<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>8</volume><submitter>Xu G</submitter><pubmed_abstract>&lt;b>Aim:&lt;/b> The current study aims to investigate the critical role of the focal adhesion kinase (FAK) oncogenic signaling pathway in mediating drug resistance to epidermal growth factor receptor (EGFR)-tyrosine kinase inhibitors (EGFR-TKIs) and evaluate the potential of two novel FAK inhibitors, 10k and 10l, as therapeutic strategies for drug resistant non-small cell lung cancer (NSCLC). &lt;b>Methods:&lt;/b> EGFR-TKI resistance in NSCLC cells was developed via stepwise drug selection. Kinases/polymerase chain reaction (PCR) arrays identified key resistance determinants, while reverse transcription quantitative polymerase chain reaction (RT-qPCR), enzyme-linked immunosorbent assay (ELISA), and immunohistochemistry evaluated FAK messenger RNA and phosphorylation levels. Antitumor activities were</pubmed_abstract><journal>Cancer drug resistance (Alhambra, Calif.)</journal><pagination>57</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC12635985</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Novel FAK inhibitors suppress tumor growth and reverse EGFR-TKI resistance in non-small cell lung cancer.</pubmed_title><pmcid>PMC12635985</pmcid><pubmed_authors>Pecoraro C</pubmed_authors><pubmed_authors>Cavazzoni A</pubmed_authors><pubmed_authors>Diana P</pubmed_authors><pubmed_authors>Assaraf YG</pubmed_authors><pubmed_authors>Vahabi M</pubmed_authors><pubmed_authors>Giovannetti E</pubmed_authors><pubmed_authors>Tiseo M</pubmed_authors><pubmed_authors>Lagrasta CAM</pubmed_authors><pubmed_authors>Xu G</pubmed_authors><pubmed_authors>Carbone D</pubmed_authors><pubmed_authors>Deng D</pubmed_authors><pubmed_authors>Zucali PA</pubmed_authors><pubmed_authors>Cascioferro SM</pubmed_authors><pubmed_authors>Avan A</pubmed_authors><pubmed_authors>Fiuji H</pubmed_authors><pubmed_authors>Peters GJ</pubmed_authors></additional><is_claimable>false</is_claimable><name>Novel FAK inhibitors suppress tumor growth and reverse EGFR-TKI resistance in non-small cell lung cancer.</name><description>&lt;b>Aim:&lt;/b> The current study aims to investigate the critical role of the focal adhesion kinase (FAK) oncogenic signaling pathway in mediating drug resistance to epidermal growth factor receptor (EGFR)-tyrosine kinase inhibitors (EGFR-TKIs) and evaluate the potential of two novel FAK inhibitors, 10k and 10l, as therapeutic strategies for drug resistant non-small cell lung cancer (NSCLC). &lt;b>Methods:&lt;/b> EGFR-TKI resistance in NSCLC cells was developed via stepwise drug selection. Kinases/polymerase chain reaction (PCR) arrays identified key resistance determinants, while reverse transcription quantitative polymerase chain reaction (RT-qPCR), enzyme-linked immunosorbent assay (ELISA), and immunohistochemistry evaluated FAK messenger RNA and phosphorylation levels. Antitumor activities were</description><dates><release>2025-01-01T00:00:00Z</release><publication>2025</publication><modification>2026-06-05T17:33:10.865Z</modification><creation>2026-05-19T03:11:52.53Z</creation></dates><accession>S-EPMC12635985</accession><cross_references><pubmed>41281943</pubmed><doi>10.20517/cdr.2025.139</doi></cross_references></HashMap>