{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Karihtala K"],"funding":["Cancer Foundation Finland sr"],"pagination":["1919-1931"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC8941476"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["6(6)"],"pubmed_abstract":["Emerging evidence indicates a major impact for the tumor microenvironment (TME) and immune escape in the pathogenesis and clinical course of classical Hodgkin lymphoma (cHL). We used gene expression profiling (n = 88), CIBERSORT, and multiplex immunohistochemistry (n = 131) to characterize the immunoprofile of cHL TME and correlated the findings with survival. Gene expression analysis divided tumors into subgroups with T cell-inflamed and -noninflamed TME. Several macrophage-related genes were upregulated in samples with the non-T cell-inflamed TME, and based on the immune cell proportions, the samples clustered according to the content of T cells and macrophages. A cluster with high proportions of checkpoint protein (programmed cell death protein 1, PD-1 ligands, indoleamine 2,3 dioxygena"],"journal":["Blood advances"],"pubmed_title":["Checkpoint protein expression in the tumor microenvironment defines the outcome of classical Hodgkin lymphoma patients."],"pmcid":["PMC8941476"],"funding_grant_id":["120102","160092","180125","200088","140136","210047","130117","110094"],"pubmed_authors":["Karihtala K","Steidl C","Karjalainen-Lindsberg ML","Chan FC","Pellinen T","Leppa S","Leivonen SK"],"additional_accession":[]},"is_claimable":false,"name":"Checkpoint protein expression in the tumor microenvironment defines the outcome of classical Hodgkin lymphoma patients.","description":"Emerging evidence indicates a major impact for the tumor microenvironment (TME) and immune escape in the pathogenesis and clinical course of classical Hodgkin lymphoma (cHL). We used gene expression profiling (n = 88), CIBERSORT, and multiplex immunohistochemistry (n = 131) to characterize the immunoprofile of cHL TME and correlated the findings with survival. Gene expression analysis divided tumors into subgroups with T cell-inflamed and -noninflamed TME. Several macrophage-related genes were upregulated in samples with the non-T cell-inflamed TME, and based on the immune cell proportions, the samples clustered according to the content of T cells and macrophages. A cluster with high proportions of checkpoint protein (programmed cell death protein 1, PD-1 ligands, indoleamine 2,3 dioxygena","dates":{"release":"2022-01-01T00:00:00Z","publication":"2022 Mar","modification":"2026-03-27T16:40:50.047Z","creation":"2025-04-03T21:30:43.085Z"},"accession":"S-EPMC8941476","cross_references":{"pubmed":["34941990"],"doi":["10.1182/bloodadvances.2021006189"]}}