<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Munoz-Galvan S</submitter><funding>Centro de Investigación Biomédica en Red Cáncer</funding><funding>Centro de Investigación Biomédica en Red Cáncer (ES)</funding><funding>Instituto de Salud Carlos III</funding><funding>Ministerio de Ciencia, Innovación y Universidades</funding><funding>Consejería de Salud, Junta de Andalucía</funding><funding>Ministerio de Economía y Competitividad</funding><pagination>234</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC6547556</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>38(1)</volume><pubmed_abstract>&lt;h4>Background&lt;/h4>Ovarian cancer is the leading cause of gynecologic cancer-related death, due in part to a late diagnosis and a high rate of recurrence. Primary and acquired platinum resistance is related to a low response probability to subsequent lines of treatment and to a poor survival. Therefore, a comprehensive understanding of the mechanisms that drive platinum resistance is urgently needed.&lt;h4>Methods&lt;/h4>We used bioinformatics analysis of public databases and RT-qPCR to quantitate the relative gene expression profiles of ovarian tumors. Many of the dysregulated genes were cancer stem cell (CSC) factors, and we analyzed its relation to therapeutic resistance in human primary tumors. We also performed clustering and in vitro analyses of therapy cytotoxicity in tumorspheres.&lt;h4>Res</pubmed_abstract><journal>Journal of experimental &amp; clinical cancer research : CR</journal><pubmed_title>New markers for human ovarian cancer that link platinum resistance to the cancer stem cell phenotype and define new therapeutic combinations and diagnostic tools.</pubmed_title><pmcid>PMC6547556</pmcid><funding_grant_id>FPU12/01380</funding_grant_id><funding_grant_id>CD16/12/00275</funding_grant_id><funding_grant_id>RTI2018-097455-B-I00</funding_grant_id><funding_grant_id>PI15/00045</funding_grant_id><funding_grant_id>PI-0096-2014</funding_grant_id><funding_grant_id>CD16/00230</funding_grant_id><pubmed_authors>Suarez-Martinez E</pubmed_authors><pubmed_authors>Dominguez-Pinol J</pubmed_authors><pubmed_authors>Otero-Albiol D</pubmed_authors><pubmed_authors>Marin JJ</pubmed_authors><pubmed_authors>Jimenez-Garcia MP</pubmed_authors><pubmed_authors>Munoz-Galvan S</pubmed_authors><pubmed_authors>Estevez-Garcia P</pubmed_authors><pubmed_authors>Verdugo-Sivianes EM</pubmed_authors><pubmed_authors>Garcia-Carrasco M</pubmed_authors><pubmed_authors>Quiroga AG</pubmed_authors><pubmed_authors>Felipe-Abrio B</pubmed_authors><pubmed_authors>Carnero A</pubmed_authors><pubmed_authors>Espinosa-Sanchez A</pubmed_authors><pubmed_authors>Garcia-Heredia JM</pubmed_authors><pubmed_authors>Navas LE</pubmed_authors></additional><is_claimable>false</is_claimable><name>New markers for human ovarian cancer that link platinum resistance to the cancer stem cell phenotype and define new therapeutic combinations and diagnostic tools.</name><description>&lt;h4>Background&lt;/h4>Ovarian cancer is the leading cause of gynecologic cancer-related death, due in part to a late diagnosis and a high rate of recurrence. Primary and acquired platinum resistance is related to a low response probability to subsequent lines of treatment and to a poor survival. Therefore, a comprehensive understanding of the mechanisms that drive platinum resistance is urgently needed.&lt;h4>Methods&lt;/h4>We used bioinformatics analysis of public databases and RT-qPCR to quantitate the relative gene expression profiles of ovarian tumors. Many of the dysregulated genes were cancer stem cell (CSC) factors, and we analyzed its relation to therapeutic resistance in human primary tumors. We also performed clustering and in vitro analyses of therapy cytotoxicity in tumorspheres.&lt;h4>Res</description><dates><release>2019-01-01T00:00:00Z</release><publication>2019 Jun</publication><modification>2026-05-07T12:19:36.007Z</modification><creation>2025-05-18T11:02:19.876Z</creation></dates><accession>S-EPMC6547556</accession><cross_references><pubmed>31159852</pubmed><doi>10.1186/s13046-019-1245-5</doi></cross_references></HashMap>