Involvement of BCL6 in chromosomal aberrations affecting band 3q27 in B-cell non-Hodgkin lymphoma Journal Article


Authors: Chaganti, S. R.; Chen, W.; Parsa, N.; Offit, K.; Louie, D. C.; Dalla-Favera, R.; Chaganti, R. S. K.
Article Title: Involvement of BCL6 in chromosomal aberrations affecting band 3q27 in B-cell non-Hodgkin lymphoma
Abstract: Chromosomal band 3q27 exhibits recurring and nonrecurring translocations and other rearrangements in approximately 8% of B-cell non-Hodgkin lymphomas (NHL) belonging to low-grade as well as diffuse aggressive histologies. The BCL6 gene, which encodes a zinc-finger transcription repressor protein and which maps to chromosomal band 3q27, is deregulated in t(3;14)(q27;q32) and other translocations by substitution of its transcription regulatory sequences by those of genes on the partner chromosomes. To delineate the cytogenetics and investigate the nature and consequence of BCL6 involvement in the spectrum of 3q27 aberrations seen in NHL, we analyzed a panel of 53 NHL tumors with 3q27 aberrations for BCL6 gene rearrangements and a subset of 32 of these for mutations. We identified four new recurring translocations involving 3q27, in addition to the previously recognized t(3;14)(q27;q32) and its variant, t(3;22)(q27;q11). Histologically, the 3q27 breaks were represented by 4% mantle cell lymphomas, 38% follicutar center cell lymphomas, and 58% diffuse large B-cell lymphomas. Approximately 50% of the tumors exhibited BCL6 rearrangements, whereas 87.5% showed mutations in the 5' noncoding region which contains the transcription regulatory sequences. These results demonstrate that a substantial proportion of cytogenetically detected 3q27 breaks in NHLs do not represent BCL6-associated translocations. They also suggest alternate breakpoints which may lead to BCL6 deregulation, or involvement of other genes in 3q27 translocations. The frequent BCL6 mutation in these tumors is consistent with our previous observation of hypermutation of the 5' noncoding region of the gene in lymphomas arising in the germinal-center B-cells.
Keywords: controlled study; human tissue; gene mutation; major clinical study; dna-binding proteins; proto-oncogene proteins; polymerase chain reaction; chromosomes, human, pair 9; chromosomes, human, pair 2; transcription factors; b cell lymphoma; gene expression regulation, neoplastic; lymphoma, b-cell; nonhodgkin lymphoma; reverse transcriptase polymerase chain reaction; lymphoma, non-hodgkin; dna, neoplasm; chromosome rearrangement; translocation, genetic; chromosome aberrations; chromosomes, human, pair 1; chromosome 14q; chromosome 3q; chromosome mapping; chromosomes, human, pair 3; chromosomes, human, pair 22; zinc fingers; chromosomes, human, pair 5; single strand conformation polymorphism; polymorphism, single-stranded conformational; chromosome banding; proto-oncogene proteins c-bcl-6; chromosomes, human, pair 14; humans; human; priority journal; article; chromosome translocation 3
Journal Title: Genes Chromosomes and Cancer
Volume: 23
Issue: 4
ISSN: 1045-2257
Publisher: Wiley Periodicals, Inc  
Date Published: 1998-12-01
Start Page: 323
End Page: 327
Language: English
DOI: 10.1002/(sici)1098-2264(199812)23:4<323::aid-gcc7>3.0.co;2-3
PUBMED: 9824205
PROVIDER: scopus
DOI/URL:
Notes: Article -- Export Date: 12 December 2016 -- Source: Scopus
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MSK Authors
  1. Kenneth Offit
    790 Offit
  2. Diane C Louie
    52 Louie
  3. Weiyi Chen
    20 Chen
  4. Raju S K Chaganti
    391 Chaganti
  5. Nasser Z. Parsa
    28 Parsa