Carcinogenesis is a multi-stage process of accumulation of changes in the genome of cells, resulting in the appearance of asocial cells characterized by morphological, functional, biochemical atypism, autonomous growth, “evasion” of cells from humoral and nervous influences, says Dr. Denis Slinkin.

The ideas about the molecular-cellular mechanisms of oncogenic transformation of cells have undergone significant evolution over the past several decades.

Dr. Denis Slinkin argues that the initiators of cell malignization of various morphofunctional organizations are carcinogens of chemical, physical and biological nature, including viruses, hormones and genotoxic products of their metabolism.

Naturally, with extreme heterogeneity of etiological factors of neoplasia development, a rather rapidly dominating concept of pathogenesis of oncogenic transformation of cells could not be formed: their activation or promotion, followed by tumor progression.

Early research on carcinogenesis focused on epigenomal mechanisms of neoplasia development, and, of course, a number of provisions of this direction are not only historical in nature, but may to some extent be associated with modern virus-genetic and oncogenic carcinogenesis theories. To date, one of the leading carcinogenesis concepts is the mutational theory that all carcinogens have mutagenic activity, although not all mutagens are carcinogens.

Dr. Denis Slinkin

An important role in carcinogenesis induction mechanisms is played by oncogenic DNA and RNA-containing viruses capable of incorporating their DNA or DNA copy into the host genome followed by possible oncogenic transformation of the cell in the case of protooncogene expression. As is known, L.A. Silber’s theory of viruses and genetics was the basis for the formation of the modern theory of carcinogenes – the theory of oncogens, protooncogens and antioncogens, says Dr. Denis Slinkin.

It has been established that the following categories of genes fundamentally participate in tumor transformation of cells arising under the influence of various carcinogenesis inductors:

  • Oncogenes – stimulators of functions.
  • Genes of growth and proliferation of cells (Myc, Ras, Los, ABL and others).
  • Antioncogens (loss of function).
  • Genes responsible for programmed cell death (apoptosis):
  • that cancel the programmed death: Bcl-2 (function stimulation);
  • genes responsible for cell death: p53 (loss of function).