Barrett's esophagus develops as a result of a severe esophageal mucosa injury from gastroesophageal reflux.
Barrett's esophagus is a premalignant lesion and plays an important role in the development of esophageal adenocarcinoma.
Dr Schmidt and colleagues from Brazil determined the expression of the proto-oncogene c-Myc in patients with Barrett's esophagus, and esophageal adenocarcinoma.
The research team evaluated the prevalence of such expression in relation to the metaplasia-dysplasia-adenocarcinoma sequence.
|c-Myc overexpression occurred in 37% of Barrett's esophagus|
|Diseases of the Esophagus|
The team identified several genetic alterations in the process that transforms a normal cell into a tumorous one.
In the development of human tumors, one of the most important genes is the proto-oncogene c-Myc.
The researchers then determined c-Myc protein expression by immunohistochemical analysis in 4 different groups.
The team reported that there were 31 patients with normal tissue, and 43 patients with Barrett's esophagus without dysphasia.
The team also identified 11 patients with dysplasia in Barrett's esophagus, and 37 patients with esophageal adenocarcinoma.
The material was obtained from esophageal biopsies or the dissection of patient esophagectomy specimens.
The researchers analyzed demographic and endoscopic data that included sex, age, race and intestinal metaplasia extension.
In addition the team assessed morphologic and histopathologic tumor characteristics.
The research team evaluated deep tumor invasion, lymph node status, and tumor differentiation.
The c-Myc expression was assessed using the Immunoreactive Scoring System.
The team found overexpression of c-Myc in only 10% of normal tissue specimens.
c-Myc overexpression occurred in 37% of Barrett's esophagus patients, and 46% of Barrett's esophagus patients with dysphasia.
In adenocarcinoma samples, the team observed c-Myc over expression in 73%.
There was no significant statistical difference among these groups.
The research team identified no correlation when the c-Myc expression was compared with morphologic and histologic tumor features or endoscopic data.
However, linear correlation of c-Myc overexpression along the metaplasia-dysplasia-adenocarcinoma sequence was observed.
Dr Schmidt's team concluded, "This study demonstrates a significant increase in the expression of c-Myc in Barrett's esophagus dysplasia and adenocarcinoma in relation to the control group.
"We also found a linear progression of this gene expression in this sequence."
"These results point out the importance of this marker in the development of esophageal adenocarcinoma from Barrett's esophagus."