Syncytial variant of classic Hodgkin lymphoma: Four cases diagnosed with the aid of CD274/programmed cell death ligand 1 immunohistochemistry

2020 ◽  
Vol 70 (2) ◽  
pp. 108-115 ◽  
Author(s):  
Kei Kohno ◽  
Ayako Sakakibara ◽  
Akari Iwakoshi ◽  
Masaki Hasegawa ◽  
Shiro Adachi ◽  
...  
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Hodgkin Lymphoma ◽  
Classic Hodgkin Lymphoma

scholarly journals Immune-Checkpoint Blockade Therapy in Lymphoma

2020 ◽  
Vol 21 (15) ◽  
pp. 5456 ◽  
Author(s):  
Ayumi Kuzume ◽  
SungGi Chi ◽  
Nobuhiko Yamauchi ◽  
Yosuke Minami
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Malignant Lymphoma ◽  
Hodgkin Lymphoma ◽  
Immune Checkpoint ◽  
Immune Cell ◽  
Immune Checkpoint Blockade ◽  
Checkpoint Blockade ◽  
Host Immune System ◽  
Cell Death Protein

Tumor cells use immune-checkpoint pathways to evade the host immune system and suppress immune cell function. These cells express programmed cell-death protein 1 ligand 1 (PD-L1)/PD-L2, which bind to the programmed cell-death protein 1 (PD-1) present on cytotoxic T cells, trigger inhibitory signaling, and reduce cytotoxicity and T-cell exhaustion. Immune-checkpoint blockade can inhibit this signal and may serve as an effective therapeutic strategy in patients with solid tumors. Several trials have been conducted on immune-checkpoint inhibitor therapy in patients with malignant lymphoma and their efficacy has been reported. For example, in Hodgkin lymphoma, immune-checkpoint blockade has resulted in response rates of 65% to 75%. However, in non-Hodgkin lymphoma, the response rate to immune-checkpoint blockade was lower. In this review, we evaluate the biology of immune-checkpoint inhibition and the current data on its efficacy in malignant lymphoma, and identify the cases in which the treatment was more effective.

scholarly journals Targeting the programmed cell death 1 pathway in Hodgkin lymphoma: the place of nivolumab

2017 ◽  
Vol 8 (5) ◽  
pp. 175-180 ◽  
Author(s):  
Nathan D. Gay ◽  
Craig Y. Okada ◽  
Andy I. Chen ◽  
Emma C. Scott
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Hodgkin Lymphoma ◽  
Brentuximab Vedotin ◽  
Post Transplantation ◽  
Future Directions ◽  
Hematopoietic Stem ◽  
Programmed Cell Death 1 ◽  
Accelerated Approval ◽  
Immunoglobulin Gamma

Nivolumab is a humanized immunoglobulin gamma-4 kappa anti-programmed cell death 1 monoclonal antibody that is currently approved in the treatment of several solid tumors and recently gained accelerated approval in classical Hodgkin lymphoma (cHL) that has relapsed or progressed following autologous hematopoietic stem-cell transplantation and post-transplantation brentuximab vedotin. The purpose of this article is to review the immunophysiologic basis, clinical efficacy, and toxicity of nivolumab in the treatment of cHL. In addition, we will review ongoing clinical trials and potential future directions of checkpoint inhibition in the treatment of cHL.

The prognostic value of toll-like receptor5 and programmed cell death-ligand1 in patients with peripheral T-cell non-Hodgkin lymphoma

2019 ◽  
Vol 60 (11) ◽  
pp. 2646-2657 ◽  
Author(s):  
Mengqi Sun ◽  
Wenjia Su ◽  
Jingrong Qian ◽  
Hongxue Meng ◽  
Hongfei Ji ◽  
...  
Keyword(s):  
Cell Death ◽  
T Cell ◽  
Programmed Cell Death ◽  
Hodgkin Lymphoma ◽  
Prognostic Value ◽  
Non Hodgkin Lymphoma

scholarly journals Programmed cell death protein-1 (PD-1)-expression in the microenvironment of classical Hodgkin lymphoma at relapse during anti-PD-1-treatment

Haematologica ◽  
2018 ◽  
Vol 104 (1) ◽  
pp. e21-e24 ◽  
Author(s):  
Stephanie Sasse ◽  
Katharina Reddemann ◽  
Arjan Diepstra ◽  
Ilske Oschlies ◽  
Antje Schnitter ◽  
...  
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Hodgkin Lymphoma ◽  
Classical Hodgkin Lymphoma ◽  
Cell Death Protein

scholarly journals High efficacy of PD-1 inhibitor after initial failure of PD-L1 inhibitor in Relapsed/Refractory classical Hodgkin Lymphoma

BMC Cancer ◽  
2022 ◽  
Vol 22 (1) ◽  
Author(s):  
Xi Chen ◽  
Haiying Kong ◽  
Linxiang Luo ◽  
Shuiyun Han ◽  
Tao Lei ◽  
...  
Keyword(s):  
Clinical Trial ◽  
Cell Death ◽  
Tumor Microenvironment ◽  
Programmed Cell Death ◽  
Hodgkin Lymphoma ◽  
Progression Free Survival ◽  
Genetic Alterations ◽  
Classical Hodgkin Lymphoma ◽  
Formalin Fixed Paraffin Embedded ◽  
Inhibitor Treatment

Abstract Purpose We sought to understand the clinical course and molecular phenotype of patients who showed disease progression after programmed cell death ligand 1 (PD-L1) inhibitor treatment but subsequently responded to PD-1 inhibitor treatment. We also explored the response to PD-1-axis targeted therapy of classical Hodgkin lymphoma (cHL) according to genetically driven PD-L1 and programmed cell death ligand 2 (PD-L2) expression. Methods Five patients in a phase II clinical trial of CS1001 (PD-L1 inhibitor) for relapsed or refractory (R/R) cHL were retrospectively reviewed. Formalin-fixed, paraffin-embedded whole tissues from the five patients were evaluated for 9p24.1 genetic alterations based on FISH and the expression of PD-L1, PD-L2, PD-1, major histocompatibility complex (MHC) class I–II, and the tumor microenvironment factorsCD163 and FOXP3 in the microenvironmental niche, as revealed by multiplex immunofluorescence. Results All five patients showed primary refractory disease during first-line treatment. Four patients received PD-1 inhibitor after dropping out of the clinical trial, and all demonstrated at least a partial response. The progression-free survival ranged from 7 to 28 months (median = 18 months), and 9p24.1 amplification was observed in all five patients at the PD-L1/PD-L2 locus. PD-L1 and PD-L2 were colocalized on Hodgkin Reed-Sternberg (HRS) cells in four of the five (80%) patients. There was differential expression of PD-L1 and PD-L2 in cells in the tumor microenvironment in cHL, especially in HRS cells, background cells and tumor-associated macrophages. Conclusions PD-L1 monotherapy may not be sufficient to block the PD-1 pathway; PD-L2 was expressed in HRS and background cells in cHL. The immunologic function of the PD-L2 pathway in anti-tumor activity may be underestimated in R/R cHL. Further study is needed to elucidate the anti-tumor mechanism of PD-1 inhibitor and PD-L1 inhibitor treatment.

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