Publications available

Posted on 3 May 2012

A list of BEACON publications and related news articles is now available on the “Publications” page.

Potential landmark paper on Barrett’s cell of origin

Posted on 30 April 2012
Gastroenterology. 2012 Apr 23. [Epub ahead of print]

Cellular Origin of Barrett’s Esophagus: Controversy and Therapeutic Implications.

Source

Institute of Medical Biology, A-STAR, Singapore; Division of Perinatal and Women’s Pathology, Department of Pathology, Brigham and Women’s Hospital, Boston, MA, USA.

Abstract

Esophageal adenocarcinoma is on the rise in the West and yet its marginal survival rate has not changed in 30 years. Preemptive approaches, including radiofrequency ablation and photodynamic therapy for Barrett’s esophagus and dysplasia, are achieving dramatic initial results. While the long-term efficacy of these non-specific ablative therapies is awaiting longitudinal studies, reports of recurrences are increasing. More targeted therapies, particularly directed at the stem cells of Barrett’s esophagus, demand knowing the origin of this intestinal metaplasia. The prevailing concept holds that Barrett’s esophagus arises from the “transcommitment” of esophageal stem cells to produce an intestine-like epithelium. Given the remarkable frequency with which Barrett’s esophagus appears in Western populations, empirical data for such a transcommitment phenomenon have been surprisingly limited. An alternative explanation derives from the discovery of a discrete population of residual embryonic cells (RECs) existing at the gastroesophageal junction in normal individuals that expands and colonizes regions of the esophagus denuded by chronic reflux. These RECs form intestinal metaplasia within days of esophageal injury, suggesting a novel mechanism of tumorigenesis. A corollary of this work is that the Barrett’s stem cell is distinct from that of the squamous epithelium and, once identified, will form the basis of new strategies for addressing Barrett’s and its related neoplasia.

Copyright © 2012 AGA Institute. Published by Elsevier Inc. All rights reserved.

EGRP Consortia Scientist Exchange Program

Posted on 12 April 2012

A opportunity of potential interest to BEACON investigators

EGRP Initiates Consortia Scientist Exchange Program, Deadline May 1

The Epidemiology and Genomics Research Program (EGRP) has initiated a new Consortia Scientist Exchange Program to foster collaborative projects within or across EGRP-supported cancer epidemiology consortia (CEC), and to help initiate long-term multidisciplinary interactions.

Proposed projects might include, but are not limited to, cross-cancer collaborative studies, as well as the sharing of expertise in laboratory methods.  Applicants should show that the proposed research or knowledge transfer will clearly expand and improve the scientific aims of the parent CEC, and enhance or expedite its ongoing research activities or infrastructures.  Some possibilities are exchanges among or across CECs or between a CEC member and an external group.  For a list of EGRP-supported CECs, see http://epi.grants.cancer.gov/Consortia.

EGRP will support domestic or foreign travel of consortia investigators (including Principal Investigators, co-investigators, and scientific staff who are involved in consortia-related research) to engage in collaborative research activities with other consortia groups.  Priority will be given to junior researchers.

Application Procedures

In Fiscal Year 2012, there will be one call for applications, and the deadline is May 1, 2012.  Applications should provide a brief background description, proposed scope of the collaborative work, and estimates of the length of the exchange and of the budget.   Applications should not exceed two pages.

The application and the applicant’s curriculum vitae should be submitted via e-mail to Eric Derycke, M.P.H., at deryckeec@mail.nih.gov.

The EGRP Consortia Scientist Exchange Program will reimburse travel expenses up to $5,000.  It is anticipated that exchanges will be 1-2 weeks in length (but consideration will be given to exchanges of more than two weeks).  Travel must occur between June 15 and September 15, 2012.

Review Criteria

An NCI committee will review the applications.  Funding decisions will be based on the availability of funds and the degree to which proposals meet the following criteria:  Scientific merit, Credentials of the applicant, Collaborative potential of the proposed research, and Potential for future contribution to the consortium scientific agenda. Successful applicants will be expected to report back on their collaborative work at the annual meeting of their parent consortium.  A written report to NCI will also be required.

Timeline

-          Application submission deadline:  May 1, 2012

-          Travel period for 1-2 week exchanges:  June 15, 2012 to September 15, 2012

-          Report back on collaborative work:  Oral report at annual consortium meeting (date to be communicated to NCI).  Written report to NCI by October 1, 2012.

BEACON Manuscript in press: Modeling odds ratios for adenocarcinoma…

Posted on 11 April 2012

Thanks to Jay Lubin, along with the writing committee, for their efforts in publishing: “The importance of exposure rate on odds ratios by cigarette smoking and alcohol consumption for esophageal adenocarcinoma and squamous cell carcinoma in the BEACON Consortium,” which is in press in the journal Cancer Epidemiology.

