MK2 and ETV1 Are Prognostic Factors in Esophageal Adenocarcinomas

Background. Esophageal cancer is ranked in the top ten of diagnosed tumors worldwide. Even though improvements in survival could be noticed over the last years, prognosis remains poor. ETS translocation variant 1 (ETV1) is a member of a family of transcription factors and is phosphorylated by mitogen-activated protein kinase (MAPK)-activated protein kinase 2 (MK2). Aim of this study was to evaluate the prognostic role of MK2 and ETV1 in esophageal cancer. Methods. Consecutive patients that underwent surgical resection at the department of surgery at the Medical University of Vienna between 1991 and 2012 were included into this study. After microscopic analysis, tissue micro arrays (TMAs) were created and immunohistochemistry was performed with antibodies against MK2 and ETV1. Results. 323 patients were included in this study. Clinical data was achieved from a prospective patient data base. Nuclear overexpression of MK2 was observed in 143 (44.3%) cases for nuclear staining and in 142 (44.0%) cases a cytoplasmic overexpression of MK2 was observed. Nuclear and cytoplasmic ETV1 overexpression was detected in 20 cases (6.2%) and 30 cases (9.3%), respectively. In univariate survival analysis, cMK2 and nETV1 were found to be significantly associated with patients' overall survival. Whereas overexpression of cMK2 was associated with shorter, nETV1 was associated with longer overall survival. In multivariate survival analysis, both cMK2 and nETV1 were found to be independent prognostic factors for the subgroup of EAC as well. Discussion. Expression of MK2 and ETV1 are prognostic factors in patients, with esophageal adenocarcinoma

RefluxStop™ Therapy - a New Minimally Invasive Technology in Anti-reflux Surgery.

The symptoms of gastroesophageal reflux disease (GERD) are very common, but cannot be reliably controlled with medication, as more than 40% of patients suffer troublesome symptoms more than twice a week even when taking maximum doses of proton pump inhibitors (PPI). Until recently, the only surgical option was anti-reflux surgery, usually performed as a hiatal hernia repair and some form of fundoplication. While this is still the gold standard, some centers note high recurrence rates and/or high rates of side effects such as dysphagia, bloating, and post-prandial discomfort. This paper describes a new surgical procedure that controls reflux symptoms through hiatal hernia repair in combination with the implantation of a silicone cube. The cube is implanted near the left side of the esophagus above the lower esophageal sphincter (LES). The details of the procedure, the indications for this new approach, the initial results, and the rate of side effects compared to Nissen fundoplication are described. Implantation of the CE-certified RefluxStop™ (Implantica, Zug, Switzerland) has been used for 3 years and the initial studies show encouraging success rates. In addition, side effects are significantly reduced. These results must be evaluated in further studies

Pancho trial (p53-adapted neoadjuvant chemotherapy for resectable esophageal cancer) completedmutation rate of the marker higher than expected

Background In operable esophageal cancer patients, neoadjuvant therapy benefits only those who respond to the treatment. The Pancho trial represents the first prospective randomized trial evaluating the relevance of the mark53 status for predicting the effect of two different neoadjuvant chemotherapies. Method Biomarker analysis was conducted using the mark53 analysis. Calculation of patient number needed was based on a 60% rate of marker positivity, deduced from the results of a phase II pilot study. Results From 20072012, the Pancho trial recruited 235 patients with operable esophageal cancer in Austria. A total of 181 patients were eligible and could be subjected to mark53 analysis and randomization. After randomizing 74 patients, the overall TP53 mutation rate was 79%. However, due to the high prevalence of marker positivity, the number of projected patients was increased to 181 patients in order to ensure a sufficient number of marker-negative patients. After completion of the trial, the overall TP53 mutation rate was 77.9%. Conclusion Due to high medical need, the recruitment for the academic trial was excellent. Mark53 analysis clearly detected more mutations in the TP53 gene as compared to the cancer-specific p53 literature. Final analysis examining the interaction between the mark53 status and the effect of chemotherapies applied in the Pancho trial is now awaited.(VLID)359159