Prevalence of Helicobacter pylori antibiotic resistance pattern in Malaysia

Helicobacter pylori is well-known for its high genomic diversity and rapid genetic mutation by both natural transformation and inter-or intra-species conjugation. Therefore, eradication of H. pylori will be made difficult when antibiotic resistence was developed towards current treatment regimen. Although previous studies had shown low resistence rate towards major antibiotics such as clarithromycin, levofloxcin, amoxicillin and tetracycline in the Malaysian population, increasing migration of foreign workers might disrupt the gene pool

Gut microbiota and Helicobacter pylori infections

Background: It has been widely accepted that Helicobacter pylori may be the only bacterium that can survive and infect the human stomach. Recently, a few studies using 16S rRNA clone library and other similar approaches showed that the gastric microbiome may be more complex than that. However, the role of interactions between H. pylori and other members of the gastric and gut microbiome in the development and progression of gastroduodenal diseases has not been extensively studied. Objective: The objective of this study is to establish the effects of gut microbiome microbiome in H. pylori infections using germ-free (GF) and specific pathogen-free (SPF) mice models. Methodology: Male GF and SPF C57BL/6 mice of 4–8 weeks of age were infected intragastrically with 109 CFU of rodent-adapted H. pylori strain 7.13 for 2, 8 and 16 weeks. At the end of the respective infection period, the animals were sacrificed. Stomach, liver and brain were harvested for microbiological and histopathological examinations. Synaptophysin and polysynaptic density protein 95 (PSD-95) levels in the brain were evaluated. Blood samples were collected for immunological and hormonal (leptin, total ghrelin and acyl ghrelin) analysis. Results: GF mouse model was established as an alternative animal model for studying H. pylori infections in a microbiota-free in vivo system. Discussion and conclusion: To further characterize the interplay between H. pylori, gut microflora and host, a meta-proteomics and meta-metabo-lomics approach will also be adopted. Outcome of this study will enhance our understanding of the pathogenesis of H. pylori-associated diseases in a systemic in vivo model against a complex multispecies environment

Whole genome analysis of Helicobacter pylori

The human gastric microbiota may be more complex than originally thought and Helicobacter pulori may not be only microorganism found in the stomach. other bacteria that have been isolated from gastric biopsies include Streptococcus and Lactobacillus species

Pan-cancer analysis of whole genomes

Cancer is driven by genetic change, and the advent of massively parallel sequencing has enabled systematic documentation of this variation at the whole-genome scale. Here we report the integrative analysis of 2,658 whole-cancer genomes and their matching normal tissues across 38 tumour types from the Pan-Cancer Analysis of Whole Genomes (PCAWG) Consortium of the International Cancer Genome Consortium (ICGC) and The Cancer Genome Atlas (TCGA). We describe the generation of the PCAWG resource, facilitated by international data sharing using compute clouds. On average, cancer genomes contained 4-5 driver mutations when combining coding and non-coding genomic elements; however, in around 5% of cases no drivers were identified, suggesting that cancer driver discovery is not yet complete. Chromothripsis, in which many clustered structural variants arise in a single catastrophic event, is frequently an early event in tumour evolution; in acral melanoma, for example, these events precede most somatic point mutations and affect several cancer-associated genes simultaneously. Cancers with abnormal telomere maintenance often originate from tissues with low replicative activity and show several mechanisms of preventing telomere attrition to critical levels. Common and rare germline variants affect patterns of somatic mutation, including point mutations, structural variants and somatic retrotransposition. A collection of papers from the PCAWG Consortium describes non-coding mutations that drive cancer beyond those in the TERT promoter; identifies new signatures of mutational processes that cause base substitutions, small insertions and deletions and structural variation; analyses timings and patterns of tumour evolution; describes the diverse transcriptional consequences of somatic mutation on splicing, expression levels, fusion genes and promoter activity; and evaluates a range of more-specialized features of cancer genomes