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Human gut microbiome composition is influenced by genetics, diet and environmental factors. We investigated the microbial composition in several gastrointestinal (GI) compartments to evaluate the impact of genetics, delivery mode, diet, household sharing and aging on microbial similarity in monozygotic and dizygotic twins.Fecal, biopsy and saliva samples were obtained from total 108 twins. DNA and/or RNA was extracted and the region V1-V2 of the 16S rRNA gene was amplified and sequenced. Bray-Curtis similarity was used for further microbiome comparisons, Mann-Whitney test was applied to evaluate the significant differences between groups and Spearman test was applied to reveal potential correlations between data.The global bacterial profiles were grouped into two clusters separating the upper and lower GI. The upper GI microbiome composition was strictly dependent on the Helicobacter pylori status. With a positivity rate of 55%, H. pylori completely colonized the stomach and separated infected twins from non-infected twins irrespective of zygosity status. Lower GI microbiome similarity between the twins was defined mainly by household-sharing and aging; whereas delivery mode and host genetics had no influence. There was a progredient decrease in the bacterial similarity with aging. Shared vs. non-shared phylotypes analysis showed that in both siblings the shared phylotypes progressively diminished with aging, while the non-shared phylotypes increased.Our findings strongly highlight the aging and shared household as they key determinants in gut microbial similarity and drift in twins irrespective of their zygotic state.This work was supported by the grant of the Research Council of Lithuania (Project no. APP-2/2016) and also partially supported by the funds of European Commission through the "European funds for regional development" (EFRE) as well as by the regional Ministry of Economy, Science and Digitalization as part of the "LiLife" Project as part of the "Autonomy in old Age" research group (Project ID: ZS/2018/11/95324).

Gastric carcinogenesis can be described as a consequence of multilevel molecular alterations that is triggered by a cascade of events. Historically, diet and environmental factors have been identified to substantially contribute to carcinogenesis before the discovery of Helicobacter pylori (H. pylori). But H. pylori infection has revolutionized the understanding of gastric carcinogenesis. Although the model of H. pylori-driven carcinogenesis remains valid, there is a continuous effort to precisely delineate the molecular pathways involved and to understand the interplay with additional risk factors including recent relevant knowledge on the stomach microbiota. In this review, we provide an updated view on the models of gastric carcinogenesis. This includes historically appreciated H. pylori-induced models and expands these taking recent molecular data into consideration. Based on the data provided, we conclude that indeed H. pylori-carcinogenesis remains one of the best-established models at least for a subset of gastric cancers. Implementation of the recently identified molecular subtypes in novel genetic animal models is required to expand our knowledge on H. pylori-independent carcinogenesis.