Overexpression of angiogenic mediators, such as vascular endothelial growth factor ( VEGF), inducible nitric oxide synthase ( iNOS), and cyclooxygenase ( COX)-2 have been associated with EA development 8, 9, 12 and prognosis 9, 13. The importance of angiogenesis specifically in EA has been supported by a large body of research, including in vitro, in vivo, and clinical studies 9. Conversely, inhibition of angiogenesis results in suppression of tumor growth 10, 11. This process facilitates tumor growth by providing oxygenation and nutrition to tumor cells 7– 9. It has been suggested that gene-environment interactions play more important role in cancer etiology than do individual factors alone 6.Īngiogenesis is a process of new blood vessel formation from endothelial precursors. However, no single factor can fully explain the rising incidence of EA.
Over recent years, it has been established that gastroesophageal reflux disease (GERD), smoking, higher body mass index (BMI) or obesity, and certain genetic variations are individually associated with EA risk 4, 5. The rapidly increasing incidence and sporadically development feature of EA suggest that environmental influences dominate its etiology 3. Esophageal adenocarcinoma (EA) has the fastest rising incidence of all solid tumors in the US and in Western Europe over the last four decades 1, 2.
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