{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"volume":["10(9)"],"submitter":["Jardin F"],"pubmed_abstract":["The tumor cells that drive classical Hodgkin lymphoma (cHL), namely, Hodgkin and Reed-Sternberg (HRS) cells, display hallmark features that include their rareness in contrast with an extensive and rich reactive microenvironment, their loss of B-cell phenotype markers, their immune escape capacity, and the activation of several key biological pathways, including the constitutive activation of the NFkB pathway. Both canonical and alternative pathways are deregulated by genetic alterations of their components or regulators, EBV infection and interaction with the microenvironment through multiple receptors, including CD30, CD40, BAFF, RANK and BCMA. Therefore, NFkB target genes are involved in apoptosis, cell proliferation, JAK/STAT pathway activation, B-cell marker expression loss, cellular i"],"journal":["Biomedicines"],"pagination":["2153"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC9495867"],"repository":["biostudies-literature"],"pubmed_title":["NFkB Pathway and Hodgkin Lymphoma."],"pmcid":["PMC9495867"],"pubmed_authors":["Jardin F"],"additional_accession":[]},"is_claimable":false,"name":"NFkB Pathway and Hodgkin Lymphoma.","description":"The tumor cells that drive classical Hodgkin lymphoma (cHL), namely, Hodgkin and Reed-Sternberg (HRS) cells, display hallmark features that include their rareness in contrast with an extensive and rich reactive microenvironment, their loss of B-cell phenotype markers, their immune escape capacity, and the activation of several key biological pathways, including the constitutive activation of the NFkB pathway. Both canonical and alternative pathways are deregulated by genetic alterations of their components or regulators, EBV infection and interaction with the microenvironment through multiple receptors, including CD30, CD40, BAFF, RANK and BCMA. Therefore, NFkB target genes are involved in apoptosis, cell proliferation, JAK/STAT pathway activation, B-cell marker expression loss, cellular i","dates":{"release":"2022-01-01T00:00:00Z","publication":"2022 Sep","modification":"2025-04-22T00:41:12.026Z","creation":"2025-04-05T19:37:43.484Z"},"accession":"S-EPMC9495867","cross_references":{"pubmed":["36140254"],"doi":["10.3390/biomedicines10092153"]}}