Helicobacter pylori infects half of the world's population, and is associated with asymptomatic gastritis and also with more serious conditions such as peptic ulcer disease and gastric carcinoma. The clinical outcome is largely dependent on the severity and distribution of the H pylori-induced gastritis, but the pathogenesis remains poorly understood. Bacterial virulence factors and environmental influences contribute to the pathogenesis, but do not explain the divergent outcomes. There is emerging evidence that host genetic factors play a key role in determining the clinical outcome of H pylori infection. In particular, proinflammatory genotypes of the interleukin-1 beta (IL-1β) gene are associated with an increased risk of gastric cancer and its precursors. The effects are most likely mediated through the induction of hypochlorhydria and severe corpus gastritis with the subsequent development of gastric atrophy. The roles of IL-1β and other host genetic factors in the pathogenesis of H pylori related cancer are discussed in this article. Key Words: Gastric cancer, Helicobacter pylori, Interleukins, Molecular epidemiology, Polymorphisms Le rôle de l'interleukine-1 béta et d'autres marqueurs génétiques potentiels comme indicateurs de risque de cancer gastriqueLe Helicobacter pylori infecte la moitié de la population mondiale et s'associe à une gastrite asymptomatique ainsi qu'à des pathologies plus graves, comme l'ulcère peptique et le carcinome gastrique. L'issue clinique dépend en grande partie de la gravité et de la répartition de la gastrite causée par le H pylori, mais la pathogenèse demeure mal comprise. Des facteurs de virulence bactérienne et des influences environnementales contribuent à la pathogenèse, mais n'expliquent pas les issues divergentes. Selon des données émergentes, des facteurs génétiques de l'hôte jouent un rôle essentiel dans la détermination de l'issue clinique d'une infection à H pylori. En particulier, les génotypes pro-inflammatoires du gène interleukine béta-1 (IL-1ß) s'associent à un risque accru de cancer gastrique et de ses précurseurs. Les effets sont plus probablement assistés par l'induction d'hypochlorhydrie et d'une gastrite du corps grave suivies par l'apparition d'une atrophie gastrique. Le rôle de l'IL-1ß et d'autres facteurs génétiques de l'hôte dans la pathogenèse du cancer relié au H pylori est abordé dans le présent article.

We have investigated the prognostic value of two novel interim 18 F-fluorodeoxyglucose positron emission tomography (FDG-PET) parameters in patients undergoing chemoradiation (CRT) for esophageal squamous cell carcinoma (ESCC): one tumor parameter (maximal standardized uptake ratio rSUR) and one normal tissue parameter (change of FDG uptake within irradiated nontumoraffected esophagus ΔSUV NTO). PET data of 134 European and Chinese patients were analyzed. Parameter establishment was based on 36 patients undergoing preoperative CRT plus surgery, validation was performed in 98 patients receiving definitive CRT. Patients received PET imaging prior and during fourth week of CRT. Clinical parameters, baseline PET parameters, and interim PET parameters (rSUR and ΔSUV NTO) were analyzed and compared to event-free survival (EFS), overall survival (OS), loco-regional control (LRC) and freedom from distant metastases (FFDM). Combining rSUR and ΔSUV NTO revealed a strong prognostic impact on EFS, OS, LRC and FFDM in patients undergoing preoperative CRT. In the definitive CRT cohort, univariate analysis with respect to EFS revealed several staging plus both previously established interim PET parameters as significant prognostic factors. Multivariate analyses revealed only rSUR and ΔSUV NTO as independent prognostic factors (p = 0.003, p = 0.008). Combination of these parameters with the cutoff Additional Supporting Information may be found in the online version of this article.