There is a specific antagonism between an aging organism and neoplasia, in which the tumor is considered to influence the local tissue. It returns to some atavistic features, including the thermodynamic approach (2nd law of thermodynamics, Fig. 1), causing the rejuvenation of the surrounding tissue. The existence of various theories of oncogenesis entitles their supplementation with the theory of inflammaging: an entropic inflammation that can potentially have an indirect influence on the oncogenesis. This theory covers the effects of various causes of aging, including genetically programmed changes, telomere dependent processes and damage of genome, epigenome and proteome particles. The paper describes the patomechanism of inflammaging, including the role of mitochondria (point mutations and deletions especially in mtDNA), oxidative stress with overproduction and accumulation of free radicals and NFkB factor (nuclear factor kappa-light chain-enhancer of activated B cells) and the possibility of the influence of inflammaging on oncogenesis (Fig. 2). The inflamma-ging is programmed by hypothalamus using the immune-neuro-endocrine system, including gonadotropin releasing hormone (GnRH) that inhibits the NFkB factor with the inactivation of kinase IKK-beta. Regardless of that, the chronic inflammation, exceeding its defensive competence, lasts for years and can also be the beginning of neoplastic cells proliferation.
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