Finding the Role of Helicobacter pylori in Colorectal Cancer.

摘要: Colorectal cancer (CRC) is the third most common and fourth leading cause of cancer-related death globally; nonetheless, its etiology still not established. CRC has a strong association with certain hereditary gene mutations, but only 3-5% cases are due to these known mutations alone. Epidemiological data established an between development various environmental factors, such as high-calorie diet obesity; however, high-risk factors there apparently contradictory evidence. Besides host genetic chronic inflammation, induced by bacteria, viruses or parasites, can also gastrointestinal tract (GIT) cancers. The human intestine rich in nutrients habitat for over 500 different bacterial species viruses, highest concentration bacteria found colon. long list infectious microbes, potentially implicated pathogenesis CRC, includes Streptococcus bovis, Helicobacter pylori (H. pylori), Escherichia coli, Bacteroides, polyoma (JC SV40), papillomavirus, Epstein Barr virus cytomegalovirus. Among microorganisms, H. pylori-induced carcinogenesis involves well deregulation cell cycle via CagA, oncoprotein that binds activates SHP2 (a oncogenic phosphatase), resulting proliferation motility. Due gastric cancer, bacterium classified class I carcinogen. Given strongly associated stomach, it may be relevant other GIT cancers, including CRC. However, infection had been highly contentious. Zumkeller et al. (2006), who conducted systematic review meta-analysis 11 published studies (between 1991 2002) involving 899 patients 1,476 controls, concluded possible small increase risk because pylori. Similarly, recent large-scale retrospective population-based case-control study, Rhine-Neckar region southwest Germany 1,712 histologically confirmed 1,669 seropositivity was reported increased confined left-sided While epidemiological showed correlative relation, remained weak. Moving beyond data, another study using hepaticus-infected mice lacking recombinase-activating gene-2 (rag2) – emulating many aspects inflammatory bowel disease (including colitis CRC) supported hypothesis Helicobacterrelated inflammation-mediated demonstrating molecular damage altered expression during progression vivo. In this issue Immuno-Gastroenterology, Kapetanakis went further demonstrate colonic mucosa, stimulating stem cells and/or recruiting bone marrow-derived cells, thereby affecting oncogenesis immune surveillance. authors suggest have impact on sequential transformation colon epithelium adenoma, moderate-severe dysplasia eventually progression. Here, detected presence histological tissue samples cresyl violet staining imunohistochemistry (IHC) anti-H. Previously, Jones (2007) visualized tissues IHC. Can truly colonize colon? Serological detection antibody against indicates past current no information site colonization. Polymerase chain reaction immunohistochemical sensitive, specific correlate present limited their inability distinguish transient from true colonization dead viable bacteria. We need direct indirect evidence extra-gastric before passing verdict. Despite having clearer understanding potential role pathological events up questions answered. likely multi-factorial process, delicate interplay genetics, agents combination multiple agents), gut microbiome factors. microbial pathogens-cancers relationship indeed complex one. Clarification will influence clinical management cancers future.