{"database":"GEO","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Other":["ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE335nnn/GSE335769/"]},"type":"primary"},"statusCode":"OK","statusCodeValue":200}],"scores":null,"additional":{"omics_type":["Transcriptomics"],"species":["Homo sapiens"],"gds_type":["Expression profiling by high throughput sequencing"],"full_dataset_link":["https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE335769"],"repository":["GEO"],"entry_type":["GSE"],"additional_accession":[]},"is_claimable":false,"name":"ARID1B loss drives sorafenib resistance through transcriptional reprogramming in hepatocellular carcinoma","description":"mRNA-seq was performed in HepG2 hepatocellular carcinoma cells to characterize transcriptional changes driven by ARID1B loss under sorafenib treatment. Wild-type (WT) and ARID1B-knockout (ARID1B-KO) HepG2 cells were treated with sorafenib (5 µM, 48 h) or DMSO vehicle, with three biological replicates per condition. DESeq2 interaction model identified ARID1B-dependent transcriptional responses to sorafenib. Preprint: https://doi.org/10.64898/2026.06.11.731725","dates":{"publication":"2026/06/19"},"accession":"GSE335769","cross_references":{"GSM":["GSM9820473","GSM9820484","GSM9820474","GSM9820482","GSM9820483","GSM9820477","GSM9820478","GSM9820475","GSM9820476","GSM9820479","GSM9820480","GSM9820481"],"GPL":["30882"],"GSE":["335769"],"taxon":["Homo sapiens"],"DOI":["10.64898/2026.06.11.731725"]}}