ArticleDrug resistance updates : reviews and commentaries in antimicrobial and anticancer chemotherapy2024
Fibroblast growth factor receptor 1 inhibition suppresses pancreatic cancer chemoresistance and chemotherapy-driven aggressiveness.
Article in Drug resistance updates : reviews and commentaries in antimicrobial and anticancer chemotherapy, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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The trial behind it
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Who cites it
9 citing papers in PubMed, 8 citations in OpenAlex.
- Dual-energy CT extracellular volume fraction for predicting the chemotherapeutic response in pancreatic ductal adenocarcinoma.Cancer imaging : the official publication of the International Cancer Imaging Society · 2026Article
- Article
- Peptides in the Diagnosis and Treatment of Pancreatic Cancer and Other Pancreatic Diseases from Basic Research to Clinical Translation.Drug design, development and therapy · 2026Review
- Derazantinib enhances gemcitabine efficacy in PDAC by attenuating the NF-κB and MAPK pathways to suppress MUC5AC expression.Medical oncology (Northwood, London, England) · 2025Article
- FGF1-FGFR2 axis regulated by nuclear receptor RORγ represents an effective strategy in intrahepatic cholangiocarcinoma.Cell death discovery · 2025Article
- Targeting IRF7 to overcome gemcitabine resistance in pancreatic ductal adenocarcinoma.iScience · 2025Article
- High FGFR4 protein expression, but not FGFR1 or FGFR2, predicts poor prognosis in pancreatic ductal adenocarcinoma.BMC cancer · 2025Article
- Inhibition Effects and Mechanism Study of rAj-HRP30, a Recombinant Histidine-Rich Peptide fromInternational journal of molecular sciences · 2025Article
- Dual-Hit Strategy for Therapeutic Targeting of Pancreatic Cancer in Patient-Derived Xenograft Tumors.Clinical cancer research : an official journal of the American Association for Cancer Research · 2024Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
aimsPancreatic ductal adenocarcinoma (PDAC) is often intrinsically-resistant to standard-of-care chemotherapies such as gemcitabine. Acquired gemcitabine resistance (GemR) can arise from treatment of initially-sensitive tumors, and chemotherapy can increase tumor aggressiveness. We investigated the molecular mechanisms of chemoresistance and chemotherapy-driven tumor aggressiveness, which are understood incompletely.
methodsDifferential proteomic analysis was employed to investigate chemotherapy-driven chemoresistance drivers and responses of PDAC cells and patient-derived tumor xenografts (PDX) having different chemosensitivities. We also investigated the prognostic value of FGFR1 expression in the efficacy of selective pan-FGFR inhibitor (FGFRi)-gemcitabine combinations.
resultsQuantitative proteomic analysis of a highly-GemR cell line revealed fibroblast growth factor receptor 1 (FGFR1) as the highest-expressed receptor tyrosine kinase. FGFR1 knockdown or FGFRi co-treatment enhanced gemcitabine efficacy and decreased GemR marker expression, implicating FGFR1 in augmentation of GemR. FGFRi treatment reduced PDX tumor progression and prolonged survival significantly, even in highly-resistant tumors in which neither single-agent showed efficacy. Gemcitabine exacerbated aggressiveness of highly-GemR tumors, based upon proliferation and metastatic markers. Combining FGFRi with gemcitabine or gemcitabine+nab-paclitaxel reversed tumor aggressiveness and progression, and prolonged survival significantly. In multiple PDAC PDXs, FGFR1 expression correlated with intrinsic tumor gemcitabine sensitivity.
conclusionFGFR1 drives chemoresistance and tumor aggressiveness, which FGFRi can reverse.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.