Next BEACON meeting set

Posted on 15 February 2012

Thanks to Wong-Ho Chow, Christian Abnet and NCI for hosting the next BEACON meeting in Bethesda on Thu/Fri 17-18 May 2012. We are also planning a BEAGESS “pre-meeting” on the afternoon of the 16th (Wed), with all BEAGESS participants welcome.

Smoking and Barrett’s paper published in Gastroenterology

Posted on 25 January 2012
Gastroenterology. 2012 Jan 11. [Epub ahead of print]

Cigarette Smoking Increases Risk of Barrett’s Esophagus: an Analysis of the Barrett’s and Esophageal Adenocarcinoma Consortium.

Abstract

BACKGROUND & AIMS:  Cigarette smoking has been implicated in the etiology of esophageal adenocarcinoma, but it is not clear if smoking is a risk factor for Barrett’s esophagus (BE). We investigated whether tobacco smoking and other factors increase risk for BE.

METHODS:  We analyzed data from 5 case-control studies included in the international Barrett’s and Esophageal Adenocarcinoma Consortium. We compared data from subjects with BE (n=1059) with those from subjects with gastroesophageal reflux disease (GERD controls, n=1332) and population-based controls (n=1143), using multivariable logistic regression models to test associations with cigarette smoking. We also tested whether cigarette smoking has synergistic effects with other exposures, which might further increase risk for BE.

RESULTS:  Subjects with BE were significantly more likely to have ever-smoked cigarettes than the population-based controls (odds ratio [OR]=1.67; 95% confidence interval [CI], 1.04-2.67) or GERD controls (OR=1.61; 95% CI, 1.33-1.96). Increasing pack-years of smoking increased the risk for BE. There was evidence for a synergy between ever-smoking and heartburn or regurgitation; the attributable proportion of disease among individuals who ever smoked and had heartburn or regurgitation was estimated to be 0.39 (0.25-0.52).

CONCLUSIONS:  Cigarette smoking is a risk factor for BE. The association strengthened with increased exposure to smoking until ~ 20 pack-years, when it began to plateau. Smoking has synergistic effects with heartburn or regurgitation, indicating that there are various pathways by which tobacco smoking might contribute to the development of BE.

NSAIDs meta-analysis published in Gastroenterology

Posted on 30 December 2011

Congratulations to LInda (Dong) Liao for her success in publishing the BEACON NSAIDs analysis. It was selected to have an accompanying CME exercise when published in March.

Gastroenterology. 2011 Nov 18. [Epub ahead of print]

Non-Steroidal Anti-Inflammatory Drug Use Reduces Risk for Adenocarcinomas of the Esophagus and Esophagogastric Junction in a Pooled Analysis.

Source: Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda, MD.

Link to PubMed

Abstract

BACKGROUND & AIMS:  Regular use of aspirin and other non-steroidal anti-inflammatory drugs (NSAID) has been reported to reduce risks for esophageal adenocarcinoma (EAC) and esophagogastric junctional adenocarcinoma (EGJA). However, individual studies have been too small to accurately assess the effects of medication type, frequency, or duration of use. We performed a pooled analysis to investigate these associations.  METHODS:We performed a pooled analysis of 6 population-based studies within the Barrett’s and Esophageal Adenocarcinoma Consortium to evaluate the association between NSAID use and the risk of EAC and EGJA, using uniform exposure definitions. We collected information from 6 studies (5 case-control and 1 cohort), with a total of 1226 EAC and 1140 EGJA cases, on aspirin and/or NSAID use. Study-specific odds ratios (ORs) and 95% confidence intervals (CIs) were estimated using multivariate adjusted logistic regression models and then pooled using a random effects meta-analysis model.  RESULTS: Compared to non-users, individuals who have used NSAIDs had a statistically significant, reduced risk of EAC (OR=0.68; 95% CI, 0.56-0.82); they also appeared to have a reduced risk of EGJA (OR=0.84; 95% CI, 0.68-1.03). Similar reductions in risk were observed among individuals who took aspirin or non-aspirin NSAIDs. The highest levels of frequency (?daily) and duration (?10 years) of NSAID use were associated with an approximately 40% reduction in risk for EAC: OR=0.56 (95% CI, 0.43-0.73; P-trend, <.001) and OR=0.63 (95% CI, 0.45-0.90; P-trend, 0.04), respectively.  CONCLUSIONS:  Although reverse causation could, in part, explain the inverse association observed between NSAID use and EAC risk, pooled analysis indicates a role for NSAIDs in prevention of adenocarcinomas of the esophagus and esophagogastric junction.