ArticleMolecular cancer therapeutics2017
Dual Inhibition of Hedgehog and c-Met Pathways for Pancreatic Cancer Treatment.
Article in Molecular cancer therapeutics, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
18 citing papers in PubMed, 58 citations in OpenAlex.
- Hepatocyte growth factor/c-Met signaling axis in human diseases: Mechanistic insights and therapeutic potential.Journal of cell communication and signaling · 2026Review
- Harnessing the power of cancer-associated fibroblasts to revolutionize pancreatic cancer treatment.Cancer biology & medicine · 2025Review
- Molecular mechanism of genetic, epigenetic, and metabolic alteration in lung cancer.Medical oncology (Northwood, London, England) · 2025Review
- Exosomal miRNA 16-5p/29a-3p from pancreatic cancer induce adipose atrophy by inhibiting adipogenesis and promoting lipolysis.iScience · 2024Article
- Pancreatic Cancer Treatment Targeting the HGF/c-MET Pathway: The MEK Inhibitor Trametinib.Cancers · 2024Review
- Targeting the hedgehog pathway in MET mutation cancers and its effects on cells associated with cancer development.Cell communication and signaling : CCS · 2023Review
- CLDN18.2 BiTE Engages Effector and Regulatory T Cells for Antitumor Immune Response in Preclinical Models of Pancreatic Cancer.Gastroenterology · 2023Article
- Design, Synthesis, and Evaluation of New Mesenchymal-Epithelial Transition Factor (c-Met) Kinase Inhibitors with Dual Chiral Centers.Molecules (Basel, Switzerland) · 2022Article
- Molecular signatures of tumor progression in pancreatic adenocarcinoma identified by energy metabolism characteristics.BMC cancer · 2022Article
- Combinational blockade of MET and PD-L1 improves pancreatic cancer immunotherapeutic efficacy.Journal of experimental & clinical cancer research : CR · 2021Article
- The tumor microenvironment in pancreatic ductal adenocarcinoma: current perspectives and future directions.Cancer metastasis reviews · 2021Review
- Review
- Lidocaine suppresses the malignant behavior of gastric cancer cells via the c-Met/c-Src pathway.Experimental and therapeutic medicine · 2021Article
- The role of MET in chemotherapy resistance.Oncogene · 2021Review
- Phase 1 trial of Vismodegib and Erlotinib combination in metastatic pancreatic cancer.Pancreatology : official journal of the International Association of Pancreatology (IAP) ... [et al.] · 2020Article
- Strategies in Developing Immunotherapy for Pancreatic Cancer: Recognizing and Correcting Multiple Immune "Defects" in the Tumor Microenvironment.Journal of clinical medicine · 2019Review
- Function of the c-Met receptor tyrosine kinase in carcinogenesis and associated therapeutic opportunities.Molecular cancer · 2018Review
- Pancreatic Cancer: Molecular Characterization, Clonal Evolution and Cancer Stem Cells.Biomedicines · 2017Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 1 institution in 2 countries.
Funding
Abstract
Pancreatic ductal adenocarcinoma (PDAC) is one of the most chemotherapy- and radiotherapy-resistant tumors. The c-Met and Hedgehog (Hh) pathways have been shown previously by our group to be key regulatory pathways in the primary tumor growth and metastases formation. Targeting both the HGF/c-Met and Hh pathways has shown promising results in preclinical studies; however, the benefits were not readily translated into clinical trials with PDAC patients. In this study, utilizing mouse models of PDAC, we showed that inhibition of either HGF/c-Met or Hh pathways sensitize the PDAC tumors to gemcitabine, resulting in decreased primary tumor volume as well as significant reduction of metastatic tumor burden. However, prolonged treatment of single HGF/c-Met or Hh inhibitor leads to resistance to these single inhibitors, likely because the single c-Met treatment leads to enhanced expression of Shh, and vice versa. Targeting both the HGF/c-Met and Hh pathways simultaneously overcame the resistance to the single-inhibitor treatment and led to a more potent antitumor effect in combination with the chemotherapy treatment.
Indexed as
Identifiers
What OpenQuestion holds
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.