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Helicobacter pylori-Induced Chronic Gastritis and Assessing Risks for Gastric Cancer
被引:42
|作者:
Carrasco, Gonzalo
[1
]
Corvalan, Alejandro H.
[2
,3
]
机构:
[1] Mt Sinai Sch Med, Dept Pathol, New York, NY 10029 USA
[2] Pontificia Univ Catolica Chile, Ctr Translat Res Oncol CITO, Santiago 8330074, Chile
[3] Pontificia Univ Catolica Chile, Dept Hematol & Oncol, Santiago 8330074, Chile
关键词:
CHRONIC ATROPHIC GASTRITIS;
III INTESTINAL METAPLASIA;
FOLLOW-UP;
PROMOTER METHYLATION;
DYSPLASIA;
INFECTION;
CLASSIFICATION;
PROGRESSION;
COLOMBIA;
STOMACH;
D O I:
10.1155/2013/393015
中图分类号:
R57 [消化系及腹部疾病];
学科分类号:
摘要:
Chronic gastritis is an inflammation of the gastric mucosa and has multiple etiologies. Here we discuss the pathological alterations induced by Helicobacter pylori (HP) leading to chronic gastritis and the epigenetic bases underlying these changes. We review the histology of the normal gastric mucosa and overview the role of HP in the multistep cascade of GC. We attempt to define the role of the Operative Link for Gastritis Assessment (OLGA) staging system in assessing the risk of GC. The epigenetic bases of chronic gastritis, mainly DNA methylation, are presented through examples such as (i) the methylation of the promoter region of E-cadherin in HP-induced chronic gastritis and its reversion after HP eradication and (ii) the association of methylation of the promoter region of Reprimo, a p53-mediated cell cycle arrest gene, with aggressive HP strains in high risk areas for GC. In addition, we discuss the finding of RPRM as a circulating cell-free DNA, offering the opportunity for noninvasive risk assessment of GC. Finally, the integration of OLGA and tissue biomarkers, by systems pathology approach, suggests that severe atrophy has a greater risk for GC development if, in addition, overexpressed p73. This trial is registered with ClinicalTrials.gov NCT01774266.
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