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Loss of PRDM1/BLIMP-1 function contributes to poor prognosis of activated B-cell-like diffuse large B-cell lymphoma.

Abstract：

:PRDM1/BLIMP-1, a master regulator of plasma-cell differentiation, is frequently inactivated in activated B-cell-like (ABC) diffuse large B-cell lymphoma (DLBCL) patients. Little is known about its genetic aberrations and relevant clinical implications. A large series of patients with de novo DLBCL was effectively evaluated for PRDM1/BLIMP-1 deletion, mutation, and protein expression. BLIMP-1 expression was frequently associated with the ABC phenotype and plasmablastic morphologic subtype of DLBCL, yet 63% of the ABC-DLBCL patients were negative for BLIMP-1 protein expression. In these patients, loss of BLIMP-1 was associated with Myc overexpression and decreased expression of p53 pathway molecules. In addition, homozygous PRDM1 deletions and PRDM1 mutations within exons 1 and 2, which encode for domains crucial for transcriptional repression, were found to show a poor prognostic impact in patients with ABC-DLBCL but not in those with germinal center B-cell-like DLBCL (GCB-DLBCL). Gene expression profiling revealed that loss of PRDM1/BLIMP-1 expression correlated with a decreased plasma-cell differentiation signature and upregulation of genes involved in B-cell receptor signaling and tumor-cell proliferation. In conclusion, these results provide novel clinical and biological insight into the tumor-suppressive role of PRDM1/BLIMP-1 in ABC-DLBCL patients and suggest that loss of PRDM1/BLIMP-1 function contributes to the overall poor prognosis of ABC-DLBCL patients.

journal_name

Leukemia

journal_title

Leukemia

authors

Xia Y,Xu-Monette ZY,Tzankov A,Li X,Manyam GC,Murty V,Bhagat G,Zhang S,Pasqualucci L,Visco C,Dybkaer K,Chiu A,Orazi A,Zu Y,Richards KL,Hsi ED,Choi WW,van Krieken JH,Huh J,Ponzoni M,Ferreri AJ,Møller MB,Parsons

doi

10.1038/leu.2016.243

subject

Has Abstract

pub_date

2017-03-01 00:00:00

pages

625-636

issue

3

eissn

0887-6924

issn

1476-5551

pii

leu2016243

journal_volume

31

pub_type

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