ArticleOncogene2006
Genomic amplification of MET with boundaries within fragile site FRA7G and upregulation of MET pathways in esophageal adenocarcinoma.
Article in Oncogene, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 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
68 citing papers in PubMed, 1 synthesis or guideline pooled it, 160 citations in OpenAlex.
- Pooled it
- Crizotinib in Patients with Tumors with MET Amplification or Exon 14 Deletion: Results from the NCI-MATCH ECOG-ACRIN Trial (EAY131) Subprotocols C1 and C2.Clinical cancer research : an official journal of the American Association for Cancer Research · 2026Article
- Clinical and structural insights into concurrent EGFR and MET exon 14 skipping mutations in NSCLC: a multi-center series.Biomarker research · 2025Article
- The genomic landscape of esophageal squamous cell carcinoma cell lines.Cancer cell international · 2025Article
- The MET Oncogene: Thirty Years of Insights into Molecular Mechanisms Driving Malignancy.Pharmaceuticals (Basel, Switzerland) · 2024Article
- An Observatory for theCancers · 2023Review
- Article
- Bromodomain proteins: protectors against endogenous DNA damage and facilitators of genome integrity.Experimental & molecular medicine · 2021Review
- Article
- Spectrum of Mesenchymal-Epithelial Transition Aberrations and Potential Clinical Implications: Insights From Integrative Pancancer Analysis.Frontiers in oncology · 2020Article
- Upregulation of ITGBL1 predicts poor prognosis and promotes chemoresistance in ovarian cancer.Cancer biomarkers : section A of Disease markers · 2020Article
- Common fragile sites: protection and repair.Cell & bioscience · 2020Review
- Radiation-Induced DNA Damage Cooperates with Heterozygosity of TP53 and PTEN to Generate High-Grade Gliomas.Cancer research · 2019Article
- MM-131, a bispecific anti-Met/EpCAM mAb, inhibits HGF-dependent and HGF-independent Met signaling through concurrent binding to EpCAM.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- BLM prevents instability of structure-forming DNA sequences at common fragile sites.PLoS genetics · 2018Article
- Is Osteopontin a Friend or Foe of Cell Apoptosis in Inflammatory Gastrointestinal and Liver Diseases?International journal of molecular sciences · 2017Review
- c-Met Overexpression in Cervical Cancer, a Prognostic Factor and a Potential Molecular Therapeutic Target.American journal of clinical oncology · 2017Article
- Crizotinib targets in glioblastoma stem cells.Cancer medicine · 2017Article
- Correlation between c-Met and ALDH1 contributes to the survival and tumor-sphere formation of ALDH1 positive breast cancer stem cells and predicts poor clinical outcome in breast cancer.Genes & cancer · 2017Article
- MET expression and copy number status in clear-cell renal cell carcinoma: prognostic value and potential predictive marker.Oncotarget · 2017Article
8 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
11 authors at 2 institutions in 2 countries.
Funding
Abstract
Esophageal adenocarcinoma (EA) is characterized by a poor prognosis making the identification of clinically targetable proteins essential for improving patient outcome. We report the involvement of multiple alterations of the MET pathway in EA development and progression. Microarray analysis of Barrett's metaplasia, dysplasia, and EA revealed overexpression of the MET oncogene in EAs but only those with MET gene amplification. STS-amplification mapping revealed that the boundary of the MET amplicon in these EAs is defined by fragile site FRA7G. We also identified an amplicon at 11p13 that resulted in amplification and overexpression of CD44, a gene involved in MET autophosphorylation upon HGF stimulation. Tissue microarrays with phospho-MET-specific antibodies demonstrated a uniformly high abundance of MET activation in primary EA and cells metastatic to lymph nodes but to a lesser extent in a subset of metaplastic and dysplastic Barrett's samples. Increased expression of multiple genes in the MET pathway associated with invasive growth, for example, many MMPs and osteopontin, also was found in EAs. Treatment of EA-derived cell lines with geldanamycin, an inhibitor for tyrosine kinases including MET receptor kinase, reduced cell migration and induced EA cell apoptosis. The data indicate that upregulation of the MET pathway may contribute to the poor outcome of EA patients and that therapeutic agents targeting this pathway may help improve patient survival.
Indexed as
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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.