ArticleCancer prevention research (Philadelphia, Pa.)2010
Genome-wide catalogue of chromosomal aberrations in barrett's esophagus and esophageal adenocarcinoma: a high-density single nucleotide polymorphism array analysis.
Article in Cancer prevention research (Philadelphia, Pa.), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.
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Who cites it
49 citing papers in PubMed, 105 citations in OpenAlex.
- Discovery of therapeutic targets in cancer using chromatin accessibility and transcriptomic data.Cell systems · 2024Article
- Molecular Pathology of Gastroesophageal Cancer.Clinics in laboratory medicine · 2024Review
- A risk variant for Barrett's esophagus and esophageal adenocarcinoma at chr8p23.1 affects enhancer activity and implicates multiple gene targets.Human molecular genetics · 2022Article
- Multi-omic cross-sectional cohort study of pre-malignant Barrett's esophagus reveals early structural variation and retrotransposon activity.Nature communications · 2022Article
- Evolutionary dynamics in Barrett oesophagus: implications for surveillance, risk stratification and therapy.Nature reviews. Gastroenterology & hepatology · 2022Review
- Reframing How Physical Activity Reduces The Incidence of Clinically-Diagnosed Cancers: Appraising Exercise-Induced Immuno-Modulation As An Integral Mechanism.Frontiers in oncology · 2022Review
- KIF26B in the Prognosis and Immune Biomarking of Various Cancers: A Pan-Cancer Study.Journal of oncology · 2022Article
- Molecular Pathology of Gastroesophageal Cancer.Surgical pathology clinics · 2021Review
- Massively Parallel Sequencing of Esophageal Brushings Enables an Aneuploidy-Based Classification of Patients With Barrett's Esophagus.Gastroenterology · 2021Article
- MicroRNA-3613-3p functions as a tumor suppressor and represents a novel therapeutic target in breast cancer.Breast cancer research : BCR · 2021Article
- Recurring Translocations in Barrett's Esophageal Adenocarcinoma.Frontiers in genetics · 2021Article
- Review
- Ingested asbestos in filtered beer, in addition to occupational exposure, as a causative factor in oesophageal adenocarcinoma.British journal of cancer · 2019Review
- Detection of Mutations in Barrett's Esophagus Before Progression to High-Grade Dysplasia or Adenocarcinoma.Gastroenterology · 2018Article
- Identification of a WNT5A-Responsive Degradation Domain in the Kinesin Superfamily Protein KIF26B.Genes · 2018Article
- Evolution of Barrett's esophagus through space and time at single-crypt and whole-biopsy levels.Nature communications · 2018Article
- Knockdown of KIF26B inhibits breast cancer cell proliferation, migration, and invasion.OncoTargets and therapy · 2018Article
- Application of a multi-gene next-generation sequencing panel to a non-invasive oesophageal cell-sampling device to diagnose dysplastic Barrett's oesophagus.The journal of pathology. Clinical research · 2017Article
- Article
- Fragile sites in cancer: more than meets the eye.Nature reviews. Cancer · 2017Review
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
Abstract
To better understand the molecular mechanisms behind esophageal adenocarcinoma (EAC) tumorigenesis, we used high-density single nucleotide polymorphism arrays to profile chromosomal aberrations at each of the four sequential progression stages, Barrett's metaplasia (BM), low-grade dysplasia (LGD), high-grade dysplasia (HGD), and EAC, in 101 patients. We observed a significant trend toward increasing loss of chromosomes with higher progression stage. For BM, LGD, HGD, and EAC, respectively, the average numbers of chromosome arms with loss per sample were 0.30, 3.21, 7.70, and 11.90 (P for trend = 4.82 x 10(-7)), and the mean percentages of single nucleotide polymorphisms with allele loss were 0.1%, 1.8%, 6.6%, and 17.2% (P for trend = 2.64 x 10(-6)). In LGD, loss of 3p14.2 (68.4%) and 16q23.1 (47.4%) was limited to narrow regions within the FHIT (3p14.2) and WWOX (16q23.1) genes, whereas loss of 9p21 (68.4%) occurred in larger regions. A significant increase in the loss of other chromosomal regions was seen in HGD and EAC. Loss of 17p (47.6%) was one of the most frequent events in EAC. Many recurrent small regions of chromosomal loss disrupted single genes, including FHIT, WWOX, RUNX1, KIF26B, MGC48628, PDE4D, C20orf133, GMDS, DMD, and PARK2, most of which are common fragile site regions in the human genome. However, RUNX1 at 21q22 seemed to be a potential tumor suppressor gene in EAC. Amplifications were less frequent than losses and mostly occurred in EAC. 8q24 (containing Myc) and 8p23.1 (containing CTSB) were the two most frequently amplified regions. In addition, a significant trend toward increasing amplification was associated with higher progression stage.
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