Prevalence of Barrett's esophagus (BE) in Luoyang, China, has not been reported, and its pathogenesis is controversial. The aim of this study was therefore to investigate the prevalence of BE and its underlying factors in the city of Luoyang.

This was a prospective study in one center. Many patients were analyzed using endoscopy who showed upper gastrointestinal symptoms between August 2006 and June 2007. In addition, the effect of apoptosis-related proteins and heat shock proteins upon BE's pathogenesis were also investigated by an immunohistochemical protocol.

Prevalence of BE was at 4.55% and the mean age of those affected was about 10 years older than for esophagitis. Typical reflux symptoms were significantly lower than with esophagitis, whereas signs of caspase-3 and HSP105 elevation were significantly higher. Expression of TERT, HSP70 and HSP90α in BE cases was significantly lower than in esophagitis. However, there was no statistical difference between the two groups in expression of HSP27.

The prevalence of BE is high in Luoyang, which could result from esophagitis despite typical reflux symptoms being relatively uncommon. Initiation and development of BE might be the result of accelerated proliferation, apoptosis and differentiation of original cells to intestinal epithelium.

The purpose of this study was to evaluate whether 2-methoxyestradiol (2-ME(2)), a promising anticancer agent, modulates Barrett's esophageal adenocarcinoma (BEAC) cell growth and behavior through a cellular pathway involving beta-catenin in partnership with E-cadherin, which seems to play a critical role in the induction of antitumor responses in cancer cells. We found that 2-ME(2) markedly reduced the BEAC cell proliferation through regulating apoptotic machinery such as Bcl-2 and Bax. It may nullify the aggressive behavior of the cells by reducing the migratory behavior. Expressions of beta-catenin and E-cadherin and binding of these two proteins is activated in a 2-ME(2)-dependent fashion in Bic-1 cells. Moreover, overexpressions of these two proteins may be due to the stabilization of these proteins by 2-ME(2). We found that 2-ME(2)-induced antimigratory effects are mediated through the beta-catenin-E-cadherin signaling pathways. In view of these results, we determined whether 2-ME(2) reduces BEAC tumor growth. Administration of 2-ME2 significantly decreased the growth of BEAC cells xenografted on the flank of nude mice. The evidence presented points out that the effect of 2-ME(2) on beta-catenin-orchestrated signal transduction plausibly plays a multifaceted functional role to inhibit the proliferation and cell migration of 2-ME(2)-treated malignant cells and it could be a potential candidate in novel treatment strategies for Barrett's esophageal adenocarcinoma.

The non-steroidal anti-inflammatory drug tolfenamic acid (TA) inhibits proliferation of SEG-1 and BIC-1 esophageal cancer cells with half-maximal growth inhibitory concentration values of 36 and 48 muM, respectively. TA also increased Annexin V staining in both cell lines, indicative of proapoptotic activity. Treatment of SEG-1 and BIC-1 cells with TA for up to 72 h decreased expression of specificity protein (Sp) transcription factors Sp1, Sp3 and Sp4 and this was accompanied by decreased expression of the well-characterized Sp-regulated genes cyclin D1, vascular endothelial growth factor and survivin. TA also decreased hepatocyte growth factor receptor, (c-Met), a receptor tyrosine kinase that is overexpressed in esophageal cancer cells and tumors and is an important drug target. Knockdown of Sp1, Sp3 and Sp4 by RNA interference in SEG-1 and BIC-1 cells also decreased c-Met expression, demonstrating that c-Met is an Sp-regulated gene in esophageal cancer cells. Sp1 was overexpressed in esophageal cancer cells and tumors and increased Sp1 staining was observed in esophageal tumors from patients. TA (20 mg/kg/day) also decreased tumor growth and weight in athymic nude mice bearing SEG-1 cells as xenografts and this was accompanied by increased apoptosis and decreased Sp1 and c-Met staining in tumors from treated mice. Thus, TA-dependent downregulation of Sp transcription factors and c-Met defines a novel chemotherapeutic approach for treatment of esophageal cancer.

Our objective was to investigate the endoscopic and clinico-pathological characteristics in patients with Barrett's esophagus (BE) in China. Using the terms 'Barrett's esophagus' and 'Barrett's esophagus, China' as key words, literatures published in Chinese and English journals were searched in Chinese data banks, as well as PubMed and ISI Web of Science from 1989 to 2007. An analysis was carried out with the standard inclusion and exclusion criteria. A total of 4120 cases were included in this study. BE was found in 2.44% of patients undergoing endoscopy for various symptoms of upper gastrointestinal tract diseases; the male : female ratio was 2.09 : 1, the average age of detection of BE was 53.15 years old, and 51% of patients with BE had typical symptoms for gastroesophageal reflux disease (GERD). The island-type BE was predominant (56.80%), and the occurrence of BE with special intestinal metaplasia (SIM) was 36.58%, but SIM was more common in tongue-type BE than island-type and circumferential-type BE (both P < 0.001), as well as in long segment BE (LSBE) than in short segment BE (SSBE) (P < 0.001). A total of 46.39% of patients had Helicobacter pylori infection. The mean length of follow up was 2 years in 492 patients. The incidence of adenocarcinoma was 0.61% patient-years of total follow up. In China, the endoscopic prevalence of BE is lower, but the average age of diagnosis is younger; a high proportion of H. pylori infection is found in patients with BE, and about half of the patients have no typical symptoms of GERD; the tongue-type BE and the LSBE are apt to SIM.

We aim to determine the expression of the proto-oncogene c-Myc in patients with Barrett's esophagus (BE) and esophageal adenocarcinoma, and to evaluate the prevalence of such expression in relation to the metaplasia-dysplasia-adenocarcinoma sequence. BE develops as a result of a severe esophageal mucosa injury from gastroesophageal reflux. BE is a premalignant lesion and plays an important role in the development of esophageal adenocarcinoma. Several genetic alterations have been identified 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 c-Myc protein expression was determined by immunohistochemical analysis in four different groups: 31 patients with normal tissue, 43 patients with BE without dysplasia, 11 patients with dysplasia in BE and 37 patients with esophageal adenocarcinoma. The material was obtained from esophageal biopsies or the dissection of patient esophagectomy specimens. Demographic and endoscopic data (sex, age, race and intestinal metaplasia extension), and morphologic and histopathologic tumor characteristics (deep tumor invasion, lymph node status, and tumor differentiation) were analyzed. The c-Myc expression was assessed using the Immunoreactive Scoring System (IRS). Overexpression of c-Myc was found in only 9.6% of normal tissue specimens, 37.2% of Barrett's esophagus, 45.5% of BE patients with dysplasia and 73% of adenocarcinoma samples, with significant statistical difference among these groups. No correlation was identified 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. 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, as well as 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 BE.