Endogenous and Exogenous Oncogenesis

Polyomaviruses. The emergence of a few SV40 simian polyomavims-induced human cancers occurred after the ingestion of the first batch of the attenuated live poliomyelitis vims vaccines reviewed in [1908]. Some slowly replicating SV40 vims particles containing only one 72 bp enhancer remained much less detectable in 

Comment. It was a response to physico-chemical inducers,that the ancient cells managed to survive by activating their cell survival pathways. Antiviral self-defense mechanisms were installed. In the end, the descendants of the single cells, and their viruses both remain in existence, forming the largest biomass on Earth. The primordial cell survival pathways remained conserved in the form of much more elaborate, and interrelated sequences In the stem and somatic cells of multicellular hosts. In addition to physico-chemical inducers, it is an armada of biological agents 

NEMO kinase (regulatory subunit IKKy), NFkB (nuclear factor kappa B lymphoma) essential modulator, inhibitor of kappa kinase gamma (IKKy). Protein kinase C-interacting protein p62/sequestosome-l, is activated by interleukin IL-IP in sequence, it activates of nuclear factor NFkB in TNFa-stimulated cells (Zotti T et al Mol Immunol 2014 58 27-31). NEMO promotes vFFlP (Fas-associated death domain-like interleukin-1-converting enzyme inhibitory protein) expression by Kaposi sarcoma associated herpesvirus (KSHV) (Tolani B et al J Virol 2014 March 26 PMID 24672029). 

tumor necrosis factor-associated factor TTRAP, TRAFATNF-R receptor associated protein. System was operational in ancestral mollusks (Yang J et al Dev Comp Immunol 2011 35 827-34). TRAF6 and p62 sequestosome suppress NEMO by ubiquitination depletion of p62 by siRNA abrogates TRAF activity. NFkB activation depends on the ubiquitinational state of NEMO (Zotti T et al Mol Immunol 2014 58 27-31). TTRAP inhibits NFkB activation (Pype S et al J Biol Chem 2000 275 18586-93). 

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