Esophageal Adenocarcinoma|OMICS International|Journal Of Neurology And Neurophysiology

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Esophageal Adenocarcinoma

Esophageal adenocarcinoma (EA) has increased in incidence over the past three decades, and in the last 10 years at a rate exceeding that of any other cancer. EA is characterized by a uniformly poor prognosis, with a median survival time following diagnosis of less than 18 months, and a five-year survival rate of less than 20% in operable tumors. Other than surgical resection of early stage disease, no other therapies alter its clinical course. Gastro-esophageal reflux disease complicated by Barrett’s esophagus (BE) is a major risk factor for esophageal adenocarcinoma. However, mechanisms of the progression from BE to EA is unknown. Acid reflux and reflux-induced inflammation may play an important role in the progression. Ambulatory pH studies show that the total exposure time of esophageal luminal pH < 4 is 1.5-16 hours per day in BE patients, which is greater than in patients with GERD. It has also been reported that acid exposure induces DNA damage in human esophageal cell lines. Cultured biopsy specimens of intestinal metaplastic cells demonstrate a significant increase in tritiated thymidine uptake when the explants are briefly exposed to acid, suggesting that in Barrett’s specimens brief, episodic acid exposure is sufficient to promote tumorigenesis by stimulating hyperproliferation. Longterm inhibition of esophageal acid exposure by administration of proton pump inhibitors (PPI) to patients with BE has been shown to decrease proliferation of metaplastic cellsand an effective anti reflux surgery may reduce the risk of Barrett’s progression.
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Last date updated on June, 2021