ArticleOncotarget2017
Targeting the HGF/c-MET pathway: stromal remodelling in pancreatic cancer.
Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
34 citing papers in PubMed, 55 citations in OpenAlex.
- Engineering exosomes with iRGD for targeted RNAi therapy against pancreatic cancer mediated by long non-coding RNA PLBD1-AS1.PloS one · 2026Article
- Comprehensive bioinformatics analysis of selected germline variants of uncertain significance identified in a cohort of Sri Lankan hereditary breast cancer patients.Human genomics · 2025Article
- C-reactive protein is a prognostic biomarker in pancreatic ductal adenocarcinoma patients.Asia-Pacific journal of clinical oncology · 2025Article
- Topographic analysis of pancreatic cancer by TMA and digital spatial profiling reveals biological complexity with potential therapeutic implications.Scientific reports · 2024Article
- Article
- HGF/c-Met pathway inhibition combined with chemotherapy increases cytotoxic T-cell infiltration and inhibits pancreatic tumour growth and metastasis.Cancer letters · 2023Article
- New insights into the role of adipocytes in pancreatic cancer progression: paving the way towards novel therapeutic targets.Theranostics · 2023Review
- The anti-oncogenic effect of 17-DMAG via the inactivation of HSP90 and MET pathway in osteosarcoma cells.Oncology research · 2023Article
- Focal adhesion kinase priming in pancreatic cancer, altering biomechanics to improve chemotherapy.Biochemical Society transactions · 2022Article
- Small extracellular vesicles: from mediating cancer cell metastasis to therapeutic value in pancreatic cancer.Cell communication and signaling : CCS · 2022Review
- Metastatic phenotype and immunosuppressive tumour microenvironment in pancreatic ductal adenocarcinoma: Key role of the urokinase plasminogen activator (PLAU).Frontiers in immunology · 2022Article
- Pancreatic stellate cells - rising stars in pancreatic pathologies.Physiological research · 2021Review
- Role of Pancreatic Stellate Cell-Derived Exosomes in Pancreatic Cancer-Related Diabetes: A Novel Hypothesis.Cancers · 2021Review
- Roles for growth factors and mutations in metastatic dissemination.Biochemical Society transactions · 2021Review
- HGF/c-Met Inhibition as Adjuvant Therapy Improves Outcomes in an Orthotopic Mouse Model of Pancreatic Cancer.Cancers · 2021Article
- Oncogenic long intervening noncoding RNA Linc00284 promotes c-Met expression by sponging miR-27a in colorectal cancer.Oncogene · 2021Article
- The role of MET in chemotherapy resistance.Oncogene · 2021Review
- Targeting HGF/c-MET Axis in Pancreatic Cancer.International journal of molecular sciences · 2020Review
- Review
- Recent advances in understanding cancer-associated fibroblasts in pancreatic cancer.American journal of physiology. Cell physiology · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Stromal-tumor interactions in pancreatic cancer (PC) impact on treatment outcomes. Pancreatic stellate cells (PSCs) produce the collagenous stroma of PC and interact with cancer cells to facilitate disease progression. A candidate growth factor pathway that may mediate this interaction is the hepatocyte growth factor (HGF)/c-MET pathway. HGF is produced by PSCs and its receptor c-MET is expressed on pancreatic cancer cells. We studied the effects on PC progression of inhibiting the HGF/c-MET pathway in the presence and absence of a representative chemotherapeutic agent, gemcitabine. Using an orthotopic model of PC we have shown that "triple therapy" (inhibition of both HGF and c-MET combined with gemcitabine) resulted in the greatest reduction in tumor volume compared to each of the treatments alone or in dual combinations. Importantly, metastasis was virtually eliminated in mice receiving triple therapy. Our
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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.