Abstract
Barrett’s esophagus (BE) is an asymptomatic condition of the distal esophagus that can progress to aggressive adenocarcinoma of the esophagus. Although BE is not malignant, the amount of deoxyribonucleic acid (DNA) damage is comparable to some malignancies such as melanoma and breast carcinoma. The purpose of this literature review is to evaluate the anomalies that underlie the transformation of the normal stratified squamous epithelium of the esophagus into metaplastic columnar epithelium with a potential of progressing into esophageal adenocarcinoma based on an appraisal and scrutiny of the literature published since 2000. A systematic search of freely available journal articles pertinent to the pathoetiology (molecular and clinical risk factors) of BE was performed within PubMed and Google Scholar. All articles published in English reporting on the risks and molecular transformation of normal esophageal mucosa into metaplastic mucosa were considered; the research did not look further to the pathoetiology of esophageal adenocarcinoma. Each journal article was assessed based on the content, relevance, and applicability to this literature review. An assessment of 118 full-length articles produced 18 articles for the qualitative analysis. We noted risk factors, such as gastroesophageal reflux of acid and bile, cause aberrations at a molecular level to alter cell cycle control to culminate in morphological changes in esophageal mucosa, producing metaplastic cells with a potential of malignant transformation. There is a need for translational research to bridge the gap between genetics and molecular knowledge to achieve clinical preventive, diagnostic, and therapeutic approaches to addressing BE.
Highlights
Background“The esophagus is part of the foregut, distal to the cricopharyngeal sphincter, which is lined by squamous epithelium [1]." Norman Rupert Barrett, consultant surgeon at St
The purpose of this literature review is to evaluate the anomalies that underlie the transformation of the normal stratified squamous epithelium of the esophagus into metaplastic columnar epithelium with a potential of progressing into esophageal adenocarcinoma based on an appraisal and scrutiny of the literature published since 2000
We noted risk factors, such as gastroesophageal reflux of acid and bile, cause aberrations at a molecular level to alter cell cycle control to culminate in morphological changes in esophageal mucosa, producing metaplastic cells with a potential of malignant transformation
Summary
“The esophagus is part of the foregut, distal to the cricopharyngeal sphincter, which is lined by squamous epithelium [1]." Norman Rupert Barrett, consultant surgeon at St. A 47-year-old obese woman presented with long-standing gastroesophageal reflux disease She had a history of gastric banding and reported a history of esophageal ulcers. There is a need to verify that all the prior cycle steps are done well before the parent cells produce two daughter cells; this verification step is the G2 phase This is followed by the mitosis stage (M-stage) where cellular stores are expended to form two diploid daughter cells. These risk factors include Caucasian race, male gender, age greater than 60 years, alcohol and smoking, obesity, history of GERD or heartburn, non-acid reflux disease, and genetic heterogeneity favoring familial BE [6]. EA is associated with BE, and the pathological processes discussed here will relate to the adenocarcinoma variety and all references to cancer will relate to this variety
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