Show simple item record

dc.creatorMolina Castro, Silvia Elena
dc.creatorRamírez Mayorga, Vanessa
dc.creatorAlpízar Alpízar, Warner
dc.description.abstractHelicobacter pylori (H. pylori) infection is a well-established risk factor for the development of gastric cancer (GC), one of the most common and deadliest neoplasms worldwide. H. pylori infection induces chronic inflammation in the gastric mucosa that, in the absence of treatment, may progress through a series of steps to GC. GC is only one of several clinical outcomes associated with this bacterial infection, which may be at least partially attributed to the high genetic variability of H. pylori. The biological mechanisms underlying how and under what circumstances H. pylori alters normal physiological processes remain enigmatic. A key aspect of carcinogenesis is the acquisition of traits that equip preneoplastic cells with the ability to invade. Accumulating evidence implicates H. pylori in the manipulation of cellular and molecular programs that are crucial for conferring cells with invasive capabilities. We present here an overview of the main findings about the involvement of H. pylori in the acquisition of cell invasive behavior, specifically focusing on the epithelial-to-mesenchymal transition, changes in cell polarity, and deregulation of molecules that control extracellular matrix remodeling.es_ES
dc.rightsAttribution-NonCommercial-NoDerivatives 4.0 Internacional*
dc.sourceWorld Journal of Gastrointestinal Oncology, vol.10(9), pp. 231-243es_ES
dc.subjectPlasminogen activation systemes_ES
dc.subjectEpithelial-to-mesenchymal transitiones_ES
dc.subjectCell polarityes_ES
dc.subjectGastric carcinogenesises_ES
dc.subjectHelicobacter pylories_ES
dc.titlePriming the seed: Helicobacter pylori alters epithelial cell invasiveness in early gastric carcinogenesises_ES
dc.description.procedenceUCR::Investigación::Unidades de Investigación::Ciencias de la Salud::Instituto de Investigaciones en Salud (INISA)es_ES

Files in this item


This item appears in the following Collection(s)

Show simple item record

Attribution-NonCommercial-NoDerivatives 4.0 Internacional
Except where otherwise noted, this item's license is described as Attribution-NonCommercial-NoDerivatives 4.0 Internacional