###### Abstract
The experimental results very likely demonstrate a disturbed protection of selectivity of chemical reactions and their randomization in cancer cells which may involve genome mutations. The pathway of chemical bonding to the genome and transferring consequences of the oncogene mutation involves a sequence of processes, each of which faces major obstacles. Access to DNA is heavily restricted, e.g., by supercoiling, limiting full access to the cell-division period. Random mutations can be corrected by DNA repair processes. If a specific oncogene mutation occurs, the oncogene expression toward mitochondrial dysfunction meets another obstacle: the cell mobilizes tumor-suppressor networks to avert the hazard of malignant transformation and to be withdrawn from the proliferative pool. One of the mechanisms, oncogene-induced apoptosis, triggers a preprogrammed death of a cell suffering from large enough DNA damage. Oncogene-induced senescence (OIS) represents a complementary mechanism depending on the response to induction of the DNA damage [23]. OIS is induced by suppression of the PDH kinase and induction of PDH phosphatase, resulting in increased respiration [24]. Mitochondrial dysfunction is an effector pathway of OIS [25]. Even if tumor-suppressor networks become inactive, the tumor-suppressor genes can be reactivated [26]. All the processes leading to cancer transformation of the cell must occur during a limited timescale of the cellular life cycle. The resulting cancer cell must then evade the supervision of the cell-mediated immunity (CMI) response involving T-lymphocytes (part CD\({}_{4}\)Ly). A specific oncogene mutation and/or overexpression, together with the loss of tumor suppressors, is a complex process which should occur simultaneously in a large enough number of cells to initiate cancer. It is therefore reasonable to assume that a production of mitochondrial dysfunction by an isolated oncogene mutation without other serious pathologies has a low probability. Oncogenic viruses play a special role as experimental models for investigating cellular networks [27]. A number of viruses associated with human cancer have been identified, e.g., Epstein-Barr virus, hepatitis B and C viruses, human herpes virus 8, human T-cell leukemia virus, and HIV-1. More than 170 individual types of human papillomavirus (HPV) have been classified [28; 29; 30; 31]. Despite their different nature related to different virus families, oncogenic viruses share key features, in particular, prolonged latency and their ability to establish long-term persistent infections instead of killing their host cells [27]. To achieve that, they must employ strategies for evading immune response of the host. A long-term interaction between a virus and its host seems to be an important factor for cancer development. Cancer is assumed to be initiated when a viral coding sequence is integrated into oncogene of the cellular genome as a result of infection. Carcinogenicity of oncogenic virusesmay be connected with their capability to disturb or overcome protection of biochemical genome bonding. Besides that, a virus as a living system requires energy to be supplied from the host cell. A reduced energy supply utilized by the cell inevitably causes lowered amplitude of the generated electromagnetic field, lowered organization forces, and possibly--at some critical stage--disturbed write protection of the DNA [9]. About 15%-20% of all human cancers are estimated to be caused by viral infections [27]; however, the role of viruses is supposed to be underappreciated [32]. In contrast to many other carcinogenic agents, they provide a direct mechanism contributing to cancer initiation (writing into DNA of the host cell), together with indirect ones (inflammation or other chronic effects). Nevertheless, the probability of such a process depends on the virus activity and cellular protection levels. It has to be admitted that the actual occurrence of cancers caused by viruses might be higher than the so far estimated figure, e.g., if further oncogenic viruses are revealed.