Open Access

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

  • Authors:
    • Joseph G. Sinkovics
  • View Affiliations

  • Published online on: November 4, 2011     https://doi.org/10.3892/ijo.2011.1248
  • Pages:305-349
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Abstract

In some inflammasomes tumor cells are generated. The internal environment of the inflammasome is conducive to the induction of malignant transformation. Epigenetic changes initiate this process. The subverted stromal connective tissue cells act to promote and sustain the process of malignant trans­formation. In its early stages, the premalignant cells depend on paracrine circuitries for the reception of growth factors. The ligands are derived from the connective tissue, and the receptors are expressed on the recipient premalignant cells. The initial events are not a direct attack on the proto-oncogenes, and thus it may be entirely reversible. Epigenetic processes of hypermethylation of the genes at the promoters of tumor suppressor genes (to silence them), and deacetylation of the histones aimed at the promoters of proto-oncogenes (to activate them) are on-going. A large number of short RNA sequences (interfering, micro-, short hairpin, non-coding RNAs) silence tumor suppressor genes, by neutralizing their mRNAs. In a serial sequence oncogenes undergo amplifications, point-mutations, translocations and fusions. In its earliest stage, the process is reversible by demethylation of the silenced suppressor gene promoters (to reactivate them), or re-acetylation of the histones of the oncogene promoters, thus de-activating them. The external administration of histone deacetylase inhibitors usually leads to the restoration of histone acetylation. In time, the uncorrected processes solidify into constitutive and irreversible gene mutations. Some of the pathogens inducing inflammations with consquential malignant transformation contain oncogenic gene sequences (papilloma viruses, Epstein-Barr virus, Kaposi's sarcoma-associated herpesvirus, hepatitis B and C viruses, Merkel cell polyoma virus, Helicobacter pylori, enterotoxigenic Bacteroides fragilis). These induced malignancies may be multifocal. Other pathogens are devoid of any known oncogenic genomic sequences (mycoplasma vav-carcinogenesis, chlamydia MALT-lymphoma genesis). In these cases the host's inflammatory reactions induce the malignant transformation in serial sequences of gene alterations initiated by hypoxia and reactive oxygen and nitrogen species generation. Carcinogenic intrinsic inflammatory processes endogenously initiated without a pathogen are recognized. Chronic inflammatory processes signal the RNA/DNA complex. In response, the DNA may revert into its ancient primordial ‘immortal’ format, which the clinics recognize as ‘oncogenesis’. The DNA remains the ultimate master of bioengineering in order to sustain life. A discussion on the most versatile and resistant primordial RNA/DNA complex and the pre-, proto-, and unicellular world in which they co-existed is included.

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February 2012
Volume 40 Issue 2

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Online ISSN:1791-2423

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APA
Sinkovics, J.G. (2012). Molecular biology of oncogenic inflammatory processes. I. Non-oncogenic and oncogenic pathogens, intrinsic inflammatory reactions without pathogens, and microRNA/DNA interactions (Review). International Journal of Oncology, 40, 305-349. https://doi.org/10.3892/ijo.2011.1248
MLA
Sinkovics, J. G."Molecular biology of oncogenic inflammatory processes. I. Non-oncogenic and oncogenic pathogens, intrinsic inflammatory reactions without pathogens, and microRNA/DNA interactions (Review)". International Journal of Oncology 40.2 (2012): 305-349.
Chicago
Sinkovics, J. G."Molecular biology of oncogenic inflammatory processes. I. Non-oncogenic and oncogenic pathogens, intrinsic inflammatory reactions without pathogens, and microRNA/DNA interactions (Review)". International Journal of Oncology 40, no. 2 (2012): 305-349. https://doi.org/10.3892/ijo.2011.1248