Gene induction and adaptive responses in irradiated cells: Mechanisms and clinical implications
- McGill Univ., Quebec (Canada)
A characteristic of living things, conserved throughout evolution, is their capacity to react to environmental insult. From bacteria to yeast to human cells, environmental inputs induce changes in the program of genes expressed. A subset of this response, of particular interest to the radiobiologists and radiation oncologists who gathered for this meeting, is the case of radiation-mediated gene induction. A large number of genes have been reported to be up/down-regulated by ionizing radiation; some of these have been identified, while others have so far preserved their anonymity as bands and blots on gels and membranes. It is safe to say that many more such genes will be discovered in the future as the scientific and clinical significance of these processes is better understood. Substantial evidence, extending back many years, suggests the existence of an adaptive response, apparent as cellular radioprotective mechanisms which can be up-regulated after a small dose of radiation. At the molecular level, the timing of the changes in expression of induced genes and of the changes in levels of nuclear and cytoplasmic proteins which they encode is such as to support involvement of these elements in induced radioresistance. The adaptive response is one component of the battery of intrinsic factors which influence the response of tumors to radiation. Radiation-induced gene products encompass a spectrum of activities including cell cycle control, DNA repair, signal transduction, apoptosis and oncogenesis, all of which can influence tumor radioresponse and contribute to the multifactorial radioresistant phenotype. Growth factors and cytokines are encoded by several early and late-responding genes whose expression is up-regulated by radiation. These must be assumed to affect the toxicity of radiation toward early- and late-responding normal tissues profoundly by promoting repair or conversely by acting synergistically to enhance radiation damage.
- OSTI ID:
- 62049
- Journal Information:
- Radiation Research, Vol. 141, Issue 1; Other Information: PBD: Jan 1995
- Country of Publication:
- United States
- Language:
- English
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