Immune mechanisms play an integral role in tumor growth establishment and metastases. Immunoediting is a dynamic process that consists of immuno surveillance and tumor progression. It describes the relation between the tumor cells and the immune system. It is made up of three phases: 1) elimination, 2) equilibrium, and 3) escape. Immune editing and infection induced inflammation in oral carcinogenesis. This will cause immuno suppressive status in the tumour micro environment.
Microbiome studies based on ‘omics’ technologies have provided the laboratory evidence on 'disease associated microbiome' in metabolic diseases and cancer with non-infectious origin. Obviously, these microbes especially bacteria are the most metabolically versatile organisms in the world, which can adopt to any environment, even changing their genetic potential, using mechanisms such as horizontal gene transfer. Furthermore, in-vitro experiment have provided substantial information on carcinogenicity of P. gingivalis and F. nucleatum.
1. Elimination: Most immunologically vulnerable tumour antigens may eliminate by elimination phase immune editing as host’s immune system is capable of recognizing these cells
2. Equilibrium: However, constant division can generate tumour cells with reduced immunogenicity that can evade the immune elimination because of the genetic instability. This state of production of new tumor cell variants balanced by the distraction has been dubbed “equilibrium”, during which the cancer cells continue to divide, accumulating mutational changes by chance or in response to immune-induced inflammation.
3. Escape: These processes gradually come to a situation where tumours are capable of reducing the capacity of the immune system, to eradicate them by achieving immune suppressive effects or by loss of target antigen expression. Consequently tumour escapes from immuno surveillance and progression of carcinogenesis will occur. Nonetheless, there may be conditions under which tumor cells are truly dormant, for example by induction of “senescence”. In this case, they would be likely to remain dormant permanently, as replicative senescence is generally believed to be irreversible.
There are only few reports on immune-modulating mechanisms of oncogenes expressed in cancer cells, immune cells or in the tumor microenvironment due to pro inflammatory oral cancer biome.
I would like to give a thought on the participation of oral cancerbiome in the third stage of immuno editing. Persistent of chronic infection due to inflammaphilic periodontopathogens which may cause immuno suppression and help tumours to escape from immuno surveillance.
At present may be a speculation but in any disease can't forget the involvement of host's immune system
Any in –vivo studies using animal models?
I invite Microbiome and Cancer researchers to join in this meaningful discussion. Immunologists are also welcome!
Found the answer.It's just a matter of combining the current knowledge on cancer immunoediting to current knowledge on emerging role of Porphyromonas gingivalis and Fusobacterium nucleatum in oral carcinogenesis.
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