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BCL2 mutations in diffuse large B-cell lymphoma.

Abstract：

:BCL2 is deregulated in diffuse large B-cell lymphoma (DLBCL) by the t(14;18) translocation, gene amplification and/or nuclear factor-κB signaling. RNA-seq data have recently shown that BCL2 is the most highly mutated gene in germinal center B-cell (GCB) DLBCL. We have sequenced BCL2 in 298 primary DLBCL biopsies, 131 additional non-Hodgkin lymphoma biopsies, 24 DLBCL cell lines and 51 germline DNAs. We found frequent BCL2 mutations in follicular lymphoma (FL) and GCB DLBCL, but low levels of BCL2 mutations in activated B-cell DLBCL, mantle cell lymphoma, small lymphocytic leukemia and peripheral T-cell lymphoma. We found no BCL2 mutations in GC centroblasts. Many mutations were non-synonymous; they were preferentially located in the flexible loop domain, with few in BCL2-homology domains. An elevated transition/transversions ratio supports that the mutations result from somatic hypermutation. BCL2 translocations correlate with, and are likely important in acquisition of, additional BCL2 mutations in GCB DLBCL and FL. DLBCL mutations were not independently associated with survival. Although previous studies of BCL2 mutations in FL have reported mutations to result in pseudo-negative BCL2 protein expression, we find this rare in de-novo DLBCL.

journal_name

Leukemia

journal_title

Leukemia

authors

Schuetz JM,Johnson NA,Morin RD,Scott DW,Tan K,Ben-Nierah S,Boyle M,Slack GW,Marra MA,Connors JM,Brooks-Wilson AR,Gascoyne RD

doi

10.1038/leu.2011.378

subject

Has Abstract

pub_date

2012-06-01 00:00:00

pages

1383-90

issue

6

eissn

0887-6924

issn

1476-5551

pii

leu2011378

journal_volume

26

pub_type

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