Risk Factors in the Development of Esophageal Adenocarcinoma

Pohl, Heiko; Wrobel, Katharina; Bojarski, Christian; Voderholzer, Winfried A.; Sonnenberg, Amnon; Rösch, Thomas; Baumgart, Daniel C.

doi:10.1038/ajg.2012.387

Cited by 141 publications

(120 citation statements)

References 35 publications

Supporting

Mentioning

108

Contrasting

Unclassified

Order By: Relevance

“…Given the low rate of progression in these patients, the low but real rate of complications of endoscopic therapy ( 149 ), and the costs associated with its delivery ( 150 ), ablative therapy cannot be recommended in patients with nondysplastic BE. Whether these therapies are warranted in subjects judged to have a higher lifetime risk of cancer, such as those with familial BE/EAC and young patients with long segments of BE, is unclear (151)(152)(153).…”

Section: Summary Of Evidencementioning

confidence: 99%

ACG Clinical Guideline: Diagnosis and Management of Barrett’s Esophagus

Shaheen

Falk

Iyer

et al. 2016

American Journal of Gastroenterology

1,356

1,412

View full text Add to dashboard Cite

Recent population studies suggest that gastroesophageal refl ux disease (GERD) is increasing in prevalence, both in the United States and worldwide ( 1,2 ). Th e diagnosis of GERD is associated with a 10-15% risk of Barrett's esophagus (BE), a change of the normal squamous epithelium of the distal esophagus to a columnar-lined intestinal metaplasia (IM). Risk factors associated with the development of BE include long-standing GERD, male gender, central obesity ( 3 ), and age over 50 years ( 4,5 ). Th e goal of a screening and surveillance program for BE is to identify individuals at risk for progression to esophageal adenocarcinoma (EAC), a malignancy that has been increasing in incidence since the 1970s ( 6,7 ).Th e purpose of this guideline is to review the defi nition and epidemiology of BE, available screening modalities for BE detection, rationale and methods for surveillance, and available treatment modalities including medical, endoscopic, and surgical techniques. In order to evaluate the level of evidence and strength of recommendations, we used the GRADE (Grading of Recommendations Assessment, Development and Evaluation) system ( 8 ). Th e level of evidence ranged from "high" (implying that further research was unlikely to change the authors' confi dence in the estimate of the eff ect) to "moderate" (further research would be likely to have an impact on the confi dence in the estimate of eff ect) to "low" (further research would be expected to have an important impact on the confi dence in the estimate of the eff ect and would be likely to change the estimate) or "very low" (any estimate of eff ect is very uncertain). Th e strength of a recommendation was graded as "strong" when the desirable eff ects of an intervention clearly outweighed the undesirable eff ects and as "conditional" when there was uncertainty about the tradeoff s. We used meta-analyses or systematic reviews when available, followed by clinical trials and cohort and case-control studies. In order to determine the level Barrett's esophagus (BE) is among the most common conditions encountered by the gastroenterologist. In this document, the American College of Gastroenterology updates its guidance for the best practices in caring for these patients. These guidelines continue to endorse screening of high-risk patients for BE; however, routine screening is limited to men with refl ux symptoms and multiple other risk factors. Acknowledging recent data on the low risk of malignant progression in patients with nondysplastic BE, endoscopic surveillance intervals are attenuated in this population; patients with nondysplastic BE should undergo endoscopic surveillance no more frequently than every 3-5 years. Neither routine use of biomarker panels nor advanced endoscopic imaging techniques (beyond high-defi nition endoscopy) is recommended at this time. Endoscopic ablative therapy is recommended for patients with BE and high-grade dysplasia, as well as T1a esophageal adenocarcinoma. Based on recent level 1 evidence, endoscopic ablative therapy is ...

