p53 protein accumulation in Barrett's metaplasia, dysplasia, and carcinoma: A follow-up study

Younes, Mamoun; Lebovitz, Russell M.; Lechago, Lia V.; Lechago, Juan

doi:10.1016/0016-5085(93)91058-p

Cited by 190 publications

(94 citation statements)

References 36 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Rioux-Leclercq et al (1999) found P53 overexpression in only 7% of tissues with low grade dysplasia, but in 60% of tissues with high grade dysplasia, and in 85% of adenocarcinomas. Similar results were obtained by Younes et al (1993) and Ramel et al (1992). However, Younes (1997) reported overexpression of P53 in 36% of areas with low grade dysplasia and this was associated with increased probability of progression to high grade dysplasia.…”

Section: Aberrant Expression Of Pro-apoptotic P53 and Apc And Of Antsupporting

confidence: 66%

“…Overexpression of P53 has been found in over 50% of adenocarcinomas arising in BE (e.g. Blount et al 1991;Flejou et al 1993;Younes et al 1993;Casson et al 1995). Rioux-Leclercq et al (1999) found P53 overexpression in only 7% of tissues with low grade dysplasia, but in 60% of tissues with high grade dysplasia, and in 85% of adenocarcinomas.…”

Section: Aberrant Expression Of Pro-apoptotic P53 and Apc And Of Antmentioning

confidence: 99%

See 1 more Smart Citation

Field defects in progression to adenocarcinoma of the colon and esophagus

Bernstein¹,

Bernstein²,

Payne³

et al. 2000

Electron. J. Biotechnol.

View full text Add to dashboard Cite

Section: Aberrant Expression Of Pro-apoptotic P53 and Apc And Of Antsupporting

confidence: 66%

Section: Aberrant Expression Of Pro-apoptotic P53 and Apc And Of Antmentioning

confidence: 99%

Field defects in progression to adenocarcinoma of the colon and esophagus

Bernstein¹,

Bernstein²,

Payne³

et al. 2000

Electron. J. Biotechnol.

View full text Add to dashboard Cite

“…22 Only sparse data are available in the literature regarding the use of FISH on endoscopic brush cytology specimens for biomarker assessment in Barrett's esophagus. Recently, a group of investigators from Denmark applied FISH to cell pellets obtained from endoscopic brushings, and analyzed the aneusomic states of chromosomes 4,8,20, and Y, as well as genomic losses of p16, p53, and retinoblastoma (Rb) gene loci. 44 This study showed that while aneusomy of chromosomes 4 and 8, and a p16 locus deletion are early changes present in the metaplastic Barrett's epithelium, p53 genomic loss (and rarely Rb loss) occurs predominantly in HGD and adenocarcinoma arising in Barrett's esophagus.…”

Section: Discussionmentioning

confidence: 99%

“…These changes include gene mutations and their frequently associated genomic losses of tumor suppressor genes including p53 (17p13.1 locus) and p16 (9p21 locus). [14][15][16][17][18][19][20] In addition, frequent gains of chromosomes 6, 7, 11, and 12 have been previously reported in adenocarcinomas and adjacent metaplastic epithelium from esophagectomy specimens. 4,21,22 By using endoscopic brushing cytology specimens, we evaluated the ability of FISH to detect molecular genetic changes previously reported to be associated with the malignant transformation in Barrett's esophagus.…”

mentioning

confidence: 99%

Chromosomal gains and genomic loss of p53 and p16 genes in Barrett's esophagus detected by fluorescence in situ hybridization of cytology specimens

