Helicobacter pylori and epigenetic mechanisms underlying gastric carcinogenesis
Author
dc.contributor.author
Valenzuela, Manuel A.
Author
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Canales, Jimena
Author
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Corvalán, Alejandro H.
Author
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Quest, Andrew F. G.
Admission date
dc.date.accessioned
2016-01-12T01:02:07Z
Available date
dc.date.available
2016-01-12T01:02:07Z
Publication date
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2015
Cita de ítem
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World J Gastroenterol 2015 December 7; 21(45): 12742-12756
en_US
Identifier
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DOI: 10.3748/wjg.v21.i45.12742
Identifier
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https://repositorio.uchile.cl/handle/2250/136357
General note
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Artículo de publicación ISI
en_US
Abstract
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The sequence of events associated with the development of gastric cancer has been described as "the gastric precancerous cascade". This cascade is a dynamic process that includes lesions, such as atrophic gastritis, intestinal metaplasia and dysplasia. According to this model, Helicobacter pylori (H. pylori) infection targets the normal gastric mucosa causing non-atrophic gastritis, an initiating lesion that can be cured by clearing H. pylori with antibiotics or that may then linger in the case of chronic infection and progress to atrophic gastritis. The presence of virulence factors in the infecting H. pylori drives the carcinogenesis process. Independent epidemiological and animal studies have confirmed the sequential progression of these precancerous lesions. Particularly long-term follow-up studies estimated a risk of 0.1% for atrophic gastritis/intestinal metaplasia and 6% in case of dysplasia for the long-term development of gastric cancer. With this in mind, a better understanding of the genetic and epigenetic changes associated with progression of the cascade is critical in determining the risk of gastric cancer associated with H. pylori infection. In this review, we will summarize some of the most relevant mechanisms and focus predominantly but not exclusively on the discussion of gene promoter methylation and miRNAs in this context.