{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Pan F"],"funding":["the Jiangsu Provincial Youth Medical Key Talents Project","the National Natural Science Foundation of China"],"pagination":["14248"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11189934"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["14(1)"],"pubmed_abstract":["Treatment of advanced triple-negative breast cancer (TNBC) is a great challenge in clinical practice. The immune checkpoints are a category of immunosuppressive molecules that cancer could hijack and impede anti-tumor immunity. Targeting immune checkpoints, such as anti-programmed cell death 1 (PD-1) therapy, is a promising therapeutic strategy in TNBC. The efficacy and safety of PD-1 monoclonal antibody (mAb) with chemotherapy have been validated in TNBC patients. However, the precise mechanisms underlying the synergistic effect of chemotherapy and anti-PD-1 therapy have not been elucidated, causing the TNBC patients that might benefit from this combination regimen not to be well selected. In the present work, we found that IL-23, an immunological cytokine, is significantly upregulated af"],"journal":["Scientific reports"],"pubmed_title":["Chemotherapy-induced high expression of IL23A enhances efficacy of anti-PD-1 therapy in TNBC by co-activating the PI3K-AKT signaling pathway of CTLs."],"pmcid":["PMC11189934"],"funding_grant_id":["QNRC2016887","82273326"],"pubmed_authors":["Liu J","Huo L","Huang G","Xie L","Zhu B","Zhu C","Liu X","Yang Y","Wang R","Pan F","Chen W","Chen Y","Gu J","Xu X","Zhao H","Xu Y"],"additional_accession":[]},"is_claimable":false,"name":"Chemotherapy-induced high expression of IL23A enhances efficacy of anti-PD-1 therapy in TNBC by co-activating the PI3K-AKT signaling pathway of CTLs.","description":"Treatment of advanced triple-negative breast cancer (TNBC) is a great challenge in clinical practice. The immune checkpoints are a category of immunosuppressive molecules that cancer could hijack and impede anti-tumor immunity. Targeting immune checkpoints, such as anti-programmed cell death 1 (PD-1) therapy, is a promising therapeutic strategy in TNBC. The efficacy and safety of PD-1 monoclonal antibody (mAb) with chemotherapy have been validated in TNBC patients. However, the precise mechanisms underlying the synergistic effect of chemotherapy and anti-PD-1 therapy have not been elucidated, causing the TNBC patients that might benefit from this combination regimen not to be well selected. In the present work, we found that IL-23, an immunological cytokine, is significantly upregulated af","dates":{"release":"2024-01-01T00:00:00Z","publication":"2024 Jun","modification":"2026-03-16T09:59:17.238Z","creation":"2025-08-15T03:07:01.302Z"},"accession":"S-EPMC11189934","cross_references":{"pubmed":["38902343"],"doi":["10.1038/s41598-024-65129-7"]}}