<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>15(6)</volume><submitter>Lu H</submitter><pubmed_abstract>There is a paucity of comprehensive knowledge pertaining to the underlying mechanisms leading to gefitinib resistance in individuals diagnosed NSCLC harboring EGFR-sensitive mutations who inevitably develop resistance to gefitinib treatment within six months to one year. In our preceding investigations, we have noted a marked upregulation of IGFBP2 in the neoplastic tissues of NSCLC, predominantly in the periphery of the tissue, implying its plausible significance in NSCLC. Consequently, in the current research, we delved into the matter and ascertained the molecular mechanisms that underlie the participation of IGFBP2 in the emergence of gefitinib resistance in NSCLC cells. Firstly, the expression of IGFBP2 in the bronchoalveolar lavage fluid and lung cancer tissues of 20 NSCLC patients w</pubmed_abstract><journal>Cell death &amp; disease</journal><pagination>447</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC11199710</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>IGFBP2/ITGA5 promotes gefitinib resistance via activating STAT3/CXCL1 axis in non-small cell lung cancer.</pubmed_title><pmcid>PMC11199710</pmcid><pubmed_authors>Zheng Y</pubmed_authors><pubmed_authors>Zhu J</pubmed_authors><pubmed_authors>Lu H</pubmed_authors><pubmed_authors>Wang S</pubmed_authors><pubmed_authors>Zhang H</pubmed_authors><pubmed_authors>Zhou W</pubmed_authors><pubmed_authors>Zhang L</pubmed_authors><pubmed_authors>Ai J</pubmed_authors></additional><is_claimable>false</is_claimable><name>IGFBP2/ITGA5 promotes gefitinib resistance via activating STAT3/CXCL1 axis in non-small cell lung cancer.</name><description>There is a paucity of comprehensive knowledge pertaining to the underlying mechanisms leading to gefitinib resistance in individuals diagnosed NSCLC harboring EGFR-sensitive mutations who inevitably develop resistance to gefitinib treatment within six months to one year. In our preceding investigations, we have noted a marked upregulation of IGFBP2 in the neoplastic tissues of NSCLC, predominantly in the periphery of the tissue, implying its plausible significance in NSCLC. Consequently, in the current research, we delved into the matter and ascertained the molecular mechanisms that underlie the participation of IGFBP2 in the emergence of gefitinib resistance in NSCLC cells. Firstly, the expression of IGFBP2 in the bronchoalveolar lavage fluid and lung cancer tissues of 20 NSCLC patients w</description><dates><release>2024-01-01T00:00:00Z</release><publication>2024 Jun</publication><modification>2025-04-26T22:39:26.225Z</modification><creation>2025-04-06T17:17:53.264Z</creation></dates><accession>S-EPMC11199710</accession><cross_references><pubmed>38918360</pubmed><doi>10.1038/s41419-024-06843-y</doi></cross_references></HashMap>