et al. 2004

View full text Add to dashboard Cite

Endoscopic brush cytology is a promising surveillance technique for Barrett's esophagus. Ancillary markers are sought to increase the sensitivity of cytology and allow identification of patients at increased risk for disease progression. To determine if there are specific genetic changes in Barrett's esophagus with associated high-grade dysplasia/intramucosal adenocarcinoma compared to those without dysplasia, we performed fluorescence in situ hybridization (FISH) on cytologic specimens using probes to chromosomes and genomic regions previously described as altered in this disease. We studied archival brush cytology slides from 40 Barrett's esophagus patients: 21 with biopsy-proven high-grade dysplasia/carcinoma and 19 with no dysplasia and a minimum 5 years of negative follow-up. Centromeric enumeration probes (CEP) for chromosomes 6, 7, 11, and 12, and locus-specific probes (LSI) for 9p21 (p16 gene), and 17p13.1 (p53 gene) loci along with their corresponding CEP (9 and 17, respectively) were used in this study. A positive FISH result was defined as the presence of cells with 42 CEP signals or with a loss of the LSI signals relative to their corresponding CEP. p53 locus loss and/or aneusomy of chromosomes 6, 7, 11, and 12 abnormalities could be detected by FISH in routinely processed endoscopic brush cytology specimens from 95% of biopsy-positive cases with a specificity of 100%. Interestingly, all five cases with cytologic changes classified as indefinite for dysplasia from patients with a positive biopsy showed changes by FISH. Loss of the p16 locus was seen commonly in patients both with and without dysplasia/carcinoma. Selected biomarkers from this study merit further investigation to determine their potential to detect genetic changes in patients with Barrett's esophagus prior to the development of high-grade dysplasia.

show abstract

“…Thus, it is important to address the hypothesis that p53 overexpression could predict progression of nondysplastic BE to adenocarcinoma. Younes et al [47] studied p53 accumulation via immunohistochemistry in 54 patients with Barrett's metaplasia, dysplasia, or adenocarcinoma; p53 accumulation increased in parallel with histological progression from metaplasia to adenocarcinoma. Follow-up biopsies were available in 23 of 54 patients who had dysplasia in at least one biopsy specimen.…”

Section: Discussionmentioning

confidence: 99%

Risk factors associated with Barrett’s epithelial dysplasia

Fujita

Nakamura

Kasashima

et al. 2014

WJG

View full text Add to dashboard Cite

AIM:To elucidate risk factors associated with dysplasia of short-segment Barrett's esophagus (BE). METHODS:A total of 151 BE patients who underwent endoscopic examination from 2004 to 2008 in Aoyama Hospital, Tokyo Women's Medical University, Japan and whose diagnosis was confirmed from biopsy specimens were enrolled in the study. BE was diagnosed based on endoscopic findings of gastric-appearing mucosa or apparent columnar-lined esophagus proximal to the esophagogastric junction. Dysplasia was classified into three grades -mild, moderate and severe -according to the guidelines of the Vienna Classification System for gastrointestinal epithelial neoplasia. Anthropometric and biochemical data were analyzed to identify risk factors for BE dysplasia. The prevalence of Helicobacter pylori (H. pylori ) infection and the expression of p53 by immunohistological staining were also investigated. RESULTS:Histological examination classified patients into three types: specialized columnar epithelium (SCE) (n = 65); junctional (n = 38); and gastric fundic (n = 48). The incidence of dysplasia or adenocarcinoma from BE of the SCE type was significantly higher than that of the other two types (P < 0.01). The univariate analysis revealed that sex, H. pylori infection, body weight, p53 overexpression, and low diastolic blood pressure (BP) were associated with BE dysplasia. In contrast, body mass index, waist circumference, metabolic syndrome complications, and variables related to glucose or lipid metabolism were not associated with dysplasia. Multivariate logistic analysis showed that overexpression of p53 [odds ratio (OR) = 13.1, P = 0.004], H. pylori infection (OR = 0.19, P = 0.066), and diastolic BP (OR = 0.87, P = 0.021) were independent risk factors for epithelial dysplasia in BE patients with the SCE type. CONCLUSION:Overexpression of p53 is a risk factor for dysplasia of BE, however, H. pylori infection and diastolic BP inversely associated with BE dysplasia might be protective.

show abstract

p53 protein accumulation in Barrett's metaplasia, dysplasia, and carcinoma: A follow-up study

Cited by 190 publications

References 36 publications

Field defects in progression to adenocarcinoma of the colon and esophagus

Field defects in progression to adenocarcinoma of the colon and esophagus

Chromosomal gains and genomic loss of p53 and p16 genes in Barrett's esophagus detected by fluorescence in situ hybridization of cytology specimens

Risk factors associated with Barrett’s epithelial dysplasia

Contact Info

Product

Resources

About