Discordance between flow cytometric abnormalities and dysplasia in Barrett's esophagus

Fennerty, M. Brian; Sampliner, Richard E.; Way, Dennis; Riddell, Robert H.; Steinbronn, Karen; Garewal, Harinder S.

doi:10.1016/0016-5085(89)91483-2

Cited by 95 publications

(29 citation statements)

References 13 publications

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“…12 DNA content, measured by flow cytometry, has been also the subject of numerous studies, reporting that aneuploidy and increased G2M/tetraploid populations may increase along with increasing dysplasia, but the results have been conflicting. 13,14 The prevalence of p53 gene mutation in esophageal carcinoma reported in the literature ranges from 42 to 67%, 6,[15][16][17] with the exception of two reports in which a low prevalence (8%) (18) and a higher prevalence (84%), 19 respectively, were observed. The prevalence of protein accumulation is more variable, ranging from 34 to 87%.…”

Section: Discussionmentioning

confidence: 99%

Evaluation of p53 mutations in premalignant esophageal lesions and esophageal adenocarcinoma using laser capture microdissection

et al. 2004

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p53 mutations have been implicated in the development of esophageal malignancies. The purpose of this study was to assess more accurately the incidence and types of p53 mutations in Barrett's esophagus (BE) with and without dysplasia and in esophageal adenocarcinoma, using pure preparations of epithelial cells obtained by laser capture microdissection (LCM). Assays were performed on paraffin-embedded tissue samples of normal antrum and premalignant and malignant esophageal samples from 57 patients, including 16 controls, 10 with BE metaplasia alone, 20 with BE-associated dysplasia, and 11 with BE-associated adenocarcinoma. All tissues were processed for LCM. DNA was extracted from isolated cells, and polymerase chain reaction (PCR) was performed using oligonucleutide primers for exons 5-8 of p53. PCR products were processed for DNA sequencing. p53 sequence abnormalities were identified in 2/16 cases of normal antrum and regenerative/ chemical gastritis, 1/10 cases of BE, 1/20 cases of BE with dysplasia, and 2/11 cases of adenocarcinomas. The abnormalities occurred in exons 7 and 8 in the form of point mutations. Our results, using LCM, show that p53 gene mutations are relatively rare in esophageal preneoplastic and neoplastic conditions. Only point mutations were detected, but no deletions/insertions were identified.

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Section: Discussionmentioning

confidence: 99%

Evaluation of p53 mutations in premalignant esophageal lesions and esophageal adenocarcinoma using laser capture microdissection

et al. 2004

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“…Enzymes (52), proliferation indices (52)(53)(54), DNA content abnormalities (55)(56)(57), genetic mutations (58 -60), and growth factors (61,62) have been investigated. A marker other than dysplasia identifying a high risk group for cancer on which to focus surveillance has not yet been established.…”

Section: Ajg -July 1998mentioning

confidence: 99%

Practice guidelines on the diagnosis, surveillance, and therapy of Barrett's esophagus

Sampliner

1998

The American Journal of Gastroenterology

105

110

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“…36 Others have reported that histologic dysplasia and aneuploidy are often discordant. 43 Most discordance between several studies can be explained by methodologic differences.…”

Section: Dna Content/aneuploidymentioning

confidence: 99%

Molecular Biology of Barrett’s Adenocarcinoma

Wijnhoven

Tilanus²,

Dinjens³

2001

Annals of Surgery

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ObjectiveTo review the current knowledge on the genetic alterations involved in the development and progression of Barrett's esophagus-associated neoplastic lesions. Summary Background DataBarrett's esophagus (BE) is a premalignant condition in which the normal squamous epithelium of the esophagus is replaced by metaplastic columnar epithelium. BE predisposes patients to the development of esophageal adenocarcinoma. Endoscopic surveillance can detect esophageal adenocarcinomas when they are early and curable, but most of the adenocarcinomas are detected at an advanced stage. Despite advances in multimodal therapy, the prognosis for invasive esophageal adenocarcinoma is poor. A better understanding of the molecular evolution of the Barrett's metaplasia to dysplasia to adenocarcinoma sequence may allow improved diagnosis, therapy, and prognosis. MethodsThe authors reviewed data from the published literature to address what is known about the molecular changes thought to be important in the pathogenesis of BE-associated neoplastic lesions. ResultsThe progression of Barrett's metaplasia to adenocarcinoma is associated with several changes in gene structure, gene expression, and protein structure. Some of the molecular alterations already showed promise as markers for early cancer detection or prognostication. Among these, alterations in the p53 and p16 genes and cell cycle abnormalities or aneuploidy appear to be the most important and well-characterized molecular changes. However, the exact sequence of events is not known, and probably multiple molecular pathways interact and are involved in the progression of BE to adenocarcinoma. ConclusionsFurther research into the molecular biology of BE-associated adenocarcinoma will enhance our understanding of the genetic events critical for the initiation and progression of Barrett's adenocarcinoma, leading to more effective surveillance and treatment.Since 1970, the incidence of adenocarcinomas of the esophagus has increased in many countries at a rate that exceeds that of any other malignancy.

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Discordance between flow cytometric abnormalities and dysplasia in Barrett's esophagus

Cited by 95 publications

References 13 publications

Evaluation of p53 mutations in premalignant esophageal lesions and esophageal adenocarcinoma using laser capture microdissection

Evaluation of p53 mutations in premalignant esophageal lesions and esophageal adenocarcinoma using laser capture microdissection

Practice guidelines on the diagnosis, surveillance, and therapy of Barrett's esophagus

Molecular Biology of Barrett’s Adenocarcinoma

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