Helicobacter pylori-Induced Chronic Gastritis and Assessing Risks for Gastric Cancer
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 mucos...
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| Format: | Article |
| Language: | English |
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Wiley
2013-01-01
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| Series: | Gastroenterology Research and Practice |
| Online Access: | http://dx.doi.org/10.1155/2013/393015 |
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| author | Gonzalo Carrasco Alejandro H. Corvalan |
| author_facet | Gonzalo Carrasco Alejandro H. Corvalan |
| author_sort | Gonzalo Carrasco |
| collection | DOAJ |
| description | 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. |
| format | Article |
| id | doaj-art-c763b1f95aab40e4b7eef8bd9a09262b |
| institution | Kabale University |
| issn | 1687-6121 1687-630X |
| language | English |
| publishDate | 2013-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | Gastroenterology Research and Practice |
| spelling | doaj-art-c763b1f95aab40e4b7eef8bd9a09262b2025-02-03T01:21:54ZengWileyGastroenterology Research and Practice1687-61211687-630X2013-01-01201310.1155/2013/393015393015Helicobacter pylori-Induced Chronic Gastritis and Assessing Risks for Gastric CancerGonzalo Carrasco0Alejandro H. Corvalan1Department of Pathology, Mount Sinai School of Medicine, 1425 Madison Ave, New York, NY 10029, USACentre for Translational Research in Oncology (CITO) and Department of Hematology and Oncology, Pontificia Universidad Catolica de Chile, Marcoleta 391, 8330074 Santiago, ChileChronic 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.http://dx.doi.org/10.1155/2013/393015 |
| spellingShingle | Gonzalo Carrasco Alejandro H. Corvalan Helicobacter pylori-Induced Chronic Gastritis and Assessing Risks for Gastric Cancer Gastroenterology Research and Practice |
| title | Helicobacter pylori-Induced Chronic Gastritis and Assessing Risks for Gastric Cancer |
| title_full | Helicobacter pylori-Induced Chronic Gastritis and Assessing Risks for Gastric Cancer |
| title_fullStr | Helicobacter pylori-Induced Chronic Gastritis and Assessing Risks for Gastric Cancer |
| title_full_unstemmed | Helicobacter pylori-Induced Chronic Gastritis and Assessing Risks for Gastric Cancer |
| title_short | Helicobacter pylori-Induced Chronic Gastritis and Assessing Risks for Gastric Cancer |
| title_sort | helicobacter pylori induced chronic gastritis and assessing risks for gastric cancer |
| url | http://dx.doi.org/10.1155/2013/393015 |
| work_keys_str_mv | AT gonzalocarrasco helicobacterpyloriinducedchronicgastritisandassessingrisksforgastriccancer AT alejandrohcorvalan helicobacterpyloriinducedchronicgastritisandassessingrisksforgastriccancer |