ArticleUpdate on cancer therapeutics2009
The MET axis as a therapeutic target.
Article in Update on cancer therapeutics, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 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
20 citing papers in PubMed, 34 citations in OpenAlex.
- Review
- Article
- BPI-9016M, a c-Met inhibitor, suppresses tumor cell growth, migration and invasion of lung adenocarcinoma via miR203-DKK1.Theranostics · 2018Article
- Potential Antitumor Activity of SIM-89 in Non-Small Cell Lung Cancer Cells.Yonsei medical journal · 2017Article
- Analysis of circulating adipokines in patients newly diagnosed with solid cancer: Associations with measures of adiposity and tumor characteristics.Oncology letters · 2017Article
- Article
- C. elegans and mutants with chronic nicotine exposure as a novel model of cancer phenotype.Cancer biology & therapy · 2016Article
- Novel Role for γ-Catenin in the Regulation of Cancer Cell Migration via the Induction of Hepatocyte Growth Factor Activator Inhibitor Type 1 (HAI-1).The Journal of biological chemistry · 2015Article
- Targeting met mediated epithelial-mesenchymal transition in the treatment of breast cancer.Clinical and translational medicine · 2014Article
- NPS-1034, a novel MET inhibitor, inhibits the activated MET receptor and its constitutively active mutants.Investigational new drugs · 2014Article
- Overexpression of MET is a new predictive marker for anti-EGFR therapy in metastatic colorectal cancer with wild-type KRAS.Cancer chemotherapy and pharmacology · 2014Article
- Dramatic antitumor effects of the dual MET/RON small-molecule inhibitor LY2801653 in non-small cell lung cancer.Cancer research · 2014Article
- Article
- c-Met inhibitors.Infectious agents and cancer · 2013Article
- Down-regulation of CMTM8 induces epithelial-to-mesenchymal transition-like changes via c-MET/extracellular signal-regulated kinase (ERK) signaling.The Journal of biological chemistry · 2012Article
- γ-Tocotrienol inhibits HGF-dependent mitogenesis and Met activation in highly malignant mammary tumour cells.Cell proliferation · 2011Article
- The Hepatocyte Growth Factor Receptor: Structure, Function and Pharmacological Targeting in Cancer.Current signal transduction therapy · 2011Article
- Medullary thyroid carcinoma: molecular signaling pathways and emerging therapies.Journal of thyroid research · 2011Article
- Receptor-tyrosine-kinase-targeted therapies for head and neck cancer.Journal of signal transduction · 2011Article
- Targeting the HGF/Met signalling pathway in cancer.European journal of cancer (Oxford, England : 1990) · 2010Review
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 at 2 institutions in 1 country.
Funding
Abstract
The MET receptor tyrosine kinase and its ligand hepatocyte growth factor (HGF) have been implicated in transformation of a variety of malignancies. Chronic or dysregulated activation of the MET/HGF pathway may lead to increased cell growth, invasion, angiogenesis, and metastasis, reduced apoptosis, altered cytoskeletal functions and other biological changes. It has been suggested that ligand activated MET stimulation can be sufficient for a transforming phenotype. In addition, amplification and activation mutations (germline and/or somatic) within the tyrosine kinase domain, juxtamembrane domain, or semaphorin domain have been identified for MET. MET gain-of-function mutations lead to either deregulated or prolonged tyrosine kinase activity, which are instrumental to its transforming activity. A number of therapeutic strategies targeting ligand-dependent activation or the kinase domain have been employed to inhibit MET. The different structural requirements for activation of signaling events and biological functions regulated by MET will be summarized. Therapeutic targets and current pre-clinical and clinical approaches will be described. Targeting the HGF/MET pathway, alone or in combination with standard therapies, is likely to improve present therapies in MET-dependent malignancies.
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.