BCL-6 and the molecular pathogenesis of B-cell lymphoma

R. Dalla-Favera, B. Hilda Ye, F. Lo Coco, C. C. Chang, K. Cechova, J. Zhang, A. Migliazza, W. Mellado, H. Niu, S. Chaganti, W. Chen, P. H. Rao, N. Z. Parsa, D. C. Louie, K. Offit, R. S K Chaganti

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Abstract

The results presented identify the first genetic lesion associated with DLCL, the most clinically relevant form of NHL. Although no proof yet exists of a role for these lesions in DLCL pathogenesis, the feature of the BCL-6 gene product, its specific pattern of expression in B cells, and the clustering of lesions disrupting its regulatory domain strongly suggest that deregulation of BCL-6 expression may contribute to DLCL development. A more precise definition of the role of BCL-6 in normal and neoplastic B-cell development is the goal of ongoing study of transgenic mice engineered either to express BCL-6 under heterologous promoters or lacking BCL-6 function due to targeted deletions. In addition to contributing to the understanding of DLCL pathogenesis, the identification of BCL-6 lesions may have relevant clinical implications. DLCL represent a heterogeneous group of neoplasms which are treated homogeneously despite the fact that only 50% of patients experience long-term disease-free survival (Schneider et al. 1990). The fact that BCL-6 rearrangements identify biologically and clinically distinct subsets of DLCL suggests that these lesions may be useful as markers in selection of differential therapeutic strategies based on different risk groups. Furthermore, the BCL-6 rearrangements can be used to identify and monitor the malignant clone with sensitive PCR-based techniques. Since clinical remission has been observed in a significant fraction of DLCL cases, these markers may serve as critical tools for sensitive monitoring of minimal residual disease and early diagnosis of relapse (Gribben et al. 1993).

Original languageEnglish (US)
Pages (from-to)117-123
Number of pages7
JournalCold Spring Harbor Symposia on Quantitative Biology
Volume59
StatePublished - 1994
Externally publishedYes

Fingerprint

B-Cell Lymphoma
lymphoma
B-lymphocytes
B-Lymphocytes
pathogenesis
Cells
Deregulation
risk groups
monitoring
early diagnosis
relapse
Residual Neoplasm
remission
disease diagnosis
Transgenic Mice
Disease-Free Survival
Cluster Analysis
Early Diagnosis
Clone Cells
Genes

ASJC Scopus subject areas

  • Agricultural and Biological Sciences(all)
  • Biochemistry, Genetics and Molecular Biology(all)
  • Biochemistry
  • Molecular Biology

Cite this

Dalla-Favera, R., Ye, B. H., Lo Coco, F., Chang, C. C., Cechova, K., Zhang, J., ... Chaganti, R. S. K. (1994). BCL-6 and the molecular pathogenesis of B-cell lymphoma. Cold Spring Harbor Symposia on Quantitative Biology, 59, 117-123.

BCL-6 and the molecular pathogenesis of B-cell lymphoma. / Dalla-Favera, R.; Ye, B. Hilda; Lo Coco, F.; Chang, C. C.; Cechova, K.; Zhang, J.; Migliazza, A.; Mellado, W.; Niu, H.; Chaganti, S.; Chen, W.; Rao, P. H.; Parsa, N. Z.; Louie, D. C.; Offit, K.; Chaganti, R. S K.

In: Cold Spring Harbor Symposia on Quantitative Biology, Vol. 59, 1994, p. 117-123.

Research output: Contribution to journalArticle

Dalla-Favera, R, Ye, BH, Lo Coco, F, Chang, CC, Cechova, K, Zhang, J, Migliazza, A, Mellado, W, Niu, H, Chaganti, S, Chen, W, Rao, PH, Parsa, NZ, Louie, DC, Offit, K & Chaganti, RSK 1994, 'BCL-6 and the molecular pathogenesis of B-cell lymphoma', Cold Spring Harbor Symposia on Quantitative Biology, vol. 59, pp. 117-123.
Dalla-Favera R, Ye BH, Lo Coco F, Chang CC, Cechova K, Zhang J et al. BCL-6 and the molecular pathogenesis of B-cell lymphoma. Cold Spring Harbor Symposia on Quantitative Biology. 1994;59:117-123.
Dalla-Favera, R. ; Ye, B. Hilda ; Lo Coco, F. ; Chang, C. C. ; Cechova, K. ; Zhang, J. ; Migliazza, A. ; Mellado, W. ; Niu, H. ; Chaganti, S. ; Chen, W. ; Rao, P. H. ; Parsa, N. Z. ; Louie, D. C. ; Offit, K. ; Chaganti, R. S K. / BCL-6 and the molecular pathogenesis of B-cell lymphoma. In: Cold Spring Harbor Symposia on Quantitative Biology. 1994 ; Vol. 59. pp. 117-123.
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abstract = "The results presented identify the first genetic lesion associated with DLCL, the most clinically relevant form of NHL. Although no proof yet exists of a role for these lesions in DLCL pathogenesis, the feature of the BCL-6 gene product, its specific pattern of expression in B cells, and the clustering of lesions disrupting its regulatory domain strongly suggest that deregulation of BCL-6 expression may contribute to DLCL development. A more precise definition of the role of BCL-6 in normal and neoplastic B-cell development is the goal of ongoing study of transgenic mice engineered either to express BCL-6 under heterologous promoters or lacking BCL-6 function due to targeted deletions. In addition to contributing to the understanding of DLCL pathogenesis, the identification of BCL-6 lesions may have relevant clinical implications. DLCL represent a heterogeneous group of neoplasms which are treated homogeneously despite the fact that only 50{\%} of patients experience long-term disease-free survival (Schneider et al. 1990). The fact that BCL-6 rearrangements identify biologically and clinically distinct subsets of DLCL suggests that these lesions may be useful as markers in selection of differential therapeutic strategies based on different risk groups. Furthermore, the BCL-6 rearrangements can be used to identify and monitor the malignant clone with sensitive PCR-based techniques. Since clinical remission has been observed in a significant fraction of DLCL cases, these markers may serve as critical tools for sensitive monitoring of minimal residual disease and early diagnosis of relapse (Gribben et al. 1993).",
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AU - Zhang, J.

AU - Migliazza, A.

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AU - Chen, W.

AU - Rao, P. H.

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AU - Louie, D. C.

AU - Offit, K.

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