{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"volume":["12(14)"],"submitter":["Jiang Y"],"pubmed_abstract":["<b>Rationale:</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. <b>Methods:</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 <sup>18</sup>F-fluorodeoxyglucose (<sup>18</sup>F-FDG) uptake assay. mTOR/PLCγ/MEK-ERK signaling blockade by specific inhibitors or"],"journal":["Theranostics"],"pagination":["6395-6408"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC9475468"],"repository":["biostudies-literature"],"pubmed_title":["<sup>18</sup>F-FDG PET as an imaging biomarker for the response to FGFR-targeted therapy of cancer cells via FGFR-initiated mTOR/HK2 axis."],"pmcid":["PMC9475468"],"pubmed_authors":["Peng X","Liang S","Zeng Q","Jiang Q","Gao J","Ding J","Zhou X","Ai J","Huang R","Wang L","Jiang Y","Lin D","Feng H","Gao Y","Wan H","Zhou H"],"additional_accession":[]},"is_claimable":false,"name":"<sup>18</sup>F-FDG PET as an imaging biomarker for the response to FGFR-targeted therapy of cancer cells via FGFR-initiated mTOR/HK2 axis.","description":"<b>Rationale:</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. <b>Methods:</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 <sup>18</sup>F-fluorodeoxyglucose (<sup>18</sup>F-FDG) uptake assay. mTOR/PLCγ/MEK-ERK signaling blockade by specific inhibitors or","dates":{"release":"2022-01-01T00:00:00Z","publication":"2022","modification":"2026-05-28T01:08:17.595Z","creation":"2025-04-19T22:46:41.419Z"},"accession":"S-EPMC9475468","cross_references":{"pubmed":["36168616"],"doi":["10.7150/thno.74848"]}}