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Risk factors for esophageal cancer: emphasis on infectious agents
Author(s) -
ElZimaity Hala,
Di Pilato Vincenzo,
Novella Ringressi Maria,
Brcic Iva,
Rajendra Shanmugarajah,
Langer Rupert,
Dislich Bastian,
Tripathi Monika,
Guindi Maha,
Riddell Robert
Publication year - 2018
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1111/nyas.13858
Subject(s) - dysplasia , esophagus , esophageal cancer , carcinogenesis , helicobacter pylori , gastroenterology , medicine , cancer research , carcinoma , biology , cancer , immunology
Risk factors for esophageal cancer include genetic factors (such as tylosis) and infectious agents. A variety of organisms have been implicated in esophageal carcinogenesis, either directly or indirectly. In this review, we explore the normal esophageal flora and how it may be controlled, and also the variety of organisms that may affect esophageal carcinogenesis, either directly or indirectly. The organisms with potential direct effects in squamous cell carcinoma include human papillomavirus (HPV), Epstein–Barr virus, and polyoma viruses. Interestingly, HPV is now implicated in esophageal adenocarcinoma (EAC), not in its initiation but in the development of dysplasia, in which HPV33 in particular has been associated. Indirectly, Helicobacter pylori has been associated with EAC by, initially, causing increased acid secretion that increases acid reflux, and by reducing lower esophageal sphincter pressure, which increases gastroesophageal reflux; the latter increases the risk of Barrett's esophagus, and hence EAC. Conversely, subsequent atrophic gastritis may normalize that risk.