Over the past years many theories of carcinogenesis have been developed. Nowadays, there are two prevalent theories of carcinogenesis - two-hit hypothesis, which considers mutations as the main factor in malignization and tissue hypothesis, which considers tissue homeostasis disruption for providing cells transformation. Both of these theories explain cancer origin basing on principles of the reactivity paradigm. This paradigm emphasizes role of different stimuli in malignization. However, this approach does not provide us with sufficient support in progress towards either understanding of cancer origin or effective treatment strategies. In contrast to the reactivity paradigm, we intend to explain oncogenesis within the activity paradigm. Upon this approach, cells' activity is goal-directed and is determined by a future event - the adaptive result. The adaptive result is a proper interaction between the cell and its environment, which provides the cell with required metabolites. To achieve this result cells have to cooperate with each other and synchronize their needs. If cells fail to satisfy their metabolic 'needs' they have to reorganize their activity. This results in morpho-functional restructuring of cells. Summing up, we consider carcinogenesis to be a part of goal-directed adaptive activity of cells. Morphological and genetic atypia of cancer cells is a variant reorganization of cells' activity. Consequently, for better treatment, we should bring both transforming cells and their microenvironment to a novel cooperation and reorganization of their activity.
Keywords: Carcinogenesis; Cells’ activity; Goal-directed activity; Systemogenesis; The activity paradigm.
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