title: The storage of energy as a cause of malignant transformation: a 7-phase model of carcinogenesis.
abstract: Although many theories for the development of cancer exist, a new hypothesis for carcinogenesis is suggested and a new 7-phase model of malignant transformation described. Both the hypothesis and the model are based on the principle of a critical point in local energy (entropy?) storage, at a certain level of structural organisation within the cells. This principle has been previously formulated by the author from the rules of non-equilibrium thermodynamics. The model introduces a new terminology and explores the concepts of both high work value of energy and bifurcation. The ability (A) of cells is suggested to be the most important cellular feature in respect to cell survival. This ability implies that the cells follow the requirement Kir > 1, even in dangerous situations and under harmful environmental influence. But, when the cells have lost their ability (A) and all levels of the cell defence machine have been exhausted, then the local energy storage may provoke a cascade of harmful events within the cells. The S-stage is the most unstable state of the cell cycle. If such harmful events take place during DNA synthesis within the 'premalignant' cell, in the phase 'promotion' at the 4th bifurcation, they lead ultimately to carcinogenesis (i.e. malignant transformation). The 7-phase model of carcinogenesis is consistent and offers many advantages in comparison to the previous hypotheses. This model could help the design of experiments, development of new drugs and optimization of medical treatment. The new hypothesis could contribute to a better understanding of the processes of carcinogenesis and the uncontrolled division, growth and lability of tumour cells.
authors.affiliation: Medical University, Stara Zagora, Bulgaria.
authors.forename: B D
authors.initials: BD
authors.lastname: Dimitrov
mesh_terms: D000818:Animals; D002453:Cell Cycle; D002471:Cell Transformation, Neoplastic; D003043:Cocarcinogenesis; D006801:Humans; D008954:Models, Biological; D009369:Neoplasms / Q000209:etiology; D013816:Thermodynamics