<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Conte M</submitter><funding>MISE: Nabucco</funding><funding>the Campania Regional Government Lotta alle Patologie Oncologiche, iCURE</funding><funding>Campania Regional Government “Lotta alle Patologie Oncologiche”, iCURE</funding><funding>MUR (PRIN 2020)</funding><funding>EU: BBMRI: CANSERV project</funding><funding>VALERE: Vanvitelli per la Ricerca Program: Adip-Care</funding><pagination>1960</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC10093005</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>15(7)</volume><pubmed_abstract>A large body of clinical and experimental evidence indicates that colorectal cancer is one of the most common multifactorial diseases. Although some useful prognostic biomarkers for clinical therapy have already been identified, it is still difficult to characterize a therapeutic signature that is able to define the most appropriate treatment. Gene expression levels of the epigenetic regulator histone deacetylase 2 (&lt;i>HDAC2&lt;/i>) are deregulated in colorectal cancer, and this deregulation is tightly associated with immune dysfunction. By interrogating bioinformatic databases, we identified patients who presented simultaneous alterations in &lt;i>HDAC2&lt;/i>, class II major histocompatibility complex transactivator (&lt;i>CIITA)&lt;/i>, and beta-2 microglobulin (&lt;i>B2M&lt;/i>) genes based on mutation lev</pubmed_abstract><journal>Cancers</journal><pubmed_title>Targeting HDAC2-Mediated Immune Regulation to Overcome Therapeutic Resistance in Mutant Colorectal Cancer.</pubmed_title><pmcid>PMC10093005</pmcid><funding_grant_id>ID263</funding_grant_id><funding_grant_id>CUPB21c17000030007</funding_grant_id><funding_grant_id>101058620</funding_grant_id><funding_grant_id>CW39SJ</funding_grant_id><funding_grant_id>1682</funding_grant_id><funding_grant_id>PRIN 2020 CW39SJ</funding_grant_id><pubmed_authors>Di Mauro A</pubmed_authors><pubmed_authors>Altucci L</pubmed_authors><pubmed_authors>Montella L</pubmed_authors><pubmed_authors>Capasso L</pubmed_authors><pubmed_authors>De Simone M</pubmed_authors><pubmed_authors>Conte M</pubmed_authors><pubmed_authors>Nebbioso A</pubmed_authors></additional><is_claimable>false</is_claimable><name>Targeting HDAC2-Mediated Immune Regulation to Overcome Therapeutic Resistance in Mutant Colorectal Cancer.</name><description>A large body of clinical and experimental evidence indicates that colorectal cancer is one of the most common multifactorial diseases. Although some useful prognostic biomarkers for clinical therapy have already been identified, it is still difficult to characterize a therapeutic signature that is able to define the most appropriate treatment. Gene expression levels of the epigenetic regulator histone deacetylase 2 (&lt;i>HDAC2&lt;/i>) are deregulated in colorectal cancer, and this deregulation is tightly associated with immune dysfunction. By interrogating bioinformatic databases, we identified patients who presented simultaneous alterations in &lt;i>HDAC2&lt;/i>, class II major histocompatibility complex transactivator (&lt;i>CIITA)&lt;/i>, and beta-2 microglobulin (&lt;i>B2M&lt;/i>) genes based on mutation lev</description><dates><release>2023-01-01T00:00:00Z</release><publication>2023 Mar</publication><modification>2026-04-08T12:35:51.482Z</modification><creation>2025-04-05T19:42:21.806Z</creation></dates><accession>S-EPMC10093005</accession><cross_references><pubmed>37046620</pubmed><doi>10.3390/cancers15071960</doi></cross_references></HashMap>