6533b833fe1ef96bd129b86d

RESEARCH PRODUCT

Role of environmental and genetic factor interaction in age-related disease development: the gastric cancer paradigm.

Arianna GulloDomenico LioCelestino BonuraAnna GiammancoCinzia CalàLetizia ScolaGiacalone AGiusi I Forte 1Calogero CarusoAntonino CrivelloMarasa' L

subject

Malemedicine.medical_specialtyAgingSettore MED/07 - Microbiologia E Microbiologia ClinicaGenotypemedicine.medical_treatmentChronic gastritisDiseaseEnvironmentGastroenterologyPolymorphism (computer science)Stomach NeoplasmsInternal medicineGenotypemedicineHumansSettore MED/05 - Patologia ClinicaDiseaseGrading (tumors)Polymorphism GeneticbiologyCancercytokine genes biomarkersHelicobacter pylorimedicine.diseasebiology.organism_classificationCytokineGastritisImmunologyCytokinesFemaleGeriatrics and GerontologyH. pylori

description

The association of Helicobacter pylori (Hp) infection with gastric cancer is well known and might be considered a paradigmatic example of the role that interaction among environmental factors and individual background might play in inducing age-associated disease. To evaluate the role of interaction of Hp infection with genetic background, gastric cancer and chronic gastritis patients as well as random selected controls were typed for five inflammation-related polymorphisms of IL-1 and IL-10 cytokine genes. No association among IL-10 or IL-1 variants with an increased risk of gastric cancer was found, whereas an Hp-independent association of IL-1beta -511T positive genotypes to an increased risk of chronic gastritis was found (Hp-/511T+ OR 1.89, 95% CI: 1.01-3.54; Hp+/-511T+ OR 1.83, 95% CI: 1.05-3.19). Stratification of gastric cancer group according to Hp infection does not allow finding a statistically significant association of Hp+ to the higher histological grading (G3) of gastric cancer (OR 1.54, 95% CI: 0.46-5.11). Our findings seem to confirm that cytokine genetic variants might contribute to determining the background for inflammaging in which H. pylori infection might facilitate cancer development.

10.1089/rej.2008.0678.http://hdl.handle.net/10447/37426