ArticleMolecular cancer research : MCR2010
Deletion at fragile sites is a common and early event in Barrett's esophagus.
Article in Molecular cancer research : MCR, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 44 citations in OpenAlex.
- Insights into common fragile site instability: DNA replication challenges at DNA repeat sequences.Emerging topics in life sciences · 2023Article
- Enhancement of DNA hypomethylation alterations by gastric and bile acids promotes chromosomal instability in Barrett's epithelial cell line.Scientific reports · 2022Article
- Article
- Somatic whole genome dynamics of precancer in Barrett's esophagus reveals features associated with disease progression.Nature communications · 2022Article
- Complex structural rearrangements are present in high-grade dysplastic Barrett's oesophagus samples.BMC medical genomics · 2019Article
- Fragile sites in cancer: more than meets the eye.Nature reviews. Cancer · 2017Review
- Chromosomal breaks at FRA18C: association with reducedNPJ precision oncology · 2017Article
- Fragility Extraordinaire: Unsolved Mysteries of Chromosome Fragile Sites.Advances in experimental medicine and biology · 2017Review
- Mutational spectrum of Barrett's stem cells suggests paths to initiation of a precancerous lesion.Nature communications · 2016Article
- Genetic Insights in Barrett's Esophagus and Esophageal Adenocarcinoma.Gastroenterology · 2015Review
- The Barrett's Gland in Phenotype Space.Cellular and molecular gastroenterology and hepatology · 2015Review
- Are common fragile sites merely structural domains or highly organized "functional" units susceptible to oncogenic stress?Cellular and molecular life sciences : CMLS · 2014Review
- Interplay between genetic and epigenetic factors governs common fragile site instability in cancer.Cellular and molecular life sciences : CMLS · 2014Review
- Comparison of cancer-associated genetic abnormalities in columnar-lined esophagus tissues with and without goblet cells.Annals of surgery · 2014Article
- Targeting chemokine pathways in esophageal adenocarcinoma.Cell cycle (Georgetown, Tex.) · 2014Article
- Temporal and spatial evolution of somatic chromosomal alterations: a case-cohort study of Barrett's esophagus.Cancer prevention research (Philadelphia, Pa.) · 2014Article
- Article
- NSAIDs modulate clonal evolution in Barrett's esophagus.PLoS genetics · 2013Article
- Fragile site instability in Saccharomyces cerevisiae causes loss of heterozygosity by mitotic crossovers and break-induced replication.PLoS genetics · 2013Article
- Cancer in light of experimental evolution.Current biology : CB · 2012Review
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Authors and funding
11 authors at 5 institutions in 1 country.
Funding
Abstract
Barrett's esophagus (BE) is a premalignant intermediate to esophageal adenocarcinoma, which develops in the context of chronic inflammation and exposure to bile and acid. We asked whether there might be common genomic alterations that could be identified as potential clinical biomarker(s) for BE by whole genome profiling. We detected copy number alterations and/or loss of heterozygosity at 56 fragile sites in 20 patients with premalignant BE. Chromosomal fragile sites are particularly sensitive to DNA breaks and are frequent sites of rearrangement or loss in many human cancers. Seventy-eight percent of all genomic alterations detected by array-CGH were associated with fragile sites. Copy number losses in early BE were observed at particularly high frequency at FRA3B (81%), FRA9A/C (71.4%), FRA5E (52.4%), and FRA 4D (52.4%), and at lower frequencies in other fragile sites, including FRA1K (42.9%), FRAXC (42.9%), FRA 12B (33.3%), and FRA16D (33.3%). Due to the consistency of the region of copy number loss, we were able to verify these results by quantitative PCR, which detected the loss of FRA3B and FRA16D, in 83% and 40% of early molecular stage BE patients, respectively. Loss of heterozygosity in these cases was confirmed through pyrosequencing at FRA3B and FRA16D (75% and 70%, respectively). Deletion and genomic instability at FRA3B and other fragile sites could thus be a biomarker of genetic damage in BE patients and a potential biomarker of cancer risk.
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