title: Ontological hypothesis of the cancer etiology: discord between cells' survival determinism and their disposition to biological altruism.
abstract: During the last decades, scientific community has implicitly viewed cancer as a number of different diseases with the same underlying phenotype. Such a view was justified for the fact that some of the genetic and phenotypic similarities, observed in different types of tumors, were perpetuated via some distinct mechanisms. Nevertheless, this manuscript aims to interpret all of these differences in a context of the same underlying cause. To do so, the epigenetic and genetic alterations observed in cancers are initially interpreted in the context of their advantage for the evolution of the early eukaryotic organisms. Subsequently, the proposed premises are further discussed with respect to their propagation in the subsequent generations of the new eukaryotic species, as well as their role in the development of the higher organisms. In the subsequent section, the role of the proposed mechanism is discussed in the context of cancer, which is proposed to originate due to the analogous underlying mechanisms. Finally, the proposed mechanism is briefly discussed in parallel with some other contemporary theories of carcinogenesis, aiming to further support its validity. Thereby, the model presents an alternative interpretation of multiple cancer-related biomedical phenomena from the aspect of a proposed evolutionary mechanism.
authors.affiliation: Functional Architecture of the Cell (B065), German Cancer Research Centre (DKFZ), Im Neuenheimer Feld 280, 69120 Heidelberg, Germany. p.krsmanovic@dkfz.de
authors.forename: Pavle
authors.initials: P
authors.lastname: Krsmanovic
mesh_terms: D000220:Adaptation, Biological / Q000502:physiology*; D005075:Biological Evolution; D002453:Cell Cycle / Q000502:physiology; D002470:Cell Survival / Q000502:physiology; D044127:Epigenesis, Genetic; D006801:Humans; D008954:Models, Biological; D009369:Neoplasms / Q000209:etiology* / Q000235:genetics* / Q000503:physiopathology; D013312:Stress, Physiological / Q000502:physiology*