Barrett’s esophagus: an overview of the molecular biology *

Aldulaimi, David; Jankowski, Janusz

doi:10.1046/j.1442-2050.1999.00043.x

Cited by 24 publications

(18 citation statements)

References 24 publications

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“…Mutations in tumor suppressor p53 gene have been detected in more than 25% of patients with Barrett’s metaplasia submitted to endoscopy and in more than 75% of Barrett’s adenocarcinomas (Aldulaimi and Jankowski 1999). …”

Section: Introductionmentioning

confidence: 99%

Analysis of R213R and 13494 g→a polymorphisms of the p53 gene in individuals with esophagitis, intestinal metaplasia of the cardia and Barrett’s Esophagus compared with a control group

Pilger

Lopez

Segal³

et al. 2007

HUGO J

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Protein p53 is the tumor suppressor involved in cell cycle control and apoptosis. There are several polymorphisms reported for p53 which can affect important regions involved in protein tumor suppressor activity. Amongst the polymorphisms described, R213R and 13949 g→a are rarely studied, with an estimate frequency not yet available for the Brazilian population. The purpose of this study was to investigate the genotype and allele frequencies and associations of these polymorphisms in a group of patients with altered esophageal tissue from South Brazil and compare with the frequency observed for a control population. A total of 35 patients for R213R and 45 for 13494 g→a polymorphisms analysis with gastroesophageal reflux disease (GERD) symptoms diagnosed by upper digestive endoscopy and confirmed by biopsy were studied. For both groups, 100 controls were used for comparison. Loss of heterozygosity (LOH) was also analyzed for a selected group of patients where normal and affected tissue was available. There was one patient with Barrett’s Esophagus (BE) showing LOH for R213R out of two heterozygous samples analyzed and two patients (esophagitis and BE) for 13494 g→a polymorphism. We also aimed to build a haplotype for both polymorphisms collectively analyzed with R27P polymorphism, previously reported by our group. There were no significant differences in allele and genotype distribution between patients and controls. Although using esophagitis, intestinal metaplasia of the cardia and BE samples, all non-neoplastic lesions, we can conclude that these sites do not represent genetic susceptibility markers for the development and early progression of GERD to BE and esophageal cancer. Additional studies are required in order to investigate other determiners of early premalignant lesions known to predispose to esophageal cancer.

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Section: Introductionmentioning

confidence: 99%

Analysis of R213R and 13494 g→a polymorphisms of the p53 gene in individuals with esophagitis, intestinal metaplasia of the cardia and Barrett’s Esophagus compared with a control group

Pilger

Lopez

Segal³

et al. 2007

HUGO J

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“…12 During the evolution of BE into adenocarcinoma, numerical and structural genomic changes are observed, thus indicating that a great number of gene variations may be involved in EAC. 16,17 The hypermethylation of CpG islands represents an important epigenetic mechanism for silencing tumor-suppressor genes and tumor associated genes during carcinogenesis. 18,19 Although molecular alterations have been recognized to be an important mechanism underlying the progression from SIM to EAC, 20,21 there has so far been limited data regarding either the genetic or epigenetic abnormalities in both SIM of BE with/without H. pylori infection.…”

mentioning

confidence: 99%

Effects of Helicobacter pylori infection on genetic instability, the aberrant CpG island methylation status and the cellular phenotype in Barrett's esophagus in a Japanese population

Moriichi

Watari

Das³

et al. 2008

Intl Journal of Cancer

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Genetic or epigenetic alterations in Barrett's esophagus (BE) with/without Helicobacter pylori (H. pylori) infection remain unclear. We examined the effects of H. pylori infection on genetic instability (GIN), the CpG island methylation status and a biomarker related to BE carcinogenesis. We analyzed 113 Japanese individuals with endoscopically suspected BE. The patients included, Group CLE (n 5 25): no specialized intestinal metaplasia (SIM) in a columnar lined epithelium (control); Group BE (n 5 88): all had SIM. Microsatellite instability and a loss of heterozygosity as GIN, the methylation status at hMLH1, E-cadherin, p16 and APC, and immunoreactivity using a monoclonal antibody (mAb) Das-1, which specifically reacts with BE, were evaluated. Nine additional patients with BE were prospectively followed up for 2 years after successful H. pylori eradication. The frequency of GIN, methylation at E-cadherin and APC, and mAb Das-1 reactivity in Group BE was significantly higher than that in Group CLE (p < 0.0001, p < 0.0001 and p < 0.005, and p < 0.0001, respectively). Furthermore, GIN, E-cadherin methylation and mAb Das-1 reactivity showed a significantly higher incidence in patients with H. pylori infection than in those without H. pylori infection (p < 0.01, p < 0.005, and p < 0.01, respectively). Interestingly, the patients from Group BE were observed to change to a stable state of molecular alterations in 60% for GIN, 42.9% for E-cadherin methylation and 55.6% for APC methylation, or a reduction of mAb Das-1 reactivity was noted in 25% following eradication. H. pylori infection may therefore affect these molecular alterations associated with the pathogenesis of BE, to some degree, in the Japanese population. '

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“…The incidence of this tumour is rapidly increasing in the United States [4][5][6]. Barrett's oesophagus is considered to be a premalignant condition as it predisposes to the development of oesophageal adenocarcinoma [7]. The risk of developing oesophageal adenocarcinoma as a complication of Barrett's oesophagus is reported to be 0.5-2% [8].…”

Section: Introductionmentioning

confidence: 99%

Barrett??s surveillance is worthwhile and detects curable cancers. A prospective cohort study addressing cancer incidence, treatment outcome and survival

Aldulaimi

Cox

Nwokolo

et al. 2005

European Journal of Gastroenterology & Hepatology

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Few Barrett's surveillance studies have addressed treatment outcomes and survival. In our study 5% of Barrett's patients undergoing endoscopy have prevalent cancers. If surveillance is performed, 4% per year develop cancer and 2% per year are cured of their cancers. Most surveillance cancers are operable and of those undergoing surgery 70% are cured. Barrett's surveillance is cost-effective compared with other cancer screening or surveillance initiatives.

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Barrett’s esophagus: an overview of the molecular biology *

Cited by 24 publications

References 24 publications

Analysis of R213R and 13494 g→a polymorphisms of the p53 gene in individuals with esophagitis, intestinal metaplasia of the cardia and Barrett’s Esophagus compared with a control group

Analysis of R213R and 13494 g→a polymorphisms of the p53 gene in individuals with esophagitis, intestinal metaplasia of the cardia and Barrett’s Esophagus compared with a control group

Effects of Helicobacter pylori infection on genetic instability, the aberrant CpG island methylation status and the cellular phenotype in Barrett's esophagus in a Japanese population

Barrett??s surveillance is worthwhile and detects curable cancers. A prospective cohort study addressing cancer incidence, treatment outcome and survival

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