ArticleNeoplasia (New York, N.Y.)2006
c-myc amplification is frequent in esophageal adenocarcinoma and correlated with the upregulation of VEGF-A expression.
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 17 papers.
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Who cites it
17 citing papers in PubMed, 39 citations in OpenAlex.
- WEE1 stabilizes MYC to promote therapeutic resistance in esophageal adenocarcinoma.Cancer letters · 2026Article
- Association of HER2 amplification or overexpression with overall survival in advanced upper gastrointestinal adenocarcinomas.BJC reports · 2025Article
- Oxidative stress-induced endothelial cells-derived exosomes accelerate skin flap survival through Lnc NEAT1-mediated promotion of endothelial progenitor cell function.Stem cell research & therapy · 2022Article
- Comparative genomic analysis of esophageal squamous cell carcinoma and adenocarcinoma: New opportunities towards molecularly targeted therapy.Acta pharmaceutica Sinica. B · 2022Review
- Histone Modifying Enzymes as Targets for Therapeutic Intervention in Oesophageal Adenocarcinoma.Cancers · 2021Review
- Therapeutic Potential of the Cyclin-Dependent Kinase Inhibitor Flavopiridol on c-Myc Overexpressing Esophageal Cancer.Frontiers in pharmacology · 2021Article
- Synthesis of Combretastatin A-4 and 3'-Aminocombretastatin A-4 derivatives with Aminoacid Containing Pendants and Study of Their Interaction with Tubulin and as Downregulators of the VEGF, hTERT and c-Myc Gene Expression.Molecules (Basel, Switzerland) · 2020Article
- Long non-coding RNA PVT1 interacts with MYC and its downstream molecules to synergistically promote tumorigenesis.Cellular and molecular life sciences : CMLS · 2019Review
- Transcriptional upregulation of c-MYC by AXL confers epirubicin resistance in esophageal adenocarcinoma.Molecular oncology · 2018Article
- The role of angiogenesis in Group 3 medulloblastoma pathogenesis and survival.Neuro-oncology · 2017Article
- Inhibition of Notch signaling enhances transdifferentiation of the esophageal squamous epithelium towards a Barrett's-like metaplasia via KLF4.Cell cycle (Georgetown, Tex.) · 2014Article
- Signaling pathways in the molecular pathogenesis of adenocarcinomas of the esophagus and gastroesophageal junction.Cancer biology & therapy · 2013Review
- Expression of CIP2A in renal cell carcinomas correlates with tumour invasion, metastasis and patients' survival.British journal of cancer · 2011Article
- The role of oncogenes in gastrointestinal cancer.Gastrointestinal cancer research : GCR · 2010Article
- Modulating the functional contributions of c-Myc to the human endothelial cell cyclic strain response.Journal of vascular research · 2010Article
- Neoplasia: the second decade.Neoplasia (New York, N.Y.) · 2008Article
- Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundDeregulation of c-myc plays a major role in the carcinogenesis of human malignancies. We investigated the amplification of the c-myc gene in a surgical series of Barrett cancers.
methodsPrimary resected esophageal (Barrett) adenocarcinomas (n = 84) were investigated for c-myc amplification using chromogene in situ hybridization. Tumor samples were assembled in a tissue microarray. c-myc gene dosage was correlated with clinicopathologic parameters, including the survival and gene expression of cyclooxygenases (COX-1 and COX-2) and proangiogenic growth factors (VEGF-A and VEGF-C).
resultsThe majority (70 of 84; 83.3%) exhibited amplification of the c-myc gene. There were low-level amplifications in 63 (75.0%) cases and high-level amplifications in 7 (8.3%) cases. No amplification was found in 14 (16.7%) cases. Tumors without c-myc amplification had lower VEGF-A, VEGF-C, and COX-2 expression levels than tumors with low-level and high-level c-myc amplification (statistically significant for VEGF-A; P = .0348). c-myc amplification was not correlated with clinicopathological parameters or survival. Only diffuse and mixed-type tumors, according to Lauren classification, exhibited c-myc amplifications more frequently (P = .0466).
conclusionsAmplifications of the c-myc gene are frequent in Barrett cancer. c-myc may be involved in the regulation of angiogenesis.
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