M G Baramiya1. 1. Department of Histology, Cytology and Embryology, Saratov State Medical University, Saratov, Russia. sansi@intsar.com
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. Copyright 2000 S. Karger AG, Basel
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. Copyright 2000 S. Karger AG, Basel