Stephen M Ansell 1 , Alexander M Lesokhin , Ivan Borrello , Ahmad Halwani , Emma C Scott , Martin Gutierrez , Stephen J Schuster , Michael M Millenson , Deepika Cattry , Gordon J Freeman , Scott J Rodig , Bjoern Chapuy , Azra H Ligon , Lili Zhu , Joseph F Grosso , Su Young Kim , John M Timmerman , Margaret A Shipp , Philippe Armand
Jan 22 2015
Preclinical studies suggest that Reed-Sternberg cells exploit the programmed death 1 (PD-1) pathway to evade immune detection. In classic Hodgkin's lymphoma, alterations in chromosome 9p24.1 increase the abundance of the PD-1 ligands, PD-L1 and PD-L2, and promote their induction through Janus kinase (JAK)-signal transducer and activator of transcription (STAT) signaling. We hypothesized that nivolumab, a PD-1-blocking antibody, could inhibit tumor immune evasion in patients with relapsed or refractory Hodgkin's lymphoma.