show abstract

Section: Summary Of Evidencementioning

confidence: 99%

ACG Clinical Guideline: Diagnosis and Management of Barrett’s Esophagus

Shaheen

Falk

Iyer

et al. 2016

American Journal of Gastroenterology

1,356

1,412

View full text Add to dashboard Cite

show abstract

“…Gastric cancer is a progressive disease. Surgical resection is the only potential curative treatment, however despite the adjuvant or neoadjuvant chemotherapy/chemoradiotherapy administered on patients, the disease recurs in majority of the patients (Cunningham et al, 2006 dietary N-nitroso compounds and endogenous nitrosation (Keszei et al, 2013;Li et al, 2013;Pohl et al, 2013). Determination of primary prevention and risk factors is important for such diseases with bad prognosis and fast progression.…”

Section: Introductionmentioning

confidence: 99%

Esophageal Cancer, Gastric Cancer and the use of Pesticides in the Southwestern of Turkey

Yıldırım¹,

Kaya²,

Yıldız³

et al. 2014

Asian Pacific Journal of Cancer Prevention

View full text Add to dashboard Cite

“…The major risk factor for esophageal adenocarcinoma (EA) is gastroesophageal reflux disease complicated by Barrett's esophagus (BE) (Lagergren et al, 1999;Kahrilas, 2011;Pohl et al, 2013). The mechanisms of the progression from BE to EA are not fully understood.…”

Section: Introductionmentioning

confidence: 99%

Silencer-of-Death Domain Mediates Acid-Induced Decrease in Cell Apoptosis in Barrett’s Associated Esophageal Adenocarcinoma Cells

Hong

Cao

2016

J Pharmacol Exp Ther

View full text Add to dashboard Cite

We have shown that NADPH oxidase (NOX)5-S may mediate the acid-induced decrease in cell apoptosis. However, mechanisms of NOX5-S-dependent decrease in cell apoptosis are not fully understood. In this study, we found that silencer-of-death domain (SODD) was significantly increased in esophageal adenocarcinoma (EA) tissues, EA cell lines FLO and OE33, and a dysplastic cell line CP-B. Strong SODD immunostaining was significantly higher in low-grade dysplasia (66.7%), high-grade dysplasia (81.2%), and EA (71.2%) than in Barrett's mucosa (10.5%). Acid treatment significantly increased SODD protein and mRNA expression and promoter activity in FLO cells, an increase that was significantly decreased by the knockdown of NOX5-S and nuclear factor kB (NF-kB)1 p50 with their small interfering RNAs. Similarly, acid-induced increase of SODD mRNA was blocked by knockdown of NOX5-S and p50 in a BE cell line CP-A. Overexpression of NOX5-S significantly increased SODD protein expression in FLO cells. Moreover, overexpression of NOX5-S or p50 significantly increased the SODD promoter activity and decreased the caspase 9 activity or apoptosis. NOX5-S overexpression-induced increase in SODD promoter activity was significantly decreased by knockdown of p50. In addition, acid treatment significantly decreased the caspase 9 activity, a decrease that was significantly inhibited by knockdown of SODD. Furthermore, chromatin immunoprecipitation assay showed that NF-kB1 p50 bound to SODD genomic DNA containing a NF-kB-binding element GGGGACACCCT. This binding element was further confirmed by a gel mobility shift assay. We conclude that acid-induced increase in SODD expression and decrease in cell apoptosis may depend on the activation of NOX5-S and NF-kB1 p50 in FLO cells.

show abstract

Risk Factors in the Development of Esophageal Adenocarcinoma

Abstract: While some risk factors act predominantly on the initial development of reflux disease, others appear to be primarily responsible for the development of more advanced disease stages.

Cited by 141 publications

References 35 publications

ACG Clinical Guideline: Diagnosis and Management of Barrett’s Esophagus

ACG Clinical Guideline: Diagnosis and Management of Barrett’s Esophagus

Esophageal Cancer, Gastric Cancer and the use of Pesticides in the Southwestern of Turkey

Silencer-of-Death Domain Mediates Acid-Induced Decrease in Cell Apoptosis in Barrett’s Associated Esophageal Adenocarcinoma Cells

Contact Info

Product

Resources

About