<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>46(7)</volume><submitter>Sutherland L</submitter><pubmed_abstract>Estrogen receptor-positive (ER+) breast cancer is common among postmenopausal women and is frequently treated with Letrozole, which inhibits aromatase from synthesizing estrogen from androgens. Decreased estrogen slows the growth of tumors and can be an effective treatment. The increase in Letrozole resistance poses a unique problem for patients. To better understand the underlying molecular mechanism(s) of Letrozole resistance, we reanalyzed transcriptomic data by comparing individuals who responded to Letrozole therapy (responders) to those who were resistant to treatment (non-responders). We identified &lt;i>SOX11&lt;/i> and &lt;i>S100A9&lt;/i> as two significant differentially expressed genes (DEGs) between these patient cohorts, with "PLK1 signaling events" being the most significant signaling pa</pubmed_abstract><journal>Current issues in molecular biology</journal><pagination>7114-7133</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC11275280</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Secondary Analysis of Human Bulk RNA-Seq Dataset Suggests Potential Mechanisms for Letrozole Resistance in Estrogen-Positive (ER+) Breast Cancer.</pubmed_title><pmcid>PMC11275280</pmcid><pubmed_authors>Lang J</pubmed_authors><pubmed_authors>Pickett BE</pubmed_authors><pubmed_authors>Sutherland L</pubmed_authors><pubmed_authors>Gonzalez-Juarbe N</pubmed_authors></additional><is_claimable>false</is_claimable><name>Secondary Analysis of Human Bulk RNA-Seq Dataset Suggests Potential Mechanisms for Letrozole Resistance in Estrogen-Positive (ER+) Breast Cancer.</name><description>Estrogen receptor-positive (ER+) breast cancer is common among postmenopausal women and is frequently treated with Letrozole, which inhibits aromatase from synthesizing estrogen from androgens. Decreased estrogen slows the growth of tumors and can be an effective treatment. The increase in Letrozole resistance poses a unique problem for patients. To better understand the underlying molecular mechanism(s) of Letrozole resistance, we reanalyzed transcriptomic data by comparing individuals who responded to Letrozole therapy (responders) to those who were resistant to treatment (non-responders). We identified &lt;i>SOX11&lt;/i> and &lt;i>S100A9&lt;/i> as two significant differentially expressed genes (DEGs) between these patient cohorts, with "PLK1 signaling events" being the most significant signaling pa</description><dates><release>2024-01-01T00:00:00Z</release><publication>2024 Jul</publication><modification>2026-04-21T03:25:11.545Z</modification><creation>2025-04-19T13:11:42.988Z</creation></dates><accession>S-EPMC11275280</accession><cross_references><pubmed>39057065</pubmed><doi>10.3390/cimb46070424</doi></cross_references></HashMap>