<HashMap><database>biostudies-other</database><scores/><additional><omics_type>Unknown</omics_type><submitter>Calvo Ezequiel</submitter><species>Homo sapiens</species><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-ECPF-GEOD-38772</full_dataset_link><project>EurocanPlatform</project><abstract>Pancreatic adenocarcinoma (PDAC) is an extremely deadly disease for which all treatments available have failed to improve life expectancy significantly. This may be explained by the high metastatic potential of PDAC cells, which results from their physiological dedifferentiation towards a mesenchymal phenotype. Some PDAC present cell-in-cell structures but their origin and significance is currently unknown. We show here that cell-incells form after cell cannibalism. We found PDAC patients whose tumors display cell cannibalism develop less metastasis than those without. In vitro, cell cannibalism was enhanced by the TGFβ and repressed by the Nuclear protein (Nupr)1, and was coupled to a defective epithelial-to-mesenchymal transition of PDAC cells. Cannibalism ends with death of PDAC cells, </abstract><repository>biostudies-other</repository><experiment_type>transcription profiling by array</experiment_type><data_source>EurocanPlatform</data_source><pubmed_authors>Lomberk Gwen</pubmed_authors><pubmed_authors>Loncle Céline</pubmed_authors><pubmed_authors>Hamidi Tewfik</pubmed_authors><pubmed_authors>Urrutia Raul</pubmed_authors><pubmed_authors>Calvo Ezequiel</pubmed_authors><pubmed_authors>Garcia Stéphane</pubmed_authors><pubmed_authors>Turrini Olivier</pubmed_authors><pubmed_authors>Bartholin Laurent</pubmed_authors><pubmed_authors>Sandí María</pubmed_authors><pubmed_authors>Secq Véronique</pubmed_authors><pubmed_authors>Cano Carla</pubmed_authors><pubmed_authors>Iovanna Juan</pubmed_authors><pubmed_authors>Kroemer Guido</pubmed_authors></additional><is_claimable>false</is_claimable><name>Cell cannibalism, a cell-death process driven by the Transforming Growth Factor-? and the Nuclear Protein 1, opposes to metastasis in pancreatic cancer</name><description>Pancreatic adenocarcinoma (PDAC) is an extremely deadly disease for which all treatments available have failed to improve life expectancy significantly. This may be explained by the high metastatic potential of PDAC cells, which results from their physiological dedifferentiation towards a mesenchymal phenotype. Some PDAC present cell-in-cell structures but their origin and significance is currently unknown. We show here that cell-incells form after cell cannibalism. We found PDAC patients whose tumors display cell cannibalism develop less metastasis than those without. In vitro, cell cannibalism was enhanced by the TGFβ and repressed by the Nuclear protein (Nupr)1, and was coupled to a defective epithelial-to-mesenchymal transition of PDAC cells. Cannibalism ends with death of PDAC cells, </description><dates><release>2016-04-14T14:12:18Z</release><modification>2016-04-14T14:12:18Z</modification><creation>2016-04-14T14:12:18Z</creation></dates><accession>S-ECPF-GEOD-38772</accession><cross_references><GEO>GSE38772</GEO><ArrayExpress>E-GEOD-38772</ArrayExpress><EFO>EFO_0000322</EFO><EFO>EFO_0002618</EFO><ArrayExpress files>E-GEOD-38772</ArrayExpress files></cross_references></HashMap>