Gastric adenocarcinoma and Helicobacter pylori: correlation with p53 mutation and p27 immunoexpression.
ABSTRACT Helicobacter pylori infection is an established risk factor for gastric cancer development, but the exact underlying mechanism still remains obscure. The inactivation of tumor suppressor genes such as p53 and p27(KIP1) is a hypothesized mechanism, although there is no consensus regarding the influence of H. pylori cagA(+) in the development of these genetic alterations.
To verify the relationship among H. pylori infection, p53 mutations and p27(Kip1) Protein (p27) expression in gastric adenocarcinomas (GA) seventy-four tissues were assayed by PCR for H. pylori and cagA presence. Mutational analysis of p53 gene was performed by single-strand conformation polymorphism (SSCP). Seventy tissues were analyzed by an immunohistochemical method for p27 expression.
From the samples examined, 95% (70/74) were H. pylori positive, 63% cagA(+). Altered p53 electrophoretic mobility was found in 72% of cases and significantly more frequent in the presence of cagA. Considerable reduction in p27 expression (19%) was found with a tendency for association between cagA(+) and p27(-), although the results were not statistically significant. Concomitant alterations of both suppressor genes were detected in 60% of cases. In the cases cagA(+), 66.7% of them had these concomitant alterations.
The data suggest that H. pylori cagA(+) contributes to p53 alteration and indicate that concomitant gene inactivation, with reduced p27 expression, may be a mechanism in which H. pylori can promote the development and progression of gastric cancer.
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ABSTRACT: Helicobacter pylori cause damage to gastric epithelial cells and alterations in the p53 gene that lead to cancer development. This study aimed to determine the correlation of p53 expression with H. pylori using immunohistochemistry, RFLP-PCR, and histopathology. Gastric biopsy samples from gastric cancer (GC) (n = 54) and gastritis (n = 31) patients were examined for histopathological changes and expression of p53 protein by immunohistochemistry. Immunohistochemical analysis of p53 protein expression in H. pylori-positive GC sections showed an average of 44.3% positive cells in tumors and 6.9% in normal tissues, as compared to 16.4% and 4.4% in H. pylori-negative sections. P53 expression showed significant association with H. pylori (P = 0.005), invasion depth (P = 0.029) and inflammation reaction (P = 0.008). In gastritis sections, no difference in the average p53 staining in H. pylori-positive or -negative sections was seen. PCR-RFLP results also showed no difference in genotype frequencies of p53 in H. pylori-positive or -negative gastritis sections. Histopathology study of H. pylori-positive GC sections showed that 97.2% were the intestinal type and 2.8% the diffuse type, while in H. pylori-negative sections 35.2% were the intestinal type and 64.8% the diffuse type. Biopsy sections from H. pylori-positive gastritis patients revealed more severe inflammation than those of H. pylori-negative patients. Our results show that H. pylori infection affects p53 expression in GC. The average p53 expression was significantly higher in tumor than in normal tissues. In gastritis sections p53 expression was significantly associated with H. pylori.The Journal of Infection in Developing Countries 09/2013; 7(9):651-7. DOI:10.3855/jidc.2993 · 1.27 Impact Factor
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ABSTRACT: AIMS: There has been limited information about the relations between Helicobacter pylori infection and expressions of apoptosis-related proteins p53, ASPP and iASPP in gastric cancer and precancerous lesions. METHODS: H. pylori in gastric mucosa were identified by W-S staining and rapid urease test. Expression of apoptosis-related proteins P53, ASPP2 and iASPP in the gastric tissues were determined by immunohistochemistry. RESULTS: The concentrations of H. pylori and expressions of p53 and iASPP in gastric carcinoma group and precancerous lesion group were higher than in benign gastric diseases group (P<0.05). The expressions of ASPP2 in gastric carcinoma and precancerous lesion group were lower than in benign gastric diseases group (P<0.05). The expressions of p53 and iASPP in H. pylori positive group were higher than in H. pylori negative group (P<0.05), whereas ASPP2 in H. pylori positive group were lower than in H. pylori negative group (P<0.05). CONCLUSION: There was a higher rate H. pylori infection, an increased expression of apoptosis inhibitor iASPP, and decreased expression of apoptosis stimulator ASPP2 in gastric cancer or precancerous tissues. These results suggest that H. pylori may cause gastric cancer by up-regulating iASPP and down-regulating ASPP2.Pathologie Biologie 03/2013; DOI:10.1016/j.patbio.2013.02.002 · 1.07 Impact Factor
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ABSTRACT: Gastroenterología RESUMEN Helicobacter pylori es una bacteria con forma helicoidal, que vive únicamente en el estómago humano. Aunque la relación del bacilo con el epitelio es de antaño debido a que gran parte de la población se halla colonizada, tan solo cerca del 10% de las personas infectadas desarrollan ciertas patologías, entre ellas la úlcera duodenal, el adenocarcinoma estomacal y el linfoma tipo MALT. En las últimas décadas, la investigación sobre el Helicobacter pylori se ha incrementado, y poco a poco, se ha deslumbrando más sobre la fi siopatología de este microorganismo, como la presencia de genes involucrados en la patogenicidad vacA, cagA babA y sabA, indicando con ello que no es precisamente una bacteria totalmente inocua, pero tampoco el del mayor patógeno en el epitelio estomacal. Mediante la presente revisión se pretende abarcar algunos aspectos sobre la bacteria, su relación y benefi cios con el huésped, así como los procesos patológicos que puede desencadenar su accionar. (MÉD.UIS. 2011;24(3):287-96). Palabras Clave: Helicobacter pylori. Úlcera péptica. Linfoma tipo MALT. Linfoma de Células B de la Zona Marginal. SUMMARY Helicobacter pylori: review of physiologic and patologic aspects Helicobacter pylori is a spiral-shaped bacterium, that lives only in the human stomach. Although the relationship of the bacillus in the epithelium has been since ancient because most of the population is colonized, only about 10% of infected people develop certain diseases, including duodenal ulcer, stomach adenocarcinoma and lymphoma MALT. In recent decades, research on Helicobacter pylori has increased, and little by little, has dazzled more about the pathophysiology of this organism, as the presence of genes involved in pathogenicity vacA, cagA, babA and sabA thereby indicating that is just a completely harmless bacteria, but neither of the major pathogen in stomach epithelium. Through this review is to cover some aspects of the bacteria, their relationship and benefi ts to the host and the pathological processes that can trigger their actions. (MÉD.UIS. 2011;24(3):287-96) Key Words: Helicobacter pylori. Peptic ulcer. Lymphoma MALT. Lymphoma. B-Cell. Marginal Zone. INTRODUCCIÓN El Helicobacter pylori (H. pylori) al microscopio óptico y con el uso de colorantes tales como hematoxilina-eosina, tinción de Warthin-Starry o el Giemsa modificada 1 , se observa en medios orgánicos como un bacilo gram negativo con forma curvilínea y multiflagelado cuyo tamaño varía a lo ancho entre 0,5 a 1 µm y a lo largo desde 2,5 hasta 6,5 µm, omitiendo el tamaño de los flagelos que pueden ser de hasta 30 µm 1-3 . El estudio el 20 de agosto de 2011 y aceptado para publicación el 3 de diciembre de 2011.