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. 2016 Jun 16;127(24):3026-34.
doi: 10.1182/blood-2015-12-686550. Epub 2016 Mar 30.

Genetic basis of PD-L1 overexpression in diffuse large B-cell lymphomas

Konstantinos Georgiou  1 , Longyun Chen  2 , Mattias Berglund  3 , Weicheng Ren  1 , Noel F C C de Miranda  4 , Susana Lisboa  5 , Marco Fangazio  6 , Shida Zhu  7 , Yong Hou  7 , Kui Wu  7 , Wenfeng Fang  8 , Xianhuo Wang  9 , Bin Meng  9 , Li Zhang  8 , Yixin Zeng  8 , Govind Bhagat  10 , Magnus Nordenskjöld  11 , Christer Sundström  12 , Gunilla Enblad  12 , Riccardo Dalla-Favera  6 , Huilai Zhang  9 , Manuel R Teixeira  5 , Laura Pasqualucci  6 , Roujun Peng  8 , Qiang Pan-Hammarström  1
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Free article

Genetic basis of PD-L1 overexpression in diffuse large B-cell lymphomas

Konstantinos Georgiou et al. Blood. .
Free article

Abstract

Diffuse large B-cell lymphoma (DLBCL) is one of the most common and aggressive types of B-cell lymphoma. Deregulation of proto-oncogene expression after a translocation, most notably to the immunoglobulin heavy-chain locus (IGH), is one of the hallmarks of DLBCL. Using whole-genome sequencing analysis, we have identified the PD-L1/PD-L2 locus as a recurrent translocation partner for IGH in DLBCL. PIM1 and TP63 were also identified as novel translocation partners for PD-L1/PD-L2 Fluorescence in situ hybridization was furthermore used to rapidly screen an expanded DLBCL cohort. Collectively, a subset of samples was found to be affected by gains (12%), amplifications (3%), and translocations (4%) of the PD-L1/PD-L2 locus. RNA sequencing data coupled with immunohistochemistry revealed that these cytogenetic alterations correlated with increased expression of PD-L1 but not of PD-L2 Moreover, cytogenetic alterations affecting the PD-L1/PD-L2 locus were more frequently observed in the non-germinal center B cell-like (non-GCB) subtype of DLBCL. These findings demonstrate the genetic basis of PD-L1 overexpression in DLBCL and suggest that treatments targeting the PD-1-PD-L1/PD-L2 axis might benefit DLBCL patients, especially those belonging to the more aggressive non-GCB subtype.

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