Helicobacter pylori y cáncer gástrico / Helicobacter pylori and gastric cancer

Introducción: El Helicobacter pylori se ha relacionado con el desarrollo de gastritis crónica atrófica, metaplasia intestinal y displasia, lesiones que pueden evolucionar a carcinoma gástrico. Existen investigaciones que demuestran que la erradicación de esta bacteria disminuye el riesgo de progresión histopatológica de las lesiones preneoplásicas, excepto la metaplasia intestinal y la displasia. Se realizó una revisión de los artículos publicados en las bases de datos Pubmed, Scielo, Medline y Cochrane, relacionados con el tema. Objetivo: Profundizar en los conocimientos relacionados con la infección por Helicobacter pylori y cáncer gástrico. Desarrollo: El adenocarcinoma es el tumor gástrico más frecuente y el Helicobacter pylori es el agente etiológico principal. En poblaciones de riesgo elevado, el adenocarcinoma gástrico de tipo intestinal, se precede de lesiones preneoplásicas (atrofia, metaplasia intestinal y displasia) que evoluciona al cáncer invasor. Conclusiones: Helicobacter pylori favorece la carcinogénesis gástrica, aunque existen otros factores de riesgo para el surgimiento del cáncer gástrico como son: la historia familiar, la pobre ingestión de frutas y vegetales y el bajo nivel socioeconómico(AU)

Introduction: Helicobacter pylori has been linked to the development of chronic atrophic gastritis, intestinal metaplasia, and dysplasia, lesions that can progress to gastric carcinoma. There is research showing that the eradication of this bacterium reduces the risk of histopathological progression of preneoplastic lesions, except for intestinal metaplasia and dysplasia. A bibliographic review was made of the articles published in the Pubmed, Scielo, Medline and Cochrane data bases, related to the topic, belonging to authors dedicated to the study of this problem. Objective: To go deepen in the knowledge related to Helicobacter pylori infection and gastric cancer. Development: Adenocarcinoma is the most frequent gastric tumor and Helicobacter pylori is the main etiologic agent. In high-risk populations, gastric adenocarcinoma of the intestinal type, is preceded by preneoplasic lesions (atrophy, intestinal metaplasia, and dysplasia), that progresses to invasive cancer. Conclusions: Helicobacter pylori favors gastric carcinogenesis, although there are other risk factors for the development of gastric cancer such as: family history, poor intake of fruits and vegetables, and low socioeconomic leve(AU)

Comparative proteomics analysis of chronic atrophic gastritis: changes of protein expression in chronic atrophic gastritis without Helicobacter pylori infection

Chronic atrophic gastritis (CAG) is a very common gastritis and one of the major precursor lesions of gastric cancer, one of the most common cancers worldwide. The molecular mechanism underlying CAG is unclear, but its elucidation is essential for the prevention and early detection of gastric cancer and appropriate intervention. A combination of two-dimensional gel electrophoresis and mass spectrometry was used in the present study to analyze the differentially expressed proteins. Samples from 21 patients (9 females and 12 males; mean age: 61.8 years) were used. We identified 18 differentially expressed proteins in CAG compared with matched normal mucosa. Eight proteins were up-regulated and 10 down-regulated in CAG when compared with the same amounts of proteins in individually matched normal gastric mucosa. Two novel proteins, proteasome activator subunit 1 (PSME1), which was down-regulated in CAG, and ribosomal protein S12 (RPS12), which was up-regulated in CAG, were further investigated. Their expression was validated by Western blot and RT-PCR in 15 CAG samples matched with normal mucosa. The expression level of RPS12 was significantly higher in CAG than in matched normal gastric mucosa (P < 0.05). In contrast, the expression level of PSME1 in CAG was significantly lower than in matched normal gastric mucosa (P < 0.05). This study clearly demonstrated that there are some changes in protein expression between CAG and normal mucosa. In these changes, down-regulation of PSME1 and up-regulation of RPS12 could be involved in the development of CAG. Thus, the differentially expressed proteins might play important roles in CAG as functional molecules.

Seroprevalences ofHelicobacter pylori infection and chronic atrophic gastritis in the united Republic of Tanzania and the Dominican Republic.

OBJECTIVE: The aim of this survey was to compare the seroprevalences ofHelicobacter Pylori (H. pylori) and chronic atrophic gastritis (CAG) in Tanzania and the Dominican Republic, both of which are tropical countries, and thereafter compare the prevalences in Tanzania and the Dominican Republic with prevalences from our previous studies done in Japan (1991) and China (1996/97). METHODS: Community-based study in which 573 inhabitants of Tanzania and 1,215 inhabitants of the Dominican Republic answered detailed questionnaires on upper digestive tract diseases, and then underwent screening for gastric cancer by serum pepsinogen and testing for antibody toH. pylori. RESULTS: After adjusting to the 'Age-Standardized Rate' (ASR) using the world population in 1995, the seroprevalences ofH. pylori infection in male and female subjects for Tanzania (m=85.3% & f=88.2%) were very high compared to those for the Dominican Republic (m=63.5% & f=62.4%) and Japan (m=62.0% & f=46.8%), and similar to those of China (m=78.0% & f=77.3%). Also, the agestandardized prevalences of CAG in males and females for Tanzania (m-0.237& f=0.458). were higher than those of the Dominican Republic (m=0.168 & f=0.211) and China (m=0.111 & f=0.107) and compared well with those of Japan (m=0.266 & f=0.352). CONCLUSIONS: Although Tanzania and the Dominican Republic are both developing countries, Tanzania had a very high age-standardized prevalence ofH. pylori and CAG compared to that of the Dominican Republic, which showed a trend similar to that of Japan.