<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>8(5)</volume><submitter>Yildiz G</submitter><pubmed_abstract>Senescence is a permanent proliferation arrest in response to cell stress such as DNA damage. It contributes strongly to tissue aging and serves as a major barrier against tumor development. Most tumor cells are believed to bypass the senescence barrier (become "immortal") by inactivating growth control genes such as TP53 and CDKN2A. They also reactivate telomerase reverse transcriptase. Senescence-to-immortality transition is accompanied by major phenotypic and biochemical changes mediated by genome-wide transcriptional modifications. This appears to happen during hepatocellular carcinoma (HCC) development in patients with liver cirrhosis, however, the accompanying transcriptional changes are virtually unknown. We investigated genome-wide transcriptional changes related to the senescence-</pubmed_abstract><journal>PloS one</journal><pagination>e64016</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC3655073</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Genome-wide transcriptional reorganization associated with senescence-to-immortality switch during human hepatocellular carcinogenesis.</pubmed_title><pmcid>PMC3655073</pmcid><pubmed_authors>Ilk O</pubmed_authors><pubmed_authors>Ozen C</pubmed_authors><pubmed_authors>Erdal E</pubmed_authors><pubmed_authors>Ilk HG</pubmed_authors><pubmed_authors>Arslan-Ergul A</pubmed_authors><pubmed_authors>Ozdag H</pubmed_authors><pubmed_authors>Mizrak D</pubmed_authors><pubmed_authors>Sagol O</pubmed_authors><pubmed_authors>Konu O</pubmed_authors><pubmed_authors>Yildiz G</pubmed_authors><pubmed_authors>Akar N</pubmed_authors><pubmed_authors>Bozkaya H</pubmed_authors><pubmed_authors>Bilen B</pubmed_authors><pubmed_authors>Karademir S</pubmed_authors><pubmed_authors>Cetin-Atalay R</pubmed_authors><pubmed_authors>Gursoy-Yuzugullu O</pubmed_authors><pubmed_authors>Yuzugullu H</pubmed_authors><pubmed_authors>Ozturk N</pubmed_authors><pubmed_authors>Bagislar S</pubmed_authors><pubmed_authors>Ozturk M</pubmed_authors></additional><is_claimable>false</is_claimable><name>Genome-wide transcriptional reorganization associated with senescence-to-immortality switch during human hepatocellular carcinogenesis.</name><description>Senescence is a permanent proliferation arrest in response to cell stress such as DNA damage. It contributes strongly to tissue aging and serves as a major barrier against tumor development. Most tumor cells are believed to bypass the senescence barrier (become "immortal") by inactivating growth control genes such as TP53 and CDKN2A. They also reactivate telomerase reverse transcriptase. Senescence-to-immortality transition is accompanied by major phenotypic and biochemical changes mediated by genome-wide transcriptional modifications. This appears to happen during hepatocellular carcinoma (HCC) development in patients with liver cirrhosis, however, the accompanying transcriptional changes are virtually unknown. We investigated genome-wide transcriptional changes related to the senescence-</description><dates><release>2013-01-01T00:00:00Z</release><publication>2013</publication><modification>2026-04-07T21:57:39.324Z</modification><creation>2026-04-07T18:19:51.054Z</creation></dates><accession>S-EPMC3655073</accession><cross_references><pubmed>23691139</pubmed><doi>10.1371/journal.pone.0064016</doi></cross_references></HashMap>