Anushka Baruah

Strategy for prevention of cancers of the esophagus

The following, from the 12th OESO World Conference: Cancers of the Esophagus, includes commentaries on the animal reflux–inflammation models for Barretts esophagus and esophageal adenocarcinoma; genomic/epigenomic analyses; eflornithine‐based combinations; the molecular derangements that promote neoplastic transformation; the role of COX‐2 inhibitors, proton pump inhibitors, and phase II trials in Barretts adenocarcinoma; statins in chemoprevention and treatment of esophageal cancer; and biomarkers as potential targets in Barretts adenocarcinoma.

Efficacy of Over-the-Scope Clips in Management of High-Risk Gastrointestinal Bleeding

Background & Aims: Standard endoscopic therapies do not control bleeding or produce complications in as many as 20% of patients with nonvariceal gastrointestinal bleeding. Most bleeding comes from ulcers with characteristics such as high‐risk vascular territories and/or large vessels. We evaluated the efficacy of using over‐the‐scope clips (OTSCs) as primary or rescue therapy for patients with bleeding from lesions that have a high risk for adverse outcomes. Methods: We performed a retrospective analysis of data from 67 patients with gastrointestinal bleeding from high‐risk lesions who were treated with OTSCs as primary (n = 49) or rescue therapy (n = 18) at a quaternary center, from December 2011 through February 2015. The definition of high‐risk lesions was lesions that were situated in the area of a major artery and larger than 2 mm in diameter and/or a deep penetrating, excavated, fibrotic ulcer with high‐risk stigmata, in which a perforation could not be ruled out or thermal therapy would cause perforation, or lesions that could not be treated by standard endoscopy. Clinical severity was determined based on the Rockall score and a modified Blatchford score. Our primary outcome was the incidence of rebleeding within 30 days after OTSC placement. We assessed risk factors for rebleeding using univariate hazard models followed by multivariable analysis. Results: Of the 67 patients, 47 (70.1%) remained free of rebleeding at 30 days after OTSC placement. We found no difference in the proportion of patients with rebleeding who received primary or rescue therapy (hazard ratio, 0.639; 95% confidence interval, 0.084–4.860; P =.6653). Only 9 rebleeding events were linked clearly to OTSCs and required intervention, indicating an OTSC success rate of 81.3%. We found no significant associations between rebleeding and clinical scores. However, on multivariable analysis, patients with coronary artery disease had a higher risk of rebleeding after OTSC independent of international normalized ratio and antiplatelet use (hazard ratio, 7.30; P =.0002). Conclusions: In a retrospective analysis of 67 patients with bleeding from high‐risk gastrointestinal lesions, we found OTSCs to prevent rebleeding in more than 80% of cases. In the past, these lesions were treated with surgical or radiologic interventions. Patients with coronary artery disease have an increased risk of rebleeding after OTSCs, suggesting the need for escalated therapies.

Translational research on Barrett's esophagus

The following, from the 12th OESO World Conference: Cancers of the Esophagus, includes commentaries on translational research on Barretts esophagus that address evidence for genetic instability in esophageal cancer; the role of microsatellite instability; the use of histologic and serum Doublecortin‐like kinase 1 expression for progression of Barretts esophagus to adenocarcinoma; the oxidative stress in Barretts tumorigenesis; the genomic alterations in esophageal cancer; in vivo modeling in Barretts esophagus; epigenetic and transcriptional regulation in Barretts esophagus and esophageal adenocarcinoma; and normal and disordered regeneration in Barretts esophagus.

Chemoprevention in Barrett's oesophagus

Increasing incidence of oesophageal adenocarcinoma along with poor survival entails novel preventive strategies. Agents that target pro-oncogenic pathways in Barretts mucosa could halt this neoplastic transformation. In this review, we will use epidemiological associations and molecular mechanisms to identify novel chemoprevention targets in Barretts oesophagus. We will also discuss recent chemoprevention trials.

Sa1965 Garcinol Interferes With Oncogenic IL1b-STAT3 and Facilitates Tumor Suppressive KLF11-Sin3A to Down-Regulate AKT1 Expression and Cell Growth in Barrett's Epithelium

ESR2 physical interactions. Surprisingly, our preliminary results showed an upregulation in EGFR signals in ERB041 treated ESR2 transfectants. Summary: In AA with adenomas, reductions in ESR2 expression might contribute to higher colon cancer incidence and worse prognosis. The in vitro studies confirmed that ESR2 suppresses colon cancer cell proliferation. We postulate that the antiproliferative effects of ESR2 involve miR-145 dependent, EGFRindependent pathways. Our study suggests that ESR2 down-regulation might play an important role in colon cancer risk and contribute to racial differences in cancer progression.