<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Krauß L</submitter><funding>DFG</funding><funding>Deutsche Krebshilfe</funding><funding>Wilhelm-Sander-Stiftung</funding><pagination>695-707</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC9359718</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>82(4)</volume><pubmed_abstract>The mortality of patients with pancreatic ductal adenocarcinoma (PDAC) is strongly associated with metastasis, a multistep process that is incompletely understood in this disease. Although genetic drivers of PDAC metastasis have not been defined, transcriptional and epigenetic rewiring can contribute to the metastatic process. The epigenetic eraser histone deacetylase 2 (HDAC2) has been connected to less differentiated PDAC, but the function of HDAC2 in PDAC has not been comprehensively evaluated. Using genetically defined models, we show that HDAC2 is a cellular fitness factor that controls cell cycle in vitro and metastasis in vivo, particularly in undifferentiated, mesenchymal PDAC cells. Unbiased expression profiling detected a core set of HDAC2-regulated genes. HDAC2 controlled expres</pubmed_abstract><journal>Cancer research</journal><pubmed_title>HDAC2 Facilitates Pancreatic Cancer Metastasis.</pubmed_title><pmcid>PMC9359718</pmcid><funding_grant_id>P12</funding_grant_id><funding_grant_id>SFB1321</funding_grant_id><funding_grant_id>P13</funding_grant_id><funding_grant_id>70113760</funding_grant_id><funding_grant_id>SFB1321 S01 and S02</funding_grant_id><funding_grant_id>959/6-1</funding_grant_id><funding_grant_id>2017.048.2</funding_grant_id><funding_grant_id>70114328</funding_grant_id><funding_grant_id>111273</funding_grant_id><funding_grant_id>329628492</funding_grant_id><funding_grant_id>2019.086.1</funding_grant_id><funding_grant_id>RE 3723/4-1</funding_grant_id><pubmed_authors>Hastreiter S</pubmed_authors><pubmed_authors>Urban BC</pubmed_authors><pubmed_authors>Terrasi A</pubmed_authors><pubmed_authors>Klement C</pubmed_authors><pubmed_authors>Cernilogar FM</pubmed_authors><pubmed_authors>de Andrade Kratzig N</pubmed_authors><pubmed_authors>Wenzel P</pubmed_authors><pubmed_authors>Wirth M</pubmed_authors><pubmed_authors>Schmid RM</pubmed_authors><pubmed_authors>Engleitner T</pubmed_authors><pubmed_authors>Kramer OH</pubmed_authors><pubmed_authors>Steiger K</pubmed_authors><pubmed_authors>Hassan Z</pubmed_authors><pubmed_authors>Schneider G</pubmed_authors><pubmed_authors>Schneider C</pubmed_authors><pubmed_authors>Ollinger R</pubmed_authors><pubmed_authors>Lankes K</pubmed_authors><pubmed_authors>Rad R</pubmed_authors><pubmed_authors>Krauß L</pubmed_authors><pubmed_authors>Reichert M</pubmed_authors><pubmed_authors>Schotta G</pubmed_authors><pubmed_authors>Saur D</pubmed_authors></additional><is_claimable>false</is_claimable><name>HDAC2 Facilitates Pancreatic Cancer Metastasis.</name><description>The mortality of patients with pancreatic ductal adenocarcinoma (PDAC) is strongly associated with metastasis, a multistep process that is incompletely understood in this disease. Although genetic drivers of PDAC metastasis have not been defined, transcriptional and epigenetic rewiring can contribute to the metastatic process. The epigenetic eraser histone deacetylase 2 (HDAC2) has been connected to less differentiated PDAC, but the function of HDAC2 in PDAC has not been comprehensively evaluated. Using genetically defined models, we show that HDAC2 is a cellular fitness factor that controls cell cycle in vitro and metastasis in vivo, particularly in undifferentiated, mesenchymal PDAC cells. Unbiased expression profiling detected a core set of HDAC2-regulated genes. HDAC2 controlled expres</description><dates><release>2022-01-01T00:00:00Z</release><publication>2022 Feb</publication><modification>2026-07-14T21:08:47.677Z</modification><creation>2025-04-06T00:53:07.646Z</creation></dates><accession>S-EPMC9359718</accession><cross_references><pubmed>34903606</pubmed><doi>10.1158/0008-5472.CAN-20-3209</doi></cross_references></HashMap>