Inflammation, Obesity, Barrett’s Esophagus, and Esophageal Adenocarcinoma

Sharma, Arunima; Elebiary, Ahmed; Chowdhury, Sonia; Buttar, Navtej

doi:10.1007/978-1-4614-6819-6_6

Cited by 1 publication

(2 citation statements)

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“…The chronic inflammatory state induced by repeated exposure to gastric acid is assumed to establish a microenvironment with a high turnover of basal epithelial cells, coupled with a propensity for mutation through generation of reactive oxygen species and other molecular pathways [13,14]. The low-pH environment is also hypothesized to promote the production of mutagens from exogenous and endogenous contents of the esophagus (such as nitrosamines from saliva [15][16][17]).…”

Section: Gastroesophageal Acid Refluxmentioning

confidence: 99%

“…Second, the visceral fat deposits that predominate in men are metabolically active-more so than the subcutaneous fat deposits that tend to accumulate preferentially in women [29]. It is hypothesized that the metabolic disturbances engendered by visceral fat [including insulin resistance and increased production of adipocytokines and insulinlike growth factors (IGFs)], may promote tumor development through their anti-apoptotic and pro-proliferative effects [13,30,31].…”

Section: Obesitymentioning

confidence: 99%

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Esophageal Cancer: Priorities for Prevention

Whiteman

2014

Curr Epidemiol Rep

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Making a sizeable contribution to worldwide cancer mortality, adenocarcinomas and squamous cell carcinomas of the esophagus appear to be caused largely by environmental factors. Descriptive epidemiologic analyses demonstrate that these cancers occur at markedly different rates in populations around the world. Moreover, their incidences have changed greatly over time, strongly suggesting that their causes are modifiable. For adenocarcinomas, the risk factors identified consistently in analytic studies include gastroesophageal acid reflux, obesity, smoking, and male sex. Squamous cell carcinomas in Western countries have been attributed largely to smoking, high levels of alcohol consumption, and poor nutrition. In other parts of the world, poor-quality diets, thermal injury, exposure to polycyclic aromatic hydrocarbons, and poor oral health have been implicated. Prevention strategies targeting these exposures offer a logical foundation for action, although the outcomes of prevention trials have been frustratingly ineffective to date. Novel approaches to early detection are currently under development and may prove useful for disease control in high-incidence settings.

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