Gastrointestinal cancers have many possible causes. Although genetics and environment have a clear impact, the influence of gastric microbiota has been studied extensively.
Gastrointestinal cancers are a real public health concern: 20% of the budget for cancer is dedicated to cancers of the gastrointestinal tract. Research is accelerating to identify the causes: recent discoveries show a connection between bacteria and cancer in relation to certain dysbioses.
Helicobacter pylori is a significant example; this gastric bacteria belonging to the Helicobacteraceae family has been implicated in the development of stomach cancer. This adenocarcinoma is the second leading cause of cancer-related mortality in the world1 . Its role in carcinogenesis has nevertheless proven to be insufficient in explaining the development of gastric cancer. Other factors are suspected, like the appearance of gastric dysbiosis: the populations of Firmicutes, Bacteroidetes, and Actinobacteria are reduced in H. pylori infection, to the benefit of Proteobacteria, Spirochaetes, and Acidobacteria, which leads to acidosis2.
In the case of colorectal cancer, whose incidence and mortality have significantly risen in recent years3 , it has been shown that a specific diet-related dysbiosis is present4 and increases the risk of colorectal cancer. Other studies on intestinal microbiota have shown the influence of the bacterial population that adheres to the mucous membrane: when the Firmicutes / Bacteroidetes / Proteobacteria equilibrium is disrupted, the multiplication of Fusobacterium nucleatum5,6 indicates the start of the carcinogenic process in the majority of cases; other bacteria like Escherichia coli and Streptococcus gallolyticus7 also seem to play a role in colon carcinogenesis.
1. Polk D et al. Helicobacter pylori: gastric cancer and beyond. Nat Rev Cancer 2010 ; 10 : 403-14. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2957472/
2. Maldonado-Contreras A et al. Structure of the human gastric bacterial community in relation to Helicobacter pylori status. ISME J 2011 ; 5 : 574-9. https://www.ncbi.nlm.nih.gov/pubmed/20927139
3. Belot A et al. Cancer incidence and mortality in France over the period 1980-2005. Rev Dépidémiologie Santé Publique 2008 ; 56 : 159-75. https://www.ncbi.nlm.nih.gov/pubmed/18547762
4. O’Keefe SJD et al. Fat, fibre and cancer risk in African Americans and rural Africans. Nature Communications 2015 ; 6 : 6342. http://www.nature.com/articles/ncomms7342
5. Castellarin M et al. Fusobacterium nucleatum infection is prevalent in human colorectal carcinoma. Genome Res 2012 ; 22 : 299-306. https://www.ncbi.nlm.nih.gov/pubmed/22009989
6. Flanagan L, Schmid J, Ebert M, et al. Fusobacterium nucleatum associates with stages of colorectal neoplasia development, colorectal cancer and disease outcome. Eur J Clin Microbiol Infect Dis Off Publ Eur Soc Clin Microbiol 2014 ; 33 : 1381-90. http://epubs.rcsi.ie/cgi/viewcontent.cgi?article=1050&context=physiolart
7. Tjalsma H et al. A bacterial driver-passenger model for colorectal cancer: beyond the usual suspects. Nat Rev Microbiol 2012 ; 10 : 575-82. https://www.ncbi.nlm.nih.gov/pubmed/22728587