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Risk factors for esophageal cancer: emphasis on infectious agents.
El-Zimaity, Hala; Di Pilato, Vincenzo; Novella Ringressi, Maria; Brcic, Iva; Rajendra, Shanmugarajah; Langer, Rupert; Dislich, Bastian; Tripathi, Monika; Guindi, Maha; Riddell, Robert.
Afiliación
  • El-Zimaity H; Dynacare Laboratories, Brampton, Ontario, Canada.
  • Di Pilato V; Department of Clinical and Experimental Medicine, University of Florence, Florence, Italy.
  • Novella Ringressi M; Department of Surgery and Translational Medicine, University of Florence, Florence, Italy.
  • Brcic I; Gastrointestinal Surgery Unit, Florence Careggi University Hospital, Florence, Italy.
  • Rajendra S; Institute of Pathology, Medical University of Graz, Graz, Austria.
  • Langer R; Gastro-Intestinal Viral Oncology Group, Ingham Institute for Applied Medical Research, Liverpool, Sydney, New South Wales, Australia.
  • Dislich B; South Western Sydney Clinical School, University of New South Wales, Kensington, Sydney, New South Wales, Australia.
  • Tripathi M; Department of Gastroenterology & Hepatology, Bankstown-Lidcombe Hospital, South Western Sydney Local Health Network, Bankstown, Sydney, New South Wales, Australia.
  • Guindi M; Institute of Pathology, University of Bern, Bern, Switzerland.
  • Riddell R; Institute of Pathology, Kantonsspital Baselland, Liestal, Switzerland.
Ann N Y Acad Sci ; 1434(1): 319-332, 2018 12.
Article en En | MEDLINE | ID: mdl-29851130
ABSTRACT
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.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Esófago de Barrett / Neoplasias Esofágicas / Adenocarcinoma / Reflujo Gastroesofágico / Infecciones por Helicobacter / Infecciones por Virus de Epstein-Barr / Esófago Tipo de estudio: Etiology_studies / Risk_factors_studies Idioma: En Revista: Ann N Y Acad Sci Año: 2018 Tipo del documento: Article País de afiliación: Canadá

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Esófago de Barrett / Neoplasias Esofágicas / Adenocarcinoma / Reflujo Gastroesofágico / Infecciones por Helicobacter / Infecciones por Virus de Epstein-Barr / Esófago Tipo de estudio: Etiology_studies / Risk_factors_studies Idioma: En Revista: Ann N Y Acad Sci Año: 2018 Tipo del documento: Article País de afiliación: Canadá
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