This volume explores in detail the molecular biology, genetics and immunology of the bacterium Helicobacter pylori that causes serious gastric diseases such as gastric cancer. The book provides in-depth insights into the mechanisms of H. pylori -induced pathogenicity, gives an overview of how the bacterium colonizes the human gut, how it manages to persist in the body and which factors play a role in the development of H. pylori -induced gastric cancer. Furthermore, the interaction between the Gram-negative bacterium and the human gut microbiome is explored, and clinical management and treatment strategies to combat gastric cancer are discussed.

Helicobacter pylori is an extremely successful pathogen that persistently colonizes the gut of about 50% of the world's population. H. pylori and its human host share a long co-evolutionary relationship that dates back for at least last 100,000 years and possibly longer. Infection by thisbacterium is a high-risk factor for the development of gastric diseases, including gastric cancer. Gastric cancer is associated with high morbidity and mortality and represents the 5th most common malignant tumour and the 4th leading cause of cancer-related death worldwide. H. pylori is the first bacterium that has been classified as a type-I carcinogen by the International Agency for Research on Cancer (IARC). Recent research progress identified crucial bacterial, host and environmental factors which control H. pylori -induced gastric malignancy. New studies also suggest that specific human germline mutations and other genetic aberrations have an important impact on H. pylori -induced pathology. In this volume, all these recently discovered mechanisms are reviewed in the light of gastric cancer development, and H. pylori epidemiology, virulence factors, immune evasion, pathophysiology, cancer signalling and novel therapeutic protocols are presented.

This volume is aimed at researchers in the fields of immunology, genetics, microbiology and medicine who are interested in the detailed mechanisms of the pathogenicity of this carcinogenic stomach bacterium .

Discusses the underlying molecular mechanisms of Helicobacter pylori-induced gastric cancer Provides strategies for clinical management and treatment of gastric cancer Reviews how Helicobacter pylori interacts with its human host

Autorentext
Steffen Backert is full Professor of Microbiology in the Department of Biology at the Friedrich Alexander-Universität Erlangen-Nürnberg, Germany. His group has been working in the field of Microbial Pathogenesis for over 25 years, investigating molecular signalling pathways during host-pathogen interactions in enteric and gastric infections such as that of Campylobacter jejuni and Helicobacter pylori. His research interests focus on the identification and characterization of new bacterial virulence factors (secreted or injected), which could represent potential novel targets for therapeutic intervention. He authored more than 220 peer-reviewed publications and edited eight scientific books. He is Associate Editor of various highly ranked research journals and has a strong and consistent record of gaining competitive research funding. Professor Backert is inventor on seven patents.

Inhalt

Gastric stem cell biology and Helicobacter pylori infection.- Clinical pathogenesis and molecular mechanisms of gastric cancerogenesis.- Helicobacter pylori metabolism and mitochondrial dysfunction in gastric cancer development .- Immune biology and persistence of Helicobacter pylori in gastric diseases.- Pathogenomics of Helicobacter pylori infection.- Helicobacter pylori interactions with the microbiota and gastric cancer development.- Helicobacter pylori- induced host cell DNA damage and gastric carcinogenesis.- Gastric inflammation and oncogenic signal transduction networks by Helicobacter pylori.- Impact of Helicobacter pylori oncoprotein CagA and vacuolating cytotoxin VacA in gastric cancer.- Role of proteases in Helicobacter pylori infections and gastric diseases.- Clinical management of gastric cancer treatment regimes.