%0 Journal Article
%T Carcinog¨¦nesis g¨¢strica Gastric carcinogenesis
%A William Otero Regino
%A Mart¨ªn A G¨®mez
%A Denny Castro
%J Revista Colombiana de Gastroenterologia
%D 2009
%I Asociaci¨®n Colombiana de Gastroenterolog¨ªa
%X El c¨¢ncer g¨¢strico (CG) es la segunda causa de muerte por c¨¢ncer. M¨¢s del 90% de los CG son adenocarcinomas y el principal agente etiol¨®gico es H. pylori y aunque este es necesario, no es suficiente ya que solo 1-2% de los infectados desarrolla CG. Su origen es multifactorial, e involucra factores gen¨¦ticos del individuo, factores medioambientales y la infecci¨®n por H. pylori. Los mecanismos por los cuales H. pylori participa en la carcinog¨¦nesis no son claros pero hay dos v¨ªas involucradas: mecanismos indirectos a trav¨¦s de la inflamaci¨®n persistente inducida por la infecci¨®n, acompa ada de hiperproliferaci¨®n celular, y da o del DNA por radicales libres, con participaci¨®n adicional de c¨¦lulas progenitoras de la m¨¦dula ¨®sea que ser¨ªa el "stem cell" para el CG. La segunda v¨ªa involucra acciones directas de prote¨ªnas de H. pylori sobre las c¨¦lulas g¨¢stricas. Entre los factores gen¨¦ticos del hu¨¦sped hay evidencia de que polimorfismos gen¨¦ticos de IL-1B, TNF, IL-8, INF gama e IL-10 entre otros, inducen una fuerte respuesta inflamatoria que se asocia con mayor riesgo de CG. Gastric cancer is second among cancers as a cause of death. More than 90% of all gastric cancers are adenocarcinomas whose principal cause is Helicobacter pylori. Although H. Pylori is a necessary condition, it is not a sufficient condition since only 1-2% of those infected develop gastric cancer. There are multiple factors besides H. Pylori infection involved in the etiology of this cancer. They include genetic factors related to the individual and environmental factors. Although the ways in which H. Pylori participates in this carcinogenesis are not completely clear, two different mechanisms are involved. H. Pylori infection induces persistent inflammation accompanied by hyperproliferation of cells, and it causes damage to DNA from free radicals in which progenitor cells from the bone marrow participate. These cells could be the "stem cells" of gastric cancer. The second path involves the direct action of proteins from H. Pylori on gastric cells. Among the genetic factors involved there is evidence that IL-1B, TNF, IL-8, and INF gama e IL-10 polymorphisms, among others, induce B inflammatory responses which are associated with higher risks of gastric cancer.
%K Helicobacter pylori
%K carcinog¨¦nesis
%K c¨¦lulas progenitoras
%K polimorfismos
%K Helicobacter pylori
%K carcinogenesis
%K stem cell
%K polymorphisms
%U http://www.scielo.org.co/scielo.php?script=sci_arttext&pid=S0120-99572009000300014