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Low-dose ionizing radiation: induction of differential intracellular signalling possibly affecting intercellular
James E Trosko1, Chia-Cheng Chang, Brad L Upham
1Department of Pediatrics and Human Development, Michigan State University, East Lansing, MI 48824, USA. james.trosko@ht.msu.edu
Radiation and Environmental Biophysics
|April 12, 2005
Summary
Reexamining radiation carcinogenesis is crucial due to the complexity of low-dose ionizing radiation effects. New understanding of epigenetic events and cellular interactions challenges the traditional linear no-threshold (LNT) model for cancer risk.
Area of Science:
- Radiation biology
- Carcinogenesis
- Epigenetics
Background:
- The carcinogenic process is complex, with limited mechanistic understanding of low-dose ionizing radiation effects.
- Current paradigms extrapolate from high-dose to low-dose radiation effects, necessitating reevaluation.
- The linear no-threshold (LNT) model for radiation carcinogenesis is widely accepted but faces challenges.
Purpose of the Study:
- To reexamine concepts and paradigms in radiation carcinogenesis, particularly concerning low-dose exposures.
- To address the discrepancy between observed low-dose radiation effects and the known protective/repair mechanisms in the human body.
- To integrate new knowledge of epigenetic events and cellular interactions into radiation carcinogenesis models.
Main Methods:
- Review and reevaluation of existing concepts and paradigms in radiation carcinogenesis.
- Consideration of molecular/biochemical and biological bases for health effects from low-dose radiation.
- Integration of recent findings on epigenetic events, stem cell targets, and cell-cell communication in radiation carcinogenesis.
Main Results:
- Low-dose ionizing radiation can induce epigenetic events, challenging the DNA damage-centric LNT model.
- Health effects from low-dose radiation require molecular/biochemical and biological validation.
- Cellular effects in surrogate systems do not automatically imply corresponding human health effects.
Conclusions:
- The traditional LNT model for radiation carcinogenesis needs reevaluation in light of new mechanistic insights.
- Epigenetic modifications and cell-cell communication are critical factors in understanding low-dose radiation's role in cancer.
- Future research should consider stem cells as targets and intercellular communication in radiation carcinogenesis, including adaptive and bystander effects.