Furthermore, the specific association between oesophageal adenocarcinoma and the locus near HTR3C and ABCC5 might constitute a novel genetic marker for prediction of the transition from Barrett's oesophagus to oesophageal adenocarcinoma.
CDX2 and PITX1 messenger RNA (mRNA) expression levels, relative to the control gene beta-actin, were measured by reverse transcription-polymerase chain reaction in specimens of Barrett's IM (n = 21), dysplasia (n = 18), adenocarcinoma (n = 20), and matching normal squamous esophagus tissues (n = 39) collected from 19 patients with Barrett's esophagus and 20 patients with esophageal adenocarcinoma.
Patient samples also showed increased mRNA expression of ADAM12 in esophagitis, of ADAM9 in BE, and of ADAMs 9, 12 and 19 in Barrett's dysplasia, as compared to controls.
Using linear correlation analysis we found the positive correlation between AdipoR1 expression in Barrett's epithelium compared to squamous epithelium in the same patients (N) (r=0.5; p=0.008) and between ObR expression in BE and N (r=0.8; p<0.001).
Expression of adiponectin receptors 1 and 2 protein (AdipoR1, AdipoR2) as well as leptin receptor protein (ObR) in biopsies from 27 BE and normal squamous epithelium (N) in the same patients as well as in obese and normal controls were assessed with Western-blot analysis.
We compared markers of EMT and cell motility in trans-well and 3-dimensional organotypic culture systems among dysplastic BE epithelial cell lines, nondysplastic telomerase-immortalized BE cell lines (BAR-T), and BAR-T cells exposed acutely or for 20 weeks to acidic bile salts.
We looked for evidence of acid-induced DNA damage, including DSBs, in benign Barrett's epithelial (BAR-T) cell lines in vitro and in patients with Barrett's esophagus in vivo.
AGR2 preferentially engages with MUC-5 as a primary client and is coexpressed with the acidic mucin in Barrett's esophagus and esophageal adenocarcinoma tissue.
The results support the deduction that BE is a tissue with enhanced glycoprotein synthesis machinery (DPP4, ATP2A3, AGR2) designed to provide strong mucosal defenses aimed at resisting gastro-esophageal reflux.
It was found that seven of 28 (25%) super-minute dysplasia lesions in the Barrett's esophagus showed K-ras mutation, and were a single mutation, with AGT being detected in three lesions and GAT being detected in four lesions.
AID activation is widely observed in gastrointestinal tissues with cancer-associated inflammation, such as chronic viral hepatitis, Helicobacter pylori-related gastritis, Barrett's esophagus and inflammatory bowel disease.
Immunoreactivity for endogenous AID was observed in 24 of 28 (85.7%) specimens of the columnar cell-lined Barrett's oesophagus and in 20 of 22 (90.9%) of Barrett's adenocarcinoma, whereas weak or no AID protein expression was detectable in normal squamous epithelial cells of the oesophagus.
Proteomic screening of a cell line model of esophageal carcinogenesis identifies cathepsin D and aldo-keto reductase 1C2 and 1B10 dysregulation in Barrett's esophagus and esophageal adenocarcinoma.
Proteomic screening of a cell line model of esophageal carcinogenesis identifies cathepsin D and aldo-keto reductase 1C2 and 1B10 dysregulation in Barrett's esophagus and esophageal adenocarcinoma.