ArticleNeoplasia (New York, N.Y.)2006
Inhibition of c-Met as a therapeutic strategy for esophageal adenocarcinoma.
Article in Neoplasia (New York, N.Y.), 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.
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
19 citing papers in PubMed, 1 synthesis or guideline pooled it, 36 citations in OpenAlex.
- Clinical and Prognostic Implications ofDisease markers · 2020Pooled it
- Non-muscle myosin heavy chain IIA regulates cell morphology, stress fibre structure, and cell migration in FLO-1 oesophageal adenocarcinoma cells.Human cell · 2025Article
- Development of a contacting transwell co-culture system for theFrontiers in cell and developmental biology · 2023Article
- A novel gene signature based on the hub genes of COVID-19 predicts the prognosis of idiopathic pulmonary fibrosis.Frontiers in pharmacology · 2022Article
- Radiosensitizing effect of c-Met kinase inhibitor BPI-9016M in esophageal squamous cell carcinoma cellsAnnals of translational medicine · 2021Article
- Article
- EGFR family and cMet expression profiles and prognostic significance in esophagogastric adenocarcinoma.Journal of gastrointestinal oncology · 2016Article
- Small molecule inhibitor of c-Met (PHA665752) suppresses the growth of ovarian cancer cells and reverses cisplatin resistance.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016Article
- Study of critical role of c-Met and its inhibitor SU11274 in colorectal carcinoma.Medical oncology (Northwood, London, England) · 2013Article
- Barrett's Esophagus: A Review of Biology and Therapeutic Approaches.Gastrointestinal cancer research : GCR · 2012Article
- Targeted therapy in the management of advanced gastric cancer: are we making progress in the era of personalized medicine?The oncologist · 2012Article
- Coexpression of activated c-Met and death receptor 5 predicts better survival in colorectal carcinoma.The American journal of pathology · 2011Article
- Inhibition of the MET Receptor Tyrosine Kinase as a Novel Therapeutic Strategy in Medulloblastoma.Translational oncology · 2010Article
- Article
- Barrett's oesophagus: an ideal model to study cancer genetics.Human genetics · 2009Review
- Tolfenamic acid inhibits esophageal cancer through repression of specificity proteins and c-Met.Carcinogenesis · 2009Article
- Neoplasia: the second decade.Neoplasia (New York, N.Y.) · 2008Article
- Altered fibroblast growth factor receptor 4 stability promotes prostate cancer progression.Neoplasia (New York, N.Y.) · 2008Article
- Met expression is an independent prognostic risk factor in patients with oesophageal adenocarcinoma.British journal of cancer · 2008Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The hepatocyte growth factor (HGF) receptor c-Met is a tyrosine kinase receptor with established oncogenic properties. We have previously shown that c-Met is usually overexpressed in esophageal adenocarcinoma (EA), yet the implications of c-Met inhibition in EA remain unknown. Three c-Met-overexpressing EA cell lines (Seg-1, Bic-1, and Flo-1) were used to examine the effects of a c-Met-specific small molecule inhibitor (PHA665752) on cell viability, apoptosis, motility, invasion, and downstream signaling pathways. PHA665752 demonstrated dose-dependent inhibition of constitutive and/or HGF-induced phosphorylation of c-Met, which correlated with reduced cell viability and inhibition of extracellular regulated kinase 1/2 phosphorylation in all three EA cell lines. In contrast, PHA665752 induced apoptosis and reduced motility and invasion in only one EA cell line, Flo-1. Interestingly, Flo-1 was the only cell line in which phosphatidylinositol 3-kinase (PI3K)/Akt was induced following HGF stimulation. The PI3K inhibitor LY294002 produced effects equivalent to those of PHA665752 in these cells. We conclude that inhibition of c-Met may be a useful therapeutic strategy for EA. Factors other than receptor overexpression, such as c-Met-dependent PI3K/Akt signaling, may be predictive of an individual tumor's response to c-Met inhibition.
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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.