{"database":"GEO","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Other":["ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE309nnn/GSE309171/"]},"type":"primary"},"statusCode":"OK","statusCodeValue":200}],"scores":null,"additional":{"omics_type":["Transcriptomics"],"species":["Mus musculus"],"gds_type":["Expression profiling by high throughput sequencing"],"full_dataset_link":["https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE309171"],"repository":["GEO"],"entry_type":["GSE"],"additional_accession":[]},"is_claimable":false,"name":"Necroptosis serves as a backup for Caspase-8-mediated apoptosis in B cells and blocks lymphomagenesis","description":"Alteration of apoptosis is a hallmark of B-cell lymphoma. While mitochondrial apoptosis is critical for lymphomagenesis, the role of extrinsic apoptosis, involving Caspase-8, remains elusive. Caspase-8 initiates apoptosis, suppresses necroptosis, and promotes inflammation independent of cell death. Due to this functional versatility, previous research failed to delineate its role in lymphomagenesis. Here, we demonstrate that B-cell-specific inhibition of Caspase-8 caused an aggressive B-cell malignancy in a subset of mice, resembling human DLBCL. However, most B cells lacking Caspase-8 activity underwent necroptosis, preventing tumor development. Consistently, combined inhibition of Caspase-8 and necroptosis markedly increased lymphoma incidence and mortality. Using both, mouse models and DLBCL patient samples, our study indicates that extrinsic apoptosis and necroptosis act as barriers against lymphomagenesis.","dates":{"publication":"2026/09/24"},"accession":"GSE309171","cross_references":{"GSM":["GSM9262445","GSM9262450","GSM9262448","GSM9262449","GSM9262446","GSM9262447"],"GPL":["24247"],"GSE":["309171"],"taxon":["Mus musculus"]}}