ReviewCurrent oncology reports2007
c-Met and hepatocyte growth factor: potential as novel targets in cancer therapy.
Review in Current oncology reports, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 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
61 citing papers in PubMed.
- Comparative analysis of whole-genome sequencing of tumor and cfDNA in a neuroblastoma patient: a case report.Frontiers in oncology · 2025Article
- Establishment of Stable Knockdown of MACC1 Oncogene in Patient-Derived Ovarian Cancer Organoids.Methods and protocols · 2024Article
- Prognostic value of PAX8 in small cell lung cancer.Heliyon · 2024Article
- Development of a novelEuropean journal of nuclear medicine and molecular imaging · 2024Article
- Successful Treatment with Crizotinib to Overcome Drug Resistance Possibly Due to Mesenchymal-epithelial Transition Amplification in a Lung Cancer Patient with the Echinoderm Microtubule-associated Protein-like 4-anaplastic Lymphoma Kinase Fusion Gene.Internal medicine (Tokyo, Japan) · 2023Article
- Design, Synthesis and Antitumor Activity of Novel Selenium-Containing Tepotinib Derivatives as Dual Inhibitors of c-Met and TrxR.Molecules (Basel, Switzerland) · 2023Article
- The impacts ofJournal of Cancer · 2023Article
- Advanced hepatocellular carcinoma with MET-amplified contained excellent response to crizotinib: a case report.Frontiers in oncology · 2023Article
- Hsa_circ_0005100 regulates tumorigenicity of colorectal carcinoma via miR-145-5p/MACC1 axis.Journal of clinical laboratory analysis · 2022Article
- Emerging Mechanisms and Treatment Progress on Liver Metastasis of Colorectal Cancer.OncoTargets and therapy · 2021Review
- Detection of colonic neoplasia in vivo using near-infrared-labeled peptide targeting cMet.Scientific reports · 2019Article
- Patient-derived xenograft models to optimize kidney cancer therapies.Translational andrology and urology · 2019Review
- Targeting Tyrosine kinases in Renal Cell Carcinoma: "New Bullets against Old Guys".International journal of molecular sciences · 2019Review
- MACC1 promotes angiogenesis in cholangiocarcinoma by upregulating VEGFA.OncoTargets and therapy · 2019Article
- Boswellia frereana suppresses HGF-mediated breast cancer cell invasion and migration through inhibition of c-Met signalling.Journal of translational medicine · 2018Article
- Renal Injury during Long-Term Crizotinib Therapy.International journal of molecular sciences · 2018Article
- BPI-9016M, a c-Met inhibitor, suppresses tumor cell growth, migration and invasion of lung adenocarcinoma via miR203-DKK1.Theranostics · 2018Article
- Potential role of HGF-PARP-1 signaling in invasion of ovarian cancer cells.International journal of clinical and experimental pathology · 2018Article
- TargetingChronic diseases and translational medicine · 2017Review
- Expression and mutational analysis of c-CBL and its relationship to the MET receptor in head and neck squamous cell carcinoma.Oncotarget · 2017Article
1 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
Abstract
Receptor tyrosine kinases have come to fruition as therapeutic targets in a variety of malignancies. In this group of targets, the c-Met receptor tyrosine kinase plays an important role in increased cell growth, reduced apoptosis, altered cytoskeletal function, increased metastasis, and other biologic changes. The ligand for c-Met is hepatocyte growth factor (HGF), also known as scatter factor. Met is overexpressed and mutated in a variety of malignancies, among which germline mutations are of particular interest. Most mutations of Met have been found in the juxtamembrane, the tyrosine kinase, and the semaphorin domain. Met gain-of-function mutations lead to deregulated or prolonged tyrosine kinase activity, which is instrumental to its transforming activity. This review summarizes the biologic functions regulated by Met and its structural requirements as well as related developments in targeted therapy. Treatment approaches, including antagonism of HGF binding to Met, targeting of RNA and the Met protein, and inhibition of the tyrosine kinase domain of Met, are highlighted. Targeting of the HGF/Met pathway, alone or in combination with standard therapies, is likely to improve current therapies in Met-dependent malignancies.
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17288874What 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.