PMID- 16519699 OWN - NLM STAT- MEDLINE DCOM- 20060505 LR - 20161124 IS - 0902-4441 (Print) IS - 0902-4441 (Linking) VI - 76 IP - 4 DP - 2006 Apr TI - New chromosome abnormalities and lack of BCL-6 gene rearrangements in Argentinean diffuse large B-cell lymphomas. PG - 284-93 AB - OBJECTIVES: Diffuse large B-cell lymphoma (DLBCL) is the most common form of non-Hodgkin lymphomas. Cytogenetic studies have revealed a broad spectrum of clonal genetic abnormalities and complex karyotypes. The purpose of this study was to contribute to the understanding of the genomic alterations associated with this group of lymphomas. METHODS: Cytogenetic, fluorescence in situ hybridization (FISH) and molecular analyses were performed in 30 cases with DLBCL: 20 de novo DLBCL (dn-DLBCL) and 10 DLBCL secondary to follicular lymphoma (S-DLBCL). RESULTS: A total of 37 different structural chromosomal rearrangements were found: 27% translocations, 54% deletions, and 19% other alterations. Chromosomes 8, 6, 2, and 9 were the most commonly affected. Interestingly, translocation t(3;14)(q27;q32) and/or BCL-6 gene rearrangements were not observed either by cytogenetic studies or by FISH analysis. Fifteen novel cytogenetic alterations were detected, among them translocations t(2;21)(p11;q22) and t(8;18)(q24;p11.3) appeared as sole structural abnormalities. Translocation t(14;18)(q32;q21) and/or BCL-2-IGH gene rearrangements were the genomic alterations most frequently observed: 50% of S-DLBCL and 30% of dn-DLBCL. Deletions del(4)(q21), del(6)(q27), del(8)(q11), and del(9)(q11) were recurrent. The most common gains involved chromosome regions at 12q13-q24, 7q10-q32, and 17q22-qter; 6q was the most frequently deleted region, followed by losses at 2q35-qter, 7q32-qter, and 9q13-qter. Four novel regions of loss were identified: 5q13-q21, 2q35-qter (both recurrent in our series), 4p11-p12, and 17q11-q12. CONCLUSIONS: These studies emphasize the value of combining conventional cytogenetics with FISH and molecular studies to allow a more accurate definition of the genomic aberrations involved in DLBCL. FAU - Cerretini, Roxana AU - Cerretini R AD - Departamento de Genetica, Instituto de Investigaciones Hematologicas Mariano R. Castex, Academia Nacional de Medicina, Buenos Aires, Argentina. rcerretini@argentina.com FAU - Noriega, Maria F AU - Noriega MF FAU - Narbaitz, Marina AU - Narbaitz M FAU - Slavutsky, Irma AU - Slavutsky I LA - eng PT - Journal Article PT - Research Support, Non-U.S. Gov't PL - England TA - Eur J Haematol JT - European journal of haematology JID - 8703985 RN - 0 (BCL6 protein, human) RN - 0 (DNA-Binding Proteins) RN - 0 (Proto-Oncogene Proteins c-bcl-6) SB - IM MH - Adolescent MH - Adult MH - Aged MH - Argentina MH - Chromosomes, Human/*genetics MH - DNA-Binding Proteins/genetics MH - Female MH - Humans MH - In Situ Hybridization, Fluorescence/methods MH - Karyotyping MH - Lymphoma, B-Cell/*genetics/pathology MH - Lymphoma, Follicular/*genetics/pathology MH - Lymphoma, Large B-Cell, Diffuse/*genetics/pathology MH - Male MH - Middle Aged MH - Neoplasms, Second Primary/*genetics/pathology MH - Proto-Oncogene Proteins c-bcl-6 MH - Sequence Deletion/genetics MH - Translocation, Genetic/*genetics EDAT- 2006/03/08 09:00 MHDA- 2006/05/06 09:00 CRDT- 2006/03/08 09:00 PHST- 2006/03/08 09:00 [pubmed] PHST- 2006/05/06 09:00 [medline] PHST- 2006/03/08 09:00 [entrez] AID - EJH616 [pii] AID - 10.1111/j.1600-0609.2005.00616.x [doi] PST - ppublish SO - Eur J Haematol. 2006 Apr;76(4):284-93. doi: 10.1111/j.1600-0609.2005.00616.x.