Hu, Shimin5; Xu-Monette, Zijun Y5; Balasubramanyam, Aarthi5; Manyam, Ganiraju C5; Visco, Carlo5; Tzankov, Alexander5; Liu, Wei-min5; Miranda, Roberto N5; Zhang, Li5; Montes-Moreno, Santiago5; Dybkær, Karen6; Chiu, April5; Orazi, Attilio5; Zu, Youli5; Bhagat, Govind5; Richards, Kristy L5; Hsi, Eric D5; Choi, William W L5; Han van Krieken, J5; Huang, Qin5; Huh, Jooryung5; Ai, Weiyun5; Ponzoni, Maurilio5; Ferreri, Andrés J M5; Zhao, Xiaoying5; Winter, Jane N5; Zhang, Mingzhi5; Li, Ling5; Møller, Michael7; Piris, Miguel A5; Li, Yong5; Go, Ronald S5; Wu, Lin5; Medeiros, L Jeffrey5; Young, Ken H5
1 The Faculty of Medicine, Aalborg University, VBN2 Aalborg University Hospital, The Faculty of Medicine, Aalborg University, VBN3 Klinik Medicin, The Faculty of Medicine, Aalborg University, VBN4 Blodsygdomme (Hæmatologi), The Faculty of Medicine, Aalborg University, VBN5 unknown6 Department of Clinical Medicine, The Faculty of Medicine, Aalborg University, VBN7 Klinisk Institut
a report from the International DLBCL Rituximab-CHOP Consortium Program Study
CD30, originally identified as a cell-surface marker of Reed-Sternberg and Hodgkin cells of classical Hodgkin lymphoma, is also expressed by several types of non-Hodgkin lymphoma, including a subset of diffuse large B-cell lymphoma (DLBCL). However, the prognostic and biological importance of CD30 expression in DLBCL is unknown. Here we report that CD30 expression is a favorable prognostic factor in a cohort of 903 de novo DLBCL patients. CD30 was expressed in ∼14% of DLBCL patients. Patients with CD30(+) DLBCL had superior 5-year overall survival (CD30(+), 79% vs CD30(-), 59%; P = .001) and progression-free survival (P = .003). The favorable outcome of CD30 expression was maintained in both the germinal center B-cell and activated B-cell subtypes. Gene expression profiling revealed the upregulation of genes encoding negative regulators of nuclear factor κB activation and lymphocyte survival, and downregulation of genes encoding B-cell receptor signaling and proliferation, as well as prominent cytokine and stromal signatures in CD30(+) DLBCL patients, suggesting a distinct molecular basis for its favorable outcome. Given the superior prognostic value, unique gene expression signature, and significant value of CD30 as a therapeutic target for brentuximab vedotin in ongoing successful clinical trials, it seems appropriate to consider CD30(+) DLBCL as a distinct subgroup of DLBCL.