<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>12(14)</volume><submitter>Jiang Y</submitter><pubmed_abstract>&lt;b>Rationale:&lt;/b> The overall clinical response to FGFR inhibitor (FGFRi) is far from satisfactory in cancer patients stratified by FGFR aberration, the current biomarker in clinical practice. A novel biomarker to evaluate the therapeutic response to FGFRi in a non-invasive and dynamic manner is thus greatly desired. &lt;b>Methods:&lt;/b> Six FGFR-aberrant cancer cell lines were used, including four FGFRi-sensitive ones (NCI-H1581, NCI-H716, RT112 and Hep3B) and two FGFRi-resistant ones (primary for NCI-H2444 and acquired for NCI-H1581/AR). Cell viability and tumor xenograft growth analyses were performed to evaluate FGFRi sensitivities, accompanied by corresponding &lt;sup>18&lt;/sup>F-fluorodeoxyglucose (&lt;sup>18&lt;/sup>F-FDG) uptake assay. mTOR/PLCγ/MEK-ERK signaling blockade by specific inhibitors or</pubmed_abstract><journal>Theranostics</journal><pagination>6395-6408</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC9475468</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>&lt;sup>18&lt;/sup>F-FDG PET as an imaging biomarker for the response to FGFR-targeted therapy of cancer cells via FGFR-initiated mTOR/HK2 axis.</pubmed_title><pmcid>PMC9475468</pmcid><pubmed_authors>Peng X</pubmed_authors><pubmed_authors>Liang S</pubmed_authors><pubmed_authors>Zeng Q</pubmed_authors><pubmed_authors>Jiang Q</pubmed_authors><pubmed_authors>Gao J</pubmed_authors><pubmed_authors>Ding J</pubmed_authors><pubmed_authors>Zhou X</pubmed_authors><pubmed_authors>Ai J</pubmed_authors><pubmed_authors>Huang R</pubmed_authors><pubmed_authors>Wang L</pubmed_authors><pubmed_authors>Jiang Y</pubmed_authors><pubmed_authors>Lin D</pubmed_authors><pubmed_authors>Feng H</pubmed_authors><pubmed_authors>Gao Y</pubmed_authors><pubmed_authors>Wan H</pubmed_authors><pubmed_authors>Zhou H</pubmed_authors></additional><is_claimable>false</is_claimable><name>&lt;sup>18&lt;/sup>F-FDG PET as an imaging biomarker for the response to FGFR-targeted therapy of cancer cells via FGFR-initiated mTOR/HK2 axis.</name><description>&lt;b>Rationale:&lt;/b> The overall clinical response to FGFR inhibitor (FGFRi) is far from satisfactory in cancer patients stratified by FGFR aberration, the current biomarker in clinical practice. A novel biomarker to evaluate the therapeutic response to FGFRi in a non-invasive and dynamic manner is thus greatly desired. &lt;b>Methods:&lt;/b> Six FGFR-aberrant cancer cell lines were used, including four FGFRi-sensitive ones (NCI-H1581, NCI-H716, RT112 and Hep3B) and two FGFRi-resistant ones (primary for NCI-H2444 and acquired for NCI-H1581/AR). Cell viability and tumor xenograft growth analyses were performed to evaluate FGFRi sensitivities, accompanied by corresponding &lt;sup>18&lt;/sup>F-fluorodeoxyglucose (&lt;sup>18&lt;/sup>F-FDG) uptake assay. mTOR/PLCγ/MEK-ERK signaling blockade by specific inhibitors or</description><dates><release>2022-01-01T00:00:00Z</release><publication>2022</publication><modification>2026-05-28T01:08:17.595Z</modification><creation>2025-04-19T22:46:41.419Z</creation></dates><accession>S-EPMC9475468</accession><cross_references><pubmed>36168616</pubmed><doi>10.7150/thno.74848</doi></cross_references></HashMap>