Aging and Carcinogenesis – Insufficient Metabolic Cell Repair as the Common Link

Abstract

Background: The mechanisms of the development of cancer in old age and also the mechanisms of aging are not well understood. This paper tries to interpret consequences of malignant tissue transformation from the viewpoint of aging, or in other words, from an insufficient cell adaptation to the needs of repair and proliferation. Subject: A hypothesis is presented that a unified but quite opposite at different stages of ontogenesis mechanism is the basis of atypical growth and embryonic development. In the beginning of a malignant dedifferentiation is an insufficiency of an effective self-renovation and disturbed preservation of its adaptation capability. The suppression of regenerating cell proliferation is the primary event of the development of a dedifferentiated tissue growth. The transformation of normal cells into tumor cells is an adaptive reaction in reply to a shortage of self-regeneration capability and repair. Allowing for the process of rebirth, i.e. the complete restoration of tissues leading to the restrain of senescence proceeds by the type of embryonic growth of tissues, the possibility to use the potential of transformed cells for restraining senescence is proposed. The latter will permit to direct the process of transformation to an integrated growth channel, to prevent the clinical phenomenon of malignancy, and use the potential of transformed cells for realization of the self-renovation program and program of unlimited life duration of the whole organism. Conclusion: By a stimulation or compensation of the age-induced shortage of cell metabolism, two effects can be expected: prevention of cancer and retardation of aging.

From Cancer to Rejuvenation: Incomplete Regeneration As the Missing Link (Part I: the Same origin, Different outcomes)

“…As we noted earlier when presenting our unified model of aging and loss of regenerative potential [2], cancer cells are normal cells with a blocked entry to the normal growth path and redifferentiation, and the last feature is the only marker of malignant growth. It is this blocking and nonlimited execution of a developmental program in reverse order that is the cause of the disintegrative character of its growth or, in other words, the cause that transforms rejuvenation into DG -not the expression of the so-called oncogenes.…”

From Autonomy to Integration, From Integration to Dynamically Balanced Integrated Co-existence: Non-aging as the Third Stage of Development

“…There is reason to believe that Homo sapiens have not yet reached the pinnacle of evolution. Therefore, completing here our series of publications (Baramiya, 1988;Baramiya, 2000;Baramiya, 2018;Salnikov and Baramiya, 2020) on the theoretical substantiation of a new section of developmental biology, we propose to call it Developmental Biogerontology. financial interest in or financial conflict with the subject matter or materials discussed in the manuscript.…”

“…In other words, the solution is in absolute immunological tolerance to antigens associated with early stages of embryonic development, for which the adult organism does not have memory. This is the essence of the proposed solution, to which we have lead in our previous publications (Baramiya, 2000;.…”

Risk assessment for cancer surgery in elderly patients

“…The correlation between immune system and cancer development/progression are currently poorly understood (Ling et al 2000; Schindowski et al 2002; Zhang et al 2002). Prolonged tumor-associated antigen exposure associated with immune ‘exhaustion’ and absence of repair genes is the predominance of a ‘frail’ gene variant (Baramiya 2000; Franceschi et al 2000; Ling et al 2000). …”