<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Pan F</submitter><funding>the Jiangsu Provincial Youth Medical Key Talents Project</funding><funding>the National Natural Science Foundation of China</funding><pagination>14248</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC11189934</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>14(1)</volume><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</pubmed_abstract><journal>Scientific reports</journal><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.</pubmed_title><pmcid>PMC11189934</pmcid><funding_grant_id>QNRC2016887</funding_grant_id><funding_grant_id>82273326</funding_grant_id><pubmed_authors>Liu J</pubmed_authors><pubmed_authors>Huo L</pubmed_authors><pubmed_authors>Huang G</pubmed_authors><pubmed_authors>Xie L</pubmed_authors><pubmed_authors>Zhu B</pubmed_authors><pubmed_authors>Zhu C</pubmed_authors><pubmed_authors>Liu X</pubmed_authors><pubmed_authors>Yang Y</pubmed_authors><pubmed_authors>Wang R</pubmed_authors><pubmed_authors>Pan F</pubmed_authors><pubmed_authors>Chen W</pubmed_authors><pubmed_authors>Chen Y</pubmed_authors><pubmed_authors>Gu J</pubmed_authors><pubmed_authors>Xu X</pubmed_authors><pubmed_authors>Zhao H</pubmed_authors><pubmed_authors>Xu Y</pubmed_authors></additional><is_claimable>false</is_claimable><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.</name><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</description><dates><release>2024-01-01T00:00:00Z</release><publication>2024 Jun</publication><modification>2026-03-16T09:59:17.238Z</modification><creation>2025-08-15T03:07:01.302Z</creation></dates><accession>S-EPMC11189934</accession><cross_references><pubmed>38902343</pubmed><doi>10.1038/s41598-024-65129-7</doi></cross_references></HashMap>