By M. Bortolotti
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Extra resources for Gastroesophageal Reflux Disease
Although intestinal bacteria are an important factor in the inflammation and tumorigenesis, their precise role remains elusive. One theory 32 Gastroesophageal Reflux Disease is that both “protective” species and “harmful” species exist within the normal enteric microbiome. A healthy balance between these two populations in a normal host might be detrimental for an inflammation-prone host. Alternatively, a breakdown in the balance between the two populations, termed “dysbiosis”, could by itself promote inflammation in a normal host.
There is a vital need to explore factors other than symptoms that not only may elucidate the pathophysiology of BE development but also that may be predictive of progression to EAC. Significant advances have been made along key areas such as cell cycle abnormalities, growth factors, adiposity, and the gut microbiome. This chapter aims to review some of these elements as well as the prognostic value of biomarkers for progression from BE to EAC. , 2009). 2. Cell cycle abnormalities The normal cell cycle by which cells proliferate is comprised of an intricate system of checkpoints and regulations designed to carefully modulate growth.
2006). , 2008). , 2003) and inhibition of apoptosis, which may predispose to an increased risk of BE and esophageal adenocarcinoma (Beales and Ogunwobi, 2007). These effects have been demonstrated to be synergistic when leptin is combined with acid pulses (Beales and Ogunwobi, 2007). The most current research has demonstrated a complex signaling pathway by which leptin causes these aberrations, however the exact mechanism has not been completely elucidated. It is postulated that leptin stimulates a transmembrane leptin receptor, which activates both P38 MAP kinase and janus kinase JAK2 pathways.