bone marrow collected at diagnosis in 71 patients with B-DLCL, all treated with an antracycline-containing chemotherapy regimen. Results: Rearrangement of bcl-6 was found in 11 patients (15%), rearranged bcl-2 in 12 (17%), 6(q) deletions in 10 patients (14%) and c-myc rearrangement in four (6%). Patients with rearranged bcl-6 tended to have a more aggressive disease than patients with germ-line bcl-6 (intermediate–high/high risk according to IPI criteria: 73% vs. 43%), but there were no differences in three-year survival rates (62% vs. 42%) between the two groups. The numbers of involved extranodal sites were similar in patients with rearranged and those with germ-line bcl-6. Patients with bcl-2 rearrangement appeared to have a less aggressive disease than those with germ-line bcl-2 (low/low–intermediate risk 75% vs. 47%) and a slightly better three-year survival rate (70% vs. 41%) but again the difference was not significant. Both groups with or without 6(q) deletion had similar clinical characteristics and outcomes. The four patients with c-myc rearrangement had aggressive disease and did poorly. Conclusions: The analysis of molecular lesions in B-DLCL may be useful for a better diagnostic definition; however, in this study we were unable to show that the evaluated genetic lesions had a significant impact on clinical outcome.
    Type of Medium: Electronic Resource
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