title: Cellular and molecular aspects of gastric cancer.
abstract: Gastric cancer remains a global killer with a shifting burden from the developed to the developing world. The cancer develops along a multistage process that is defined by distinct histological and pathophysiological phases. Several genetic and epigenetic alterations mediate the transition from one stage to another and these include mutations in oncogenes, tumour suppressor genes and cell cycle and mismatch repair genes. The most significant advance in the fight against gastric cancer came with the recognition of the role of Helicobacter pylori (H pylori) as the most important acquired aetiological agent for this cancer. Recent work has focussed on elucidating the complex host/microbial interactions that underlie the neoplastic process. There is now considerable insight into the pathogenesis of this cancer and the prospect of preventing and eradicating the disease has become a reality. Perhaps more importantly, the study of H pylori-induced gastric carcinogenesis offers a paradigm for understanding more complex human cancers. In this review, we examine the molecular and cellular events that underlie H pylori-induced gastric cancer.
authors.affiliation: Department of Medicine and Therapeutics, Institute of Medical Sciences, Aberdeen University, Foresterhill, Aberdeen AB25 2ZD, Scotland, United Kingdom.
authors.forename: Malcolm-G
authors.initials: MG
authors.lastname: Smith
authors.forename: Georgina-L
authors.initials: GL
authors.lastname: Hold
authors.forename: Eiichi
authors.initials: E
authors.lastname: Tahara
authors.forename: Emad-M
authors.initials: EM
authors.lastname: El-Omar
mesh_terms: D018797:Cell Cycle Proteins / Q000235:genetics / Q000502:physiology; D016207:Cytokines / Q000235:genetics / Q000502:physiology; D004249:DNA Damage; D015972:Gene Expression Regulation, Neoplastic / Q000502:physiology*; D052138:Genes, Neoplasm / Q000502:physiology; D016147:Genes, Tumor Suppressor / Q000502:physiology; D006133:Growth Substances / Q000235:genetics / Q000502:physiology; D016481:Helicobacter Infections / Q000150:complications* / Q000503:physiopathology; D016480:Helicobacter pylori / Q000472:pathogenicity; D006801:Humans; D007249:Inflammation / Q000382:microbiology / Q000503:physiopathology; D009154:Mutation; D016328:NF-kappa B / Q000235:genetics / Q000502:physiology; D009362:Neoplasm Metastasis / Q000235:genetics; D011519:Proto-Oncogenes / Q000235:genetics / Q000502:physiology; D017382:Reactive Oxygen Species; D013274:Stomach Neoplasms / Q000209:etiology / Q000235:genetics* / Q000382:microbiology / Q000473:pathology*; D014774:Virulence
chemical_list: D018797:Cell Cycle Proteins; D016207:Cytokines; D006133:Growth Substances; D016328:NF-kappa B; D017382:Reactive Oxygen Species