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In some inflammasomes tumor cells are generated. The internal environmentof the inflammasome is conducive to the induction of malignant transformation.Epigenetic changes initiate this process. The subverted stromal connective tissuecells act to promote and sustain the process of malignant trans-formation. Inits early stages, the premalignant cells depend on paracrine circuitries for thereception of growth factors. The ligands are derived from the connective tissue,and the receptors are expressed on the recipient premalignant cells. The initialevents are not a direct attack on the proto-oncogenes, and thus it may be entirelyreversible. Epigenetic processes of hypermethylation of the genes at the promotersof tumor suppressor genes (to silence them), and deacetylation of the histonesaimed at the promoters of proto-oncogenes (to activate them) are on-going. A largenumber of short RNA sequences (interfering, micro-, short hairpin, non-codingRNAs) silence tumor suppressor genes, by neutralizing their mRNAs. In a serialsequence oncogenes undergo amplifications, point-mutations, translocations andfusions. In its earliest stage, the process is reversible by demethylation ofthe silenced suppressor gene promoters (to reactivate them), or re-acetylationof the histones of the oncogene promoters, thus de-activating them. The externaladministration of histone deacetylase inhibitors usually leads to the restorationof histone acetylation. In time, the uncorrected processes solidify into constitutiveand irreversible gene mutations. Some of the pathogens inducing inflammationswith consquential malignant transformation contain oncogenic gene sequences (papillomaviruses, Epstein-Barr virus, Kaposi's sarcoma-associated herpesvirus, hepatitis Band C viruses, Merkel cell polyoma virus, Helicobacter pylori, enterotoxigenicBacteroides fragilis). These induced malignancies may be multifocal. Other pathogensare devoid of any known oncogenic genomic sequences (mycoplasma vav-carcinogenesis,chlamydia MALT-lymphoma genesis). In these cases the host's inflammatory reactionsinduce the malignant transformation in serial sequences of gene alterations initiatedby hypoxia and reactive oxygen and nitrogen species generation. Carcinogenic intrinsicinflammatory processes endogenously initiated without a pathogen are recognized.Chronic inflammatory processes signal the RNA/DNA complex. In response, the DNAmay revert into its ancient primordial 'immortal' format, which the clinics recognizeas 'oncogenesis'. The DNA remains the ultimate master of bioengineering in orderto sustain life. A discussion on the most versatile and resistant primordial RNA/DNAcomplex and the pre-, proto-, and unicellular world in which they co-existed isincluded.

international journal of oncology

Molecular biology of oncogenic inflammatory processes. I. Non-oncogenic and oncogenic pathogens, intrinsic inflammatory reactions without pathogens, and microRNA/DNA interactions (Review)