As there is some evidence that bacteria may be directly carcinogenic. The strongest evidence to date involves the bacterium H. pylori and its role in gastric cancer
As there is some evidence that bacteria may be directly carcinogenic. The strongest evidence to date involves the bacterium H. pylori and its role in gastric cancer
This is not bacteria related, but it's in the same theme of your question. There is evidence that fungi also have a causative role in carcinogenesis. Aflatoxin from Aspergillus for example is highly carcinogenic (and a good reason not to eat mouldy walnuts).
Hi thanks for your responses and the exemples given of suspected bacteria, yes the question is about bacteria, but Alasdair evoque fungi why not, I think after all microorganisms either viruses, bacteria, fungi, parasites, non conventionnel agents would probably play a role in cancer, the relation is established with viruses, because they have the ability to integrate human genome. Is the same mecanism would concern especially bacteria. I was thinking about the relation between oral cancer and oral microbiome, it s so complexe, because viruses, bacteria parasites and fungi coexist in the oral environment and the interactions are not clear and even difficult to study.
All chronic infection could be related to cancerogenesis but may be the mecanism are diferrent betwween intracellular bacteries growth to extracellular one , i think intracellular bactery are more konown probably we know better the mecanism ! virus had the merit for This !
Indian J Med Paediatr Oncol. 2010 Oct;31(4):126-31.
Different bacteria have been proposed to induce carcinogenesis either through induction of chronic inflammation or by interference, either directly or indirectly, with eukaryotic cell cycle and signaling pathways, or by metabolism of potentially carcinogenic substances like acetaldehyde causing mutagenesis.
The bacteria in the gut are connected to inflammation levels, and therefore cancer. They are also involved in producing beneficial compounds, and potentially metabolizing carcinogens that get ingested.
Some bacteria (like E. coli, A. actinomycetemcomitans, Haem. ducreyi, Shig. dysenteriae, etc.) can express a genotoxin called Cytolethal Distending Toxin (CDT) . It's known to cause DNA damage in eukaryotic cells. To date, there is no evident link between this toxin and human cancers, but H. hepaticus can cause hepatic cancers in a mouse model when this bacteria express CDT. I hope it helps.
The Link between biological factors: Virues ( Hep C, VIH, Papiloma...) Bacterias (Hellicobacter, Haemophillus...) parasits (Eschistosoma, Malaria...) is so evident, that in low income countries, the field where I am working, the 1th cause of Cancer and the main prevalents cancers are of biological aethiology. And their prevalence maps are superponible to the poverty map (world bank
Now, finally we are looking at something. To those who have followed my previous posts on the importance of immunologic paralysis in cancer, bacteria and fungi have the capacity to incapacitate our immune system so as to place the natural killer cells, for example, incapable of killing cancer cells: this is actually where cancer progression takes place. And as many of you have stated, viruses have established roles in cancer initiation.
As has been previously stated, any microorganism that can induce chronic inflammation can contribute to the promotion phase of carcinogenesis. These toxins produced by these microorganisms can induce immune cells to sectrete various cytokines which, in turn, trigger intracellular signaling in "initiated" epithelial or fibroblast cells, and reversibly inhibits gap junctional communication between these cells in solid tissues[ see : Trosko, J.E. and Tai, M.-H., " Adult stem cell theory of the multi-stage, multi-mechanism theory of carcinogenesis: Role of inflammation on the promotion of initiated stem cells. In: Infection and Inflammation: Impacts on Oncogenesis. Dittmar, T. and Zaenker, K., eds., pp.45-65. Karger AG, Amsterdam, 2006.
Just exactly what are these toxins and how do they promote progression? And why should it take, on the average about "10 years," from initiation to overt clinical cancer. What it is this toxin that is so slow in its activity?
Well Friends,it is certainly unclear that how bacteria produce cancer, But one thing is sure that it is always long term host and bacteria association/ interaction that leads to cancerogenesis. Possible or postulated mechanisms involved in this interaction may be chronic inflammation or long sustained insult or chronic irritation or complex immunologic pathway or toxigenic components or products of bacteria or complex changes in local micro-environment due to localization of bacteria inflicting most likely the epigenetic alterations in addition to pre-existing or concurrent accumulation of mutations or a combination of any of these.
So chronic inflammation could be involved but it's too vague, inflammation is a very complex mecanism and is not specific for bacteria. As stated before in the exemples given bacteria byproducts such as enzymes and toxins can interact with immune cells which in turn produce cytokines that could play a role in carcinogenesis ?
Certainly the discussion is centered on bacteria although other microbes have been incriminated in chronic inflammation and possibly cancer. An interesting aspect is that bacteria that have long lasting relation with the host tissue like H pylori or Mycobacterium or in other words those inducing chronic inflammation,are better known to be associated with cancer,. Irrespective of the mechanism exerted by these agents, the cross talk between host and cancer cells is imminent in the clonal expansion and progression of the cancer, in which cytokines are essentially involved
Hi Thanks Craig and Naresh for the additional information. Chronic inflammation is highly implicated in carcinogenesis, there are a lot of papers on PuBMed http://www.ncbi.nlm.nih.gov/pubmed/22796521, http://www.ncbi.nlm.nih.gov/pubmed/22790082, http://www.ncbi.nlm.nih.gov/pubmed/22771929, http://www.ncbi.nlm.nih.gov/pubmed/22734048, http://www.ncbi.nlm.nih.gov/pubmed/22271008
it will be an interesting subject: chronic inflammation and oral cancer, I found papers that could help me to make a review on this topic. Indeed, salivary biomarkers could be a promising field in the future for the early detection of oral cancer
It should now be clear that the equation looks like this: chronic inflammation=tumor immunosuppression=immune tolerance=tumor microenvironment=clinical cancer. What is the common denominator in all these? And how is the process from an immunological point of view? What earliest upstream phenomenon in the immune response makes all these possible? This should be easy to imagine.