Esophageal COX-2 Expression Is Increased in Barrett’s Esophagus, Obesity, and Smoking

Wenker, Theresa Nguyen; Tang, Zhouwen; Younes, Mamoun; Alsarraj, Abeer; Ramsey, David J.; Fitzgerald, Stephanie; Kramer, Jennifer R.; El–Serag, Hashem B.

doi:10.1007/s10620-014-3333-x

Cited by 11 publications

(5 citation statements)

References 35 publications

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“…The main mechanism of this finding may due to the anti‐inflammatory properties of NSAIDs by blocking the production of proinflammatory prostaglandins through inhibition of COX‐2 . Notably, studies suggest that smoking can increase COX‐2 production in esophageal tissue and airway epithelia, although whether this extends to the ovary is unknown. Simultaneously, the antiplatelet effects of aspirin may prevent venous thrombosis, which is increased by smoking.…”

Section: Discussionmentioning

confidence: 73%

Prediagnosis and postdiagnosis smoking and survival following diagnosis with ovarian cancer

Wang

Townsend

Simmons

et al. 2019

Intl Journal of Cancer

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Little is known about the influence of prediagnosis and postdiagnosis smoking and smoking cessation on ovarian cancer survival. We investigated this relationship in two prospective cohort studies, the Nurses' Health Study (NHS) and NHSII. Analyses included 1,279 women with confirmed invasive, Stage I-III epithelial ovarian cancer. We used Cox proportional hazards regression models to estimate hazard ratios (HR) and 95% confidence intervals (CI) for ovarian cancer-specific mortality by smoking status, adjusting for age and year of diagnosis, tumor stage, histologic subtype, body mass index and nonsteroidal anti-inflammatory use (postdiagnosis models only). When examining prediagnosis smoking status (assessed a median of 12 months before diagnosis), risk of death was significantly increased for former smokers (HR = 1.19, 95% CI: 1.02-1.39), and suggestively for current smokers (HR = 1.21, 95% CI: 0.96-1.51) vs. never smokers. Longer smoking duration (≥20 years vs. never, HR = 1.23, 95% CI: 1.05-1.45) and higher pack-years (≥20 pack-years vs. never, HR = 1.28, 95% CI: 1.07-1.52) were also associated with worse outcome. With respect to postdiagnosis exposure, women who smoked ≥15 cigarettes per day after diagnosis (assessed a median of 11 months after diagnosis) had increased mortality compared to never smokers (HR = 2.34, 95% CI: 1.63-3.37). Those who continued smoking after diagnosis had 40% higher mortality (HR = 1.40, 95% CI: 1.05-1.87) compared to never smokers. Overall, our results suggest both prediagnosis and postdiagnosis smoking are associated with worse ovarian cancer outcomes.Additional Supporting Information may be found in the online version of this article.

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Section: Discussionmentioning

confidence: 73%

Prediagnosis and postdiagnosis smoking and survival following diagnosis with ovarian cancer

Wang

Townsend

Simmons

et al. 2019

Intl Journal of Cancer

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“…Exposure to bile acids, acid and greater adiposity are associated with increased COX-2 expression in esophageal squamous mucosa. Similarly, expression of COX-2 is significantly increased in BE and EAC compared with normal mucosa (187,188). Increased COX-2 signaling is thought to predispose to carcinogenesis though resistance to apoptosis, angiogenesis and proliferation, and increased invasiveness.…”

Section: Aspirinmentioning

confidence: 99%

Visceral Obesity, Metabolic Syndrome, and Esophageal Adenocarcinoma

Elliott

Reynolds

2021

Front. Oncol.

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Esophageal adenocarcinoma (EAC) represents an exemplar of obesity-associated carcinogenesis, with a progressive increase in EAC risk with increased body mass index. In this context, there is increased focus on visceral adipose tissue and associated metabolic dysfunction, including hypertension, diabetes mellitus and hyperlipidemia, or combinations of these in the metabolic syndrome. Visceral obesity (VO) may promote EAC via both directly impacting on gastro-esophageal reflux disease and Barrett's esophagus, as well as via reflux-independent effects, involving adipokines, growth factors, insulin resistance, and the microbiome. In this review these pathways are explored, including the impact of VO on the tumor microenvironment, and on cancer outcomes. The current evidence-based literature regarding the role of dietary, lifestyle, pharmacologic and surgical interventions to modulate the risk of EAC is explored.

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“…This raises the possibility that even when symptoms are present, they may be subclinical, easily managed by over the counter medications, and not come to the attention of a physician. As a result, recent Barrett's prediction models challenge the presence of reflux symptoms and emphasise other factors such as central obesity and smoking …”

Section: Discussionmentioning

confidence: 99%

Systematic review with meta‐analysis: prevalent vs. incident oesophageal adenocarcinoma and high‐grade dysplasia in Barrett's oesophagus

Visrodia

Singh

Krishnamoorthi

et al. 2016

Aliment Pharmacol Ther

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Esophageal COX-2 Expression Is Increased in Barrett’s Esophagus, Obesity, and Smoking

Cited by 11 publications

References 35 publications

Prediagnosis and postdiagnosis smoking and survival following diagnosis with ovarian cancer

Prediagnosis and postdiagnosis smoking and survival following diagnosis with ovarian cancer

Visceral Obesity, Metabolic Syndrome, and Esophageal Adenocarcinoma

Systematic review with meta‐analysis: prevalent vs. incident oesophageal adenocarcinoma and high‐grade dysplasia in Barrett's oesophagus

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