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  • Chronic lymphocytic leukemia  (2)
  • oncogene  (2)
  • Blastic transformation  (1)
  • 1
    Electronic Resource
    Electronic Resource
    Analysis of microsatellite instability in chronic lymphoproliferative disorders (1996)
    Springer
    Annals of hematology 72 (1996), S. 67-71 
    Details
    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
    URL: http://dx.doi.org/10.1007/BF00641310
    Library Location Call Number Volume/Issue/Year Availability
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    Paper (German National Licenses)
    Fulltext
  • 2
    Electronic Resource
    Electronic Resource
    Genetic analysis of p53 and RB1 tumor-suppressor genes in blast crisis of chronic myeloid leukemia (1994)
    Springer
    Annals of hematology 68 (1994), S. 3-7 
    Details
    ISSN: 1432-0584
    Keywords: Chronic myeloid leukemia ; Tumor suppressor genes ; Blastic transformation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary We have investigated the involvement of the p53 and RB1 tumor-suppressor genes in 26 cases of chronic myeloid leukemia (CML) blast crisis, including 17 myeloid, eight lymphoid, and one megakaryoblastic crisis. The presence of p53 mutations in exons 5 through 9 was tested by the PCR-single-strand conformation polymorphism (SSCP) assay, followed by PCR-direct sequencing; in addition, loss of heterozygosity (LOH) at 17p13, the site of the p53 gene, was assayed by Southern blot. Given the variability of the mechanisms of inactivation of the RB1 gene in human tumors, a combination of Southern blot and mutational analysis by PCR-SSCP was used. p53 mutations were restricted to one case of myeloid blast crisis, showing a CGC→TGC (Arg→Cys) mutation at codon 283; two additional cases displayed LOH at 17p13 in the absence of p53 mutations. No molecular lesions of the RB1 gene were detected in any of the cases analyzed. These data indicate that inactivation of p53 and RB1 is a rare event in the molecular pathogenesis of CML acute transformation.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01695912
    Library Location Call Number Volume/Issue/Year Availability
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    Paper (German National Licenses)
    Fulltext
  • 3
    Electronic Resource
    Electronic Resource
    Analysis of microsatellite instability in chronic lymphoproliferative disorders (1996)
    Springer
    Annals of hematology 72 (1996), S. 67-71 
    Details
    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
    URL: http://dx.doi.org/10.1007/BF00641310
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 4
    Electronic Resource
    Electronic Resource
    Involvement of the bcl-6 gene in AIDS-related lymphomas (1997)
    Springer
    Annals of oncology 8 (1997), S. 105-108 
    Details
    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
    URL: http://dx.doi.org/10.1023/A:1008254921497
    Library Location Call Number Volume/Issue/Year Availability
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    Paper (German National Licenses)
    Fulltext
  • 5
    Electronic Resource
    Electronic Resource
    Involvement of the bcl-6 gene in AIDS-related lymphomas (1997)
    Springer
    Annals of oncology 8 (1997), S. 105-108 
    Details
    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
    URL: http://dx.doi.org/10.1023/A:1008254921497
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
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