pylori and who also had mutant p53, than in subjects who were negative for both. Other studies have documented the presence of free radicals in the gastric mucosa of persons with H. pylori infection [45–47]. The contribution of p53 to the subsequent occurrence of gastric cancer was significant in H. pylori-seropositve subjects and non in H. pylori-seronegative subjects. Oxidative damage is well documented in chronic gastric inflammatory diseases [48, 49]. Recent published Smad inhibitor results showed that mucosal oxidative damage in H. pylori infection is associated with increased inflammatory cell infiltration, enhanced apoptosis, and cell proliferation, whereas it has been

postulated that the progressive accumulation of oxidative DNA damage in certain

genes, such as p53, may contribute to gastric carcinogenesis [26]. Such data suggest that apoptosis may be induced by both the transcriptional activation of a range of target AZD1152 clinical trial genes and also by a range of other events that may presumably include signal transduction [50]. In summary, our findings suggest that H. pylori infection contributes to the development of gastric cancer by elevating the levels of mutant p53. However, although this may be a necessary promoter in the appearance of cancer, it is not in itself a risk factor in the absence of a previous triggering or initiating or find more mutagenic factor or factors and the other hand, the presence of anti-H. pylori antibodies in human sera remains one of the simplest methods of detecting H. pylori bacteria, and serological methods thus play an important role in the clinical practice. Authors’ Disclosures of Potential Conflicts of interests The authors declare that they have no competing interests. Acknowledgements The authors thank Karen Shashok for translating the original manuscript into English. This study was supported in part a grant for scientific research from the Clinica Jerez (ASISA). We would like to thank nurse specialist Francisca Cabo for their nursing assistance and providing care to the patients. References 1. Palmeiro R, Senra A, Garcia-Blanco P, Millan J: Changing patterns of gastric cancer mortality in Spain. Cancer Letters 1988,

42:99–102.PubMedCrossRef 2. Senra Varela A, Lopez Saez JB, Gomez Biondi V: Infection next by Helicobacter H. pylori in two areas with different mortality by gastric cancer. Eur J Epidemiol 1998, 14:491–494.PubMedCrossRef 3. Li-Cheng WuM: Understanding Helicobacter H. pylori . Editorial Human Pathology 2001,32(3):247–249. 4. Marshall BJ, Warren RJ: Unidentified curved bacilli in the stomach of patients with gastritis and peptic ulceration. Lancet 1984,1(8390):1311–5.PubMedCrossRef 5. Choe YH, Hwang TS, Hong YC: Higher seroprevalence of Helicobacter pylori infection in Korean adolescent athletes compared to age and sex-matched no-athletes. J Gastroenterol Hepatol 2002,17(2):131–134.PubMedCrossRef 6. Crowe SE: Helicobacter infection, chronic inflammation, and the development of malignancy.