Project description:We leveraged massively parallel sequencing approach to comprehensively characterize the spectrum of somatic mutations and genomic rearrangements in two intestinal-type gastric adenocarcinomas from patients with and without active Helicobacter pylori infections. The tumours exhibited distinct patterns of genomic changes with more than 16,000 somatic substitutions on average, focal amplifications and rearrangements in the non-active infected tumour and a 7-fold enrichment of micro-deletions in the infected tumour. Paired-end sequences from large insert libraries revealed the structure and origins of large amplicons, including one involving the oncogene KRAS. The mutational frequencies of the tumours revealed patterns of H. pylori infection and mutagenesis and a unique exome signature, providing insights into mechanisms that define the mutational landscape of gastric cancer. For the tumour with active infection, we also reconstructed the genome of the pathogenic H. pylori strain from the raw sequence reads, demonstrating the power of whole-genome shotgun sequencing for simultaneously characterizing the tumour and its associated carcinogen genome.
Project description:The aim of the study will be to analyze the microbiome in the blood and stomach in patients with intestinal metaplasia (IM) and / or gastric cancer (GC). As far as IM is concerned, it has been found that the incomplete type is related to GC mainly intestinal-type. Studies show differences in the microbiome in patients with IM and in patients with GC, but do not specify whether these differences are related to histological types.
Our intention is to further analyze the microbiome based on histological types. Most studies on stomach cancer have focused on the microbiota of gastric microbiota. Recent data have shown that the microbiome of the small intestine, especially the mucosa, can play a key role in the condition of the gastrointestinal tract. Disturbance of the microbiome of the small intestine has been found in celiac disease, chronic liver disease, diabetes and irritable bowel syndrome. However, information on the role of the microbiome in IM remains limited.
