{"database":"GEO","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Other":["ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE341nnn/GSE341740/"]},"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=GSE341740"],"repository":["GEO"],"entry_type":["GSE"],"additional_accession":[]},"is_claimable":false,"name":"GAS6 drives chemoresistance and immune escape in ovarian cancer","description":"High-grade serous ovarian cancer (HGSOC) has poor prognosis owing to widespread platinum resistance and unsatisfactory efficacy of chemo-immunotherapy, so novel mechanisms of therapeutic failure are urgently required. The GAS6/AXL axis supports tumor survival and immunosuppression, yet how chemotherapy modulates GAS6 expression remains unclear. We demonstrate that chemotherapy elevates GAS6, which activates AXL to trigger NF-κB-mediated transcription of GDF-15. This GAS6-AXL-GDF-15 cascade drives intrinsic platinum resistance and tumor immune evasion. Blocking GDF-15 reverses chemoresistance; combined with anti-PD-1 antibody, it produces synergistic anti-tumor effects. Circulating GAS6 protein reflects activation of this signaling cascade and acts as a non-invasive predictive biomarker for combined GDF-15/PD-1 blockade. Collectively, we identify a chemotherapy-activated GAS6/AXL-NF-κB-GDF-15 pathway that mediates both chemoresistance and immune escape in HGSOC, supporting translational application of GDF-15 inhibitors plus immune checkpoint inhibitors for biomarker-stratified patients.","dates":{"publication":"2026/08/03"},"accession":"GSE341740","cross_references":{"GSM":["GSM9915959","GSM9915961","GSM9915960","GSM9915964","GSM9915963","GSM9915962"],"GPL":["34284"],"GSE":["341740"],"taxon":["Homo sapiens"]}}