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Supplementary Table S7 from Multiplexed Spatial Profiling of Hodgkin Reed–Sternberg Cell Neighborhoods in Classic Hodgkin Lymphoma

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posted on 2024-09-03, 07:40 authored by Maryam Pourmaleki, Caitlin J. Jones, Sabrina D. Mellinghoff, Brian D. Greenstein, Priyadarshini Kumar, Miguel Foronda, Daniel A. Navarrete, Carl Campos, Mikhail Roshal, Nikolaus Schultz, Sohrab P. Shah, Andrea Schietinger, Nicholas D. Socci, Travis J. Hollmann, Ahmet Dogan, Ingo K. Mellinghoff

Supplementary Table S7. Summary of HRS cell states for each patient.

Funding

National Institutes of Health (NIH)

Geoffrey Beene Cancer Research Center

Cycle for Survival

National Cancer Institute (NCI)

United States Department of Health and Human Services

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ARTICLE ABSTRACT

Classic Hodgkin lymphoma (cHL) is a B-cell lymphoma that occurs primarily in young adults and, less frequently, in elderly individuals. A hallmark of cHL is the exceptional scarcity (1%–5%) of the malignant Hodgkin Reed–Sternberg (HRS) cells within a network of nonmalignant immune cells. Molecular determinants governing the relationship between HRS cells and their proximal microenvironment remain largely unknown. We performed spatially resolved multiplexed protein imaging and transcriptomic sequencing to characterize HRS cell states, cellular neighborhoods, and gene expression signatures of 23.6 million cells from 36 newly diagnosed Epstein–Barr virus (EBV)-positive and EBV-negative cHL tumors. We show that MHC-I expression on HRS cells is associated with immune-inflamed neighborhoods containing CD8+ T cells, MHC-II+ macrophages, and immune checkpoint expression (i.e., PD1 and VISTA). We identified spatial clustering of HRS cells, consistent with the syncytial variant of cHL, and its association with T-cell–excluded neighborhoods in a subset of EBV-negative tumors. Finally, a subset of both EBV-positive and EBV-negative tumors contained regulatory T-cell–high neighborhoods harboring HRS cells with augmented proliferative capacity. Our study links HRS cell properties with distinct immunophenotypes and potential immune escape mechanisms in cHL.

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