Barrett's esophagus: cancer and molecular biology

Gibson, Michael K.; Dhaliwal, Arashinder S.; Clemons, Nicholas J.; Phillips, Wayne A.; Dvorak, Katerina; Tong, Daniel; Law, Simon; Pirchi, Enrique D; Räsänen, Jari; Krasna, Mark J.; Parikh, Kaushal; Krishnadath, Kausilia K.; Chen, Yu; Griffiths, Leonard P.; Colleypriest, Benjamin J.; Farrant, J. Mark; Tosh, David; Das, Kiron M.; Bajpai, Manisha

doi:10.1111/nyas.12252

Cited by 24 publications

(26 citation statements)

References 85 publications

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“…In addition, the role of bile and gastric acids in STAT3/NF-kB signaling has been studied in HET-1A cells indicating increased activation of both following exposure compared with parental cells and supporting a role for bile and acid reflux at a signaling level [74]. Activated phospho-STAT3 has been demonstrated only in transformed Barrett's cells with resultant inhibition of apoptosis [75].…”

Section: Transcription Factors Mediate Tumor Promotion and Metastasismentioning

confidence: 98%

The role of inflammation in cancer of the esophagus

O’Sullivan

Phelan

O’Hanlon

et al. 2014

Expert Review of Gastroenterology & Hepatology

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Esophageal adenocarcinoma is the eighth most common malignancy worldwide. The overall prognosis is poor, with 5-year survival ranges of approximately 15-25%, and 30-50% for patients who can be treated with curative intent. There has been a marked increase in incidence of esophageal adenocarcinoma over the last 30 years, with chronic and severe reflux, diet and obesity identified as principal factors fuelling this rise in the West. Esophageal adenocarcinoma is an exemplar model of an inflammation-associated cancer. The key molecular pathways driving tumor development and influencing tumor biology are the subject of considerable research efforts, and is the principal focus of this review. In addition, the diverse range of changes occurring in the local immune response, tissue microenvironment, metabolic profile, intracellular signaling mechanisms and microRNA signatures are discussed, as well as novel targeted therapies.

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Section: Transcription Factors Mediate Tumor Promotion and Metastasismentioning

confidence: 98%

The role of inflammation in cancer of the esophagus

O’Sullivan

Phelan

O’Hanlon

et al. 2014

Expert Review of Gastroenterology & Hepatology

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“…It is also well known that components of gastroduodenal fluids, including conjugated bile acids and unconjugated deoxycholic acid (DCA) contribute to the development of Barrett's esophagus and esophageal adenocarcinoma, whereas DNA damage induced by bile acids on Barrett's cells correlates with constitutive activation of nuclear factor‐kappa B (NF‐κB) . In this regard, there is evidence that NF‐κB transcription factors are mediated by a mechanistic link in both esophageal squamous cell transformation to Barrett's and to adenocarcinoma in a 2‐step process . The NF‐κB pathway demonstrated in Barrett's esophagus includes acceleration of cytokine expression, interleukin (IL)‐1β, IL‐6, and IL‐8, activation of signal transducer and activator of transcription 3 (STAT3), as well as increased levels of anti‐apoptotic B‐cell lymphoma 2 (Bcl‐2), epidermal growth factor receptor (EGFR), cyclooxygenase‐2, caudal‐related homeobox transcription factor‐2, and reactive oxygen/nitrogen species …”

Section: Introductionmentioning

confidence: 99%

“…In this regard, there is evidence that NF‐κB transcription factors are mediated by a mechanistic link in both esophageal squamous cell transformation to Barrett's and to adenocarcinoma in a 2‐step process . The NF‐κB pathway demonstrated in Barrett's esophagus includes acceleration of cytokine expression, interleukin (IL)‐1β, IL‐6, and IL‐8, activation of signal transducer and activator of transcription 3 (STAT3), as well as increased levels of anti‐apoptotic B‐cell lymphoma 2 (Bcl‐2), epidermal growth factor receptor (EGFR), cyclooxygenase‐2, caudal‐related homeobox transcription factor‐2, and reactive oxygen/nitrogen species …”

Section: Introductionmentioning

confidence: 99%

In vitro model for gastroduodenal reflux–induced nuclear factor‐kappaB activation and its role in hypopharyngeal carcinogenesis

2015

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“…Over approximately the same period there has been a dramatic increase in the incidence of oesophageal adenocarcinoma (OAC), also predominantly in the western, developed world. The pathogenesis of OAC is not fully defined, although increasingly the molecular changes are being understood [Gibson et al 2013]. It seems clear that reflux of gastroduodenal contents is involved in the initiation, perpetuation and progression of the oesophageal changes.…”

Section: Introductionmentioning

confidence: 99%

The role of obesity in oesophageal cancer development

Long

Beales

2014

Therap Adv Gastroenterol

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Abstract:The incidence of oesophageal adenocarcinoma has increased dramatically in the developed world in the last half century. Over approximately the same period there has been an increase in the prevalence of obesity. Multiple epidemiological studies and metaanalyses have confirmed that obesity, especially abdominal, visceral obesity, is a risk factor for gastro-oesophageal reflux, Barrett's oesophagus and oesophageal adenocarcinoma. Although visceral obesity enhances gastro-oesophageal reflux, the available data also show that visceral obesity increases the risk of Barrett's oesophagus and adenocarcinoma via reflux-independent mechanisms. Several possible mechanisms could link obesity with the risk of oesophageal adenocarcinoma in addition to mechanical effects increasing reflux. These include reduced gastric Helicobacter pylori infection, altered intestinal microbiome, factors related to lifestyle, the metabolic syndrome and associated low-grade inflammation induced by obesity and the secretion of mediators by adipocytes which may directly influence the oesophageal epithelium. Of these adipocyte-derived mediators, increased leptin levels have been independently associated with progression to oesophageal adenocarcinoma and in laboratory studies leptin enhances malignant behaviours in cell lines. Adiponectin is also secreted by adipocytes and levels decline with obesity: decreased serum adiponectin levels are associated with malignant progression in Barrett's oesophagus and experimentally adiponectin exerts anticancer effects in Barrett's cell lines and inhibits growth factor signalling. At present there are no proven chemopreventative interventions that may reduce the incidence of obesity-associated oesophageal cancer: observational studies suggest that the combined use of a statin and aspirin or another cyclo-oxygenase inhibitor is associated with a significantly reduced cancer incidence in patients with Barrett's oesophagus.

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Barrett's esophagus: cancer and molecular biology

Cited by 24 publications

References 85 publications

The role of inflammation in cancer of the esophagus

The role of inflammation in cancer of the esophagus

In vitro model for gastroduodenal reflux–induced nuclear factor‐kappaB activation and its role in hypopharyngeal carcinogenesis

The role of obesity in oesophageal cancer development

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