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Blood, Vol. 95 No. 2 (January 15), 2000:
pp. 651-659
Distribution and pattern of BCL-6 mutations throughout
the spectrum of B-cell neoplasia
Daniela Capello,
Umberto Vitolo,
Laura Pasqualucci,
Silvia Quattrone,
Giuseppe Migliaretti,
Lucia Fassone,
Cristiano Ariatti,
Daniela Vivenza,
Annunziata Gloghini,
Cristina Pastore,
Carlo Lanza,
Josep Nomdedeu,
Barbara Botto,
Roberto Freilone,
Daniela Buonaiuto,
Vittorina Zagonel,
Eugenio Gallo,
Giorgio Palestro,
Giuseppe Saglio,
Riccardo Dalla-Favera,
Antonino Carbone, and
Gianluca Gaidano
From the Divisions of Internal Medicine and Epidemiology, Department
of Medical Sciences, Amedeo Avogadro University of Eastern Piedmont,
Novara, Italy; Division of Hematology, A. O. San Giovanni Battista
della Citta' di Torino, Torino, Italy; Division of Oncology,
Department of Pathology, College of Physicians & Surgeons, Columbia
University, New York, NY; Center for Oncologic Prevention, CPO
Piedmont, Torino; Divisions of Pathology and of Medical Oncology B,
Centro di Riferimento Oncologico, Istituto Nazionale Tumori, Aviano,
Italy; Departments of Pediatric Sciences and Adolescence and of
Biomedical Sciences and Human Oncology, University of Torino, Torino,
Italy; Department of Hematology, Hospital de la Santa Creu i Sant Pau,
Barcelona, Spain; Division of Internal Medicine and Hematology,
Department of Clinical and Biological Sciences, University of Torino,
Orbassano, Italy.
BCL-6 mutations are accumulated during B-cell transit
through the germinal center (GC) and provide a histogenetic marker for B-cell tumors. On the basis of a comprehensive analysis of 308 B-cell
neoplasms, we (1) expand the spectrum of tumors associated with
BCL-6 mutations; (2) corroborate the notion that mutations cluster with GC and post-GC B-cell neoplasms; and (3) identify heterogeneous mutation frequency among B-lineage diffuse
large cell lymphoma (B-DLCL) subsets. Mutations are virtually
absent in acute lymphoblastic leukemia (P < .001) and
mantle cell lymphoma (P < .05), whereas they occur
frequently in GC or post-GC neoplasms, including lymphoplasmacytoid
lymphoma, follicular lymphoma, MALT lymphomas, B-DLCL and Burkitt
lymphoma. Among B-DLCL, mutations occur frequently in systemic nodal
B-DLCL, primary extranodal B-DLCL, CD5+ B-DLCL,
CD30+ B-DLCL, and primary splenic B-DLCL,
suggesting a similar histogenesis of these B-DLCL subsets. Conversely,
mutations are rare in primary mediastinal B-DLCL with
sclerosis (10.0%; P < .01), supporting a distinct
histogenesis for this lymphoma. Longitudinal follow-up of
B-DLCL transformed from follicular lymphoma shows that they BCL-6 mutations may accumulate during histologic progression. Mutations also occur in some B-cell chronic lymphocytic leukemias, small lymphocytic lymphomas, and hairy cell leukemias, consistent with
the hypothesis that a fraction of these lymphoproliferations are
related to GC-like cells. Finally, the molecular pattern of 193 mutational events reinforces the hypothesis that mutations of
BCL-6 and immunoglobulin genes are caused by similar mechanisms.
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