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Merck

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

Blood (2016-04-01)
Konstantinos Georgiou, Longyun Chen, Mattias Berglund, Weicheng Ren, Noel F C C de Miranda, Susana Lisboa, Marco Fangazio, Shida Zhu, Yong Hou, Kui Wu, Wenfeng Fang, Xianhuo Wang, Bin Meng, Li Zhang, Yixin Zeng, Govind Bhagat, Magnus Nordenskjöld, Christer Sundström, Gunilla Enblad, Riccardo Dalla-Favera, Huilai Zhang, Manuel R Teixeira, Laura Pasqualucci, Roujun Peng, Qiang Pan-Hammarström
要旨

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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Sigma-Aldrich
Anti-PDL-2 antibody produced in rabbit, affinity isolated antibody, buffered aqueous solution