<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>12(5)</volume><submitter>Zhou Y</submitter><pubmed_abstract>&lt;b>Rationale:&lt;/b> Pancreatic ductal adenocarcinoma (PDAC) is a lethal disease with a dismal 5-year survival less than 10%. Most patients with PDAC exhibit poor response to single-agent immunotherapy. Multimodal therapies targeting mechanisms of resistance to immunotherapy are urgently needed. We found that the class IIa histone deacetylase (HDAC) member, HDAC5 is downregulated in multiple solid tumors and its level were associated with favorable prognosis in PDAC patients. Upregulated genes in patients harboring HDAC5 deletions were enriched in adaptive immune responses and lymphocyte-mediated immunity in The Cancer Genome Atlas (TCGA) pancreatic cancer dataset. &lt;b>Methods:&lt;/b> Tissue microarray of pancreatic cancer were used to analysis the correlation between HDAC5 and PD-L1. RNA-seq, tr</pubmed_abstract><journal>Theranostics</journal><pagination>2080-2094</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC8899586</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>HDAC5 modulates PD-L1 expression and cancer immunity via p65 deacetylation in pancreatic cancer.</pubmed_title><pmcid>PMC8899586</pmcid><pubmed_authors>Jin X</pubmed_authors><pubmed_authors>Liang X</pubmed_authors><pubmed_authors>Wang B</pubmed_authors><pubmed_authors>Zhou Y</pubmed_authors><pubmed_authors>Ren D</pubmed_authors><pubmed_authors>Sun Y</pubmed_authors><pubmed_authors>Yu H</pubmed_authors><pubmed_authors>Wu H</pubmed_authors><pubmed_authors>Pan P</pubmed_authors><pubmed_authors>Qin G</pubmed_authors><pubmed_authors>Zhao J</pubmed_authors><pubmed_authors>Chen T</pubmed_authors><pubmed_authors>Zhu S</pubmed_authors></additional><is_claimable>false</is_claimable><name>HDAC5 modulates PD-L1 expression and cancer immunity via p65 deacetylation in pancreatic cancer.</name><description>&lt;b>Rationale:&lt;/b> Pancreatic ductal adenocarcinoma (PDAC) is a lethal disease with a dismal 5-year survival less than 10%. Most patients with PDAC exhibit poor response to single-agent immunotherapy. Multimodal therapies targeting mechanisms of resistance to immunotherapy are urgently needed. We found that the class IIa histone deacetylase (HDAC) member, HDAC5 is downregulated in multiple solid tumors and its level were associated with favorable prognosis in PDAC patients. Upregulated genes in patients harboring HDAC5 deletions were enriched in adaptive immune responses and lymphocyte-mediated immunity in The Cancer Genome Atlas (TCGA) pancreatic cancer dataset. &lt;b>Methods:&lt;/b> Tissue microarray of pancreatic cancer were used to analysis the correlation between HDAC5 and PD-L1. RNA-seq, tr</description><dates><release>2022-01-01T00:00:00Z</release><publication>2022</publication><modification>2025-04-18T16:35:46.094Z</modification><creation>2025-04-07T03:54:24.235Z</creation></dates><accession>S-EPMC8899586</accession><cross_references><pubmed>35265200</pubmed><doi>10.7150/thno.69444</doi></cross_references></HashMap>