<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>29(24)</volume><submitter>Oza AM</submitter><pubmed_abstract>&lt;h4>Purpose&lt;/h4>Phosphatase and tensin homolog (PTEN) is a tumor suppressor gene, and loss of function mutations are common and appear to be important in the pathogenesis of endometrial carcinomas. Loss of PTEN causes deregulated phosphatidylinositol-3 kinase/serine-threonine kinase/mammalian target of rapamycin (PI3K/Akt/mTOR) signaling which may provide neoplastic cells with a selective survival advantage by enhancing angiogenesis, protein translation, and cell cycle progression. Temsirolimus, an ester derivative of rapamycin that inhibits mTOR, was evaluated in this setting.&lt;h4>Patients and methods&lt;/h4>Sequential phase II studies evaluated single-agent activity of temsirolimus in women with recurrent or metastatic chemotherapy-naive or chemotherapy-treated endometrial cancer. Temsirolim</pubmed_abstract><journal>Journal of clinical oncology : official journal of the American Society of Clinical Oncology</journal><pagination>3278-85</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC3158598</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Phase II study of temsirolimus in women with recurrent or metastatic endometrial cancer: a trial of the NCIC Clinical Trials Group.</pubmed_title><pmcid>PMC3158598</pmcid><pubmed_authors>Ivy P</pubmed_authors><pubmed_authors>Oza AM</pubmed_authors><pubmed_authors>Eisenhauer EA</pubmed_authors><pubmed_authors>Biagi J</pubmed_authors><pubmed_authors>Tsao MS</pubmed_authors><pubmed_authors>Kamel-Reid S</pubmed_authors><pubmed_authors>Hoskins PJ</pubmed_authors><pubmed_authors>Ghatage P</pubmed_authors><pubmed_authors>Provencher DM</pubmed_authors><pubmed_authors>Gotlieb WH</pubmed_authors><pubmed_authors>Dancey JE</pubmed_authors><pubmed_authors>Mackay HJ</pubmed_authors><pubmed_authors>Mazurka J</pubmed_authors><pubmed_authors>Tonkin KS</pubmed_authors><pubmed_authors>Sederias J</pubmed_authors><pubmed_authors>Elit L</pubmed_authors></additional><is_claimable>false</is_claimable><name>Phase II study of temsirolimus in women with recurrent or metastatic endometrial cancer: a trial of the NCIC Clinical Trials Group.</name><description>&lt;h4>Purpose&lt;/h4>Phosphatase and tensin homolog (PTEN) is a tumor suppressor gene, and loss of function mutations are common and appear to be important in the pathogenesis of endometrial carcinomas. Loss of PTEN causes deregulated phosphatidylinositol-3 kinase/serine-threonine kinase/mammalian target of rapamycin (PI3K/Akt/mTOR) signaling which may provide neoplastic cells with a selective survival advantage by enhancing angiogenesis, protein translation, and cell cycle progression. Temsirolimus, an ester derivative of rapamycin that inhibits mTOR, was evaluated in this setting.&lt;h4>Patients and methods&lt;/h4>Sequential phase II studies evaluated single-agent activity of temsirolimus in women with recurrent or metastatic chemotherapy-naive or chemotherapy-treated endometrial cancer. Temsirolim</description><dates><release>2011-01-01T00:00:00Z</release><publication>2011 Aug</publication><modification>2025-06-01T12:16:45.2Z</modification><creation>2019-03-27T00:43:09Z</creation></dates><accession>S-EPMC3158598</accession><cross_references><pubmed>21788564</pubmed><doi>10.1200/JCO.2010.34.1578</doi><doi>10.1200/jco.2010.34.1578</doi></cross_references></HashMap>