Origin of Cancer: An Information, Energy, and Matter Disease

Abstract

Cells are open, highly ordered systems that are far away from equilibrium. For this reason, the first function of any cell is to prevent the permanent threat of disintegration that is described by thermodynamic laws and to preserve highly ordered cell characteristics such as structures, the cell cycle, or metabolism. In this context, three basic categories play a central role: energy, information, and matter. Each of these three categories is equally important to the cell and they are reciprocally dependent. We therefore suggest that energy loss (e.g., through impaired mitochondria) or disturbance of information (e.g., through mutations or aneuploidy) or changes in the composition or distribution of matter (e.g., through micro-environmental changes or toxic agents) can irreversibly disturb molecular mechanisms, leading to increased local entropy of cellular functions and structures. In terms of physics, changes to these normally highly ordered reaction probabilities lead to a state that is irreversibly biologically imbalanced, but that is thermodynamically more stable. This primary change—independent of the initiator—now provokes and drives a complex interplay between the availability of energy, the composition, and distribution of matter and increasing information disturbance that is dependent upon reactions that try to overcome or stabilize this intracellular, irreversible disorder described by entropy. Because a return to the original ordered state is not possible for thermodynamic reasons, the cells either die or else they persist in a metastable state. In the latter case, they enter into a self-driven adaptive and evolutionary process that generates a progression of disordered cells and that results in a broad spectrum of progeny with different characteristics. Possibly, 1 day, one of these cells will show an autonomous and aggressive behavior—it will be a cancer cell.

Tumorigenesis as a process of gradual loss of original cell identity and gain of properties of neural precursor/progenitor cells

“…The extreme complexity of cancer has aroused many theories and hypothesis about cancer initiation and progression, typically the theories of somatic gene mutations, chromosomal instability, aneuploidy, speciation, mitochondrial dysfunction, Warburg effect, etc., each of them being partially logical and verifiable on the one hand and meeting with serious challenges on the other [ 4 , 5 ]. A general theory accounting for an exclusive cause of cancer initiation and progression has long been sought [ 124 ].…”

“…Some theories, hypotheses and concepts have been put forward to establish a unified connection between these cancer related genes, gene mutations and the acquirement of cancer properties in cells. However, each of them cannot provide an exclusive explanation for tumorigenesis because of some inconsistencies [ 4 , 5 ]. Epithelial–mesenchymal transition (EMT) is such a concept that seems to link gene expression changes during tumorigenesis and cancer malignant properties, but it has been challenged by some studies.…”

Use of real-time cellular analysis and Plackett-Burman design to develop the serum-free media for PC-3 prostate cancer cells

“…Normal cells are given priority to with aerobic metabolism of glucose, but not for the anaerobic fermentation. However, the cancer cells are just the opposite, given priority to with glucose-based anaerobic glycolysis, supplemented by aerobic glycolysis, and thus this phenomenon is called the “Warburg effect” [ 37 , 38 ]. In the screening of PC-3 cell basal medium, PC-3 cells cultured in DMEM medium with high glucose were found to have a good proliferation performance.…”

Next Generation Networks: Featuring the Potential Role of Emerging Applications in Translational Oncology

“…There are many possible ways to utilize entropy in complex biological systems, and cancer entropy has been a topic widely covered [23,24]. At a formal level, an interesting starting point for describing the complexity of a system is offered by the concept of set complexity [25,26,27].…”