<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Li JJ</submitter><funding>NICHD NIH HHS</funding><funding>Alex&amp;apos;s Lemonade Stand Foundation for Childhood Cancer</funding><funding>NCI NIH HHS</funding><funding>National Institutes of Health</funding><funding>V Foundation for Cancer Research</funding><funding>Glenn and Stacy Schiffman Pediatric Cancer Research Fund</funding><pagination>16505</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC8363632</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>11(1)</volume><pubmed_abstract>Rhabdomyosarcoma (RMS) is the most common pediatric soft tissue sarcoma. The two predominant histologic variants of RMS, embryonal and alveolar rhabdomyosarcoma (eRMS and aRMS, respectively), carry very different prognoses. While eRMS is associated with an intermediate prognosis, the 5-year survival rate of aRMS is less than 30%. The RMS subtypes are also different at the molecular level-eRMS frequently has multiple genetic alterations, including mutations in RAS and TP53, whereas aRMS often has chromosomal translocations resulting in PAX3-FOXO1 or PAX7-FOXO1 fusions, but otherwise has a "quiet" genome. Interestingly, mutations in RAS are rarely found in aRMS. In this study, we explored the role of oncogenic RAS in aRMS. We found that while ectopic oncogenic HRAS expression was tolerated i</pubmed_abstract><journal>Scientific reports</journal><pubmed_title>Expression of oncogenic HRAS in human Rh28 and RMS-YM rhabdomyosarcoma cells leads to oncogene-induced senescence.</pubmed_title><pmcid>PMC8363632</pmcid><funding_grant_id>K12 HD043494</funding_grant_id><funding_grant_id>U54 CA231630</funding_grant_id><funding_grant_id>R01 CA122706</funding_grant_id><pubmed_authors>Linardic CM</pubmed_authors><pubmed_authors>Kovach AR</pubmed_authors><pubmed_authors>Oristian KM</pubmed_authors><pubmed_authors>Li JJ</pubmed_authors><pubmed_authors>Chen C</pubmed_authors><pubmed_authors>DeMonia M</pubmed_authors><pubmed_authors>Slemmons KK</pubmed_authors></additional><is_claimable>false</is_claimable><name>Expression of oncogenic HRAS in human Rh28 and RMS-YM rhabdomyosarcoma cells leads to oncogene-induced senescence.</name><description>Rhabdomyosarcoma (RMS) is the most common pediatric soft tissue sarcoma. The two predominant histologic variants of RMS, embryonal and alveolar rhabdomyosarcoma (eRMS and aRMS, respectively), carry very different prognoses. While eRMS is associated with an intermediate prognosis, the 5-year survival rate of aRMS is less than 30%. The RMS subtypes are also different at the molecular level-eRMS frequently has multiple genetic alterations, including mutations in RAS and TP53, whereas aRMS often has chromosomal translocations resulting in PAX3-FOXO1 or PAX7-FOXO1 fusions, but otherwise has a "quiet" genome. Interestingly, mutations in RAS are rarely found in aRMS. In this study, we explored the role of oncogenic RAS in aRMS. We found that while ectopic oncogenic HRAS expression was tolerated i</description><dates><release>2021-01-01T00:00:00Z</release><publication>2021 Aug</publication><modification>2025-06-01T03:29:18.138Z</modification><creation>2025-06-01T03:29:18.138Z</creation></dates><accession>S-EPMC8363632</accession><cross_references><pubmed>34389744</pubmed><doi>10.1038/s41598-021-95355-2</doi></cross_references></HashMap>