<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Liu S</submitter><funding>Spexis Ltd</funding><funding>The National Cancer Institute through MD Anderson Cancer Center Support Grant</funding><funding>Victor and Anna Mae Beghini Charitable Foundation</funding><funding>A. Ray Weeks, Jr. Foundation</funding><pagination>62</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC10245436</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>25(1)</volume><pubmed_abstract>&lt;h4>Background&lt;/h4>Although trastuzumab and other HER2-targeted therapies have significantly improved survival in patients with HER2 overexpressed or amplified (HER2+) breast cancer, a significant proportion of patients do not respond or eventually develop clinical resistance. Strategies to reverse trastuzumab resistance remain a high clinical priority. We were the first to report the role of CXCR4 in trastuzumab resistance. The present study aims to explore the therapeutic potential of targeting CXCR4 and better understand the associated mechanisms.&lt;h4>Methods&lt;/h4>Immunofluorescent staining, confocal microscopy analysis, and immunoblotting were used to analyze CXCR4 expression. BrdU incorporation assays and flow cytometry were used to analyze dynamic CXCR4 expression. Three-dimensional co</pubmed_abstract><journal>Breast cancer research : BCR</journal><pubmed_title>Targeting CXCR4 abrogates resistance to trastuzumab by blocking cell cycle progression and synergizes with docetaxel in breast cancer treatment.</pubmed_title><pmcid>PMC10245436</pmcid><funding_grant_id>P30CA016672</funding_grant_id><pubmed_authors>Marchese A</pubmed_authors><pubmed_authors>Xie SM</pubmed_authors><pubmed_authors>Hanker AB</pubmed_authors><pubmed_authors>Neelapu SS</pubmed_authors><pubmed_authors>Hanash S</pubmed_authors><pubmed_authors>Nguyen N</pubmed_authors><pubmed_authors>Arteaga CL</pubmed_authors><pubmed_authors>Liu S</pubmed_authors><pubmed_authors>Zimmermann J</pubmed_authors><pubmed_authors>Tripathy D</pubmed_authors><pubmed_authors>Gagea M</pubmed_authors><pubmed_authors>Liu W</pubmed_authors><pubmed_authors>Singareeka Raghavendra A</pubmed_authors><pubmed_authors>Chu F</pubmed_authors><pubmed_authors>Yang-Kolodji G</pubmed_authors></additional><is_claimable>false</is_claimable><name>Targeting CXCR4 abrogates resistance to trastuzumab by blocking cell cycle progression and synergizes with docetaxel in breast cancer treatment.</name><description>&lt;h4>Background&lt;/h4>Although trastuzumab and other HER2-targeted therapies have significantly improved survival in patients with HER2 overexpressed or amplified (HER2+) breast cancer, a significant proportion of patients do not respond or eventually develop clinical resistance. Strategies to reverse trastuzumab resistance remain a high clinical priority. We were the first to report the role of CXCR4 in trastuzumab resistance. The present study aims to explore the therapeutic potential of targeting CXCR4 and better understand the associated mechanisms.&lt;h4>Methods&lt;/h4>Immunofluorescent staining, confocal microscopy analysis, and immunoblotting were used to analyze CXCR4 expression. BrdU incorporation assays and flow cytometry were used to analyze dynamic CXCR4 expression. Three-dimensional co</description><dates><release>2023-01-01T00:00:00Z</release><publication>2023 Jun</publication><modification>2025-04-27T02:20:35.319Z</modification><creation>2025-02-19T04:34:01.621Z</creation></dates><accession>S-EPMC10245436</accession><cross_references><pubmed>37280713</pubmed><doi>10.1186/s13058-023-01665-w</doi></cross_references></HashMap>