{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Wu WY"],"funding":["National Natural Science Foundation of China (National Science Foundation of China)"],"pagination":["703-714"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC12867762"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["45(6)"],"pubmed_abstract":["Capecitabine has been commonly used for the treatment of early-stage triple-negative breast cancer (TNBC) patients; however, the resistance limits its curative potential. Here, we perform multi-omics data analysis and immunohistochemical (IHC) staining of biological samples from patients in the CBCSG010 clinical trial who were randomized to receive adjuvant docetaxel-anthracycline-based chemotherapy with or without capecitabine. We find that patients with a better prognosis in the capecitabine group exhibited an immune-inflamed microenvironment and upregulation of interferon pathways. Moreover, we identify interferon-related TANK-binding kinase 1-binding protein 1 (TBKBP1) as the key gene involved in capecitabine resistance. We uncover that TBKBP1 promotes capecitabine resistance through i"],"journal":["Oncogene"],"pubmed_title":["TBKBP1 induces capecitabine resistance through negative regulation of type I interferon pathway in triple-negative breast cancer."],"pmcid":["PMC12867762"],"funding_grant_id":["82172576"],"pubmed_authors":["Di GH","Yang YS","Shao ZM","Xie YF","Andriani L","Wu WY","Li JJ"],"additional_accession":[]},"is_claimable":false,"name":"TBKBP1 induces capecitabine resistance through negative regulation of type I interferon pathway in triple-negative breast cancer.","description":"Capecitabine has been commonly used for the treatment of early-stage triple-negative breast cancer (TNBC) patients; however, the resistance limits its curative potential. Here, we perform multi-omics data analysis and immunohistochemical (IHC) staining of biological samples from patients in the CBCSG010 clinical trial who were randomized to receive adjuvant docetaxel-anthracycline-based chemotherapy with or without capecitabine. We find that patients with a better prognosis in the capecitabine group exhibited an immune-inflamed microenvironment and upregulation of interferon pathways. Moreover, we identify interferon-related TANK-binding kinase 1-binding protein 1 (TBKBP1) as the key gene involved in capecitabine resistance. We uncover that TBKBP1 promotes capecitabine resistance through i","dates":{"release":"2026-01-01T00:00:00Z","publication":"2026 Feb","modification":"2026-07-15T06:18:15.429Z","creation":"2026-06-30T03:22:50.608Z"},"accession":"S-EPMC12867762","cross_references":{"pubmed":["41606294"],"doi":["10.1038/s41388-025-03598-4"]}}