Radiation-induced genomic instability: Are epigenetic mechanisms the missing link?
Journal Article
·
· International Journal of Radiation Biology, 87(2):171-191
Purpose: This review examines the evidence for the hypothesis that epigenetics are involved in the initiation and perpetuation of radiation-induced genomic instability (RIGI). Conclusion: In addition to the extensively studied targeted effects of radiation, it is now apparent that non-targeted delayed effects such as RIGI are also important post-irradiation outcomes. In RIGI, unirradiated progeny cells display phenotypic changes at delayed times after radiation of the parental cell. RIGI is thought to be important in the process of carcinogenesis, however, the mechanism by which this occurs remains to be elucidated. In the genomically unstable clones developed by Morgan and colleagues, radiation-induced mutations, double-strand breaks, or changes in mRNA levels alone could not account for the initiation or perpetuation of RIGI. Since changes in the DNA sequence could not fully explain the mechanism of RIGI, inherited epigenetic changes may be involved. Epigenetics are known to play an important role in many cellular processes and epigenetic aberrations can lead to carcinogenesis. Recent studies in the field of radiation biology suggest that the changes in methylation patterns may be involved in RIGI. Together these clues have led us to hypothesize that epigenetics may be the missing link in understanding the mechanism behind RIGI.
- Research Organization:
- Pacific Northwest National Laboratory (PNNL), Richland, WA (US)
- Sponsoring Organization:
- USDOE
- DOE Contract Number:
- AC05-76RL01830
- OSTI ID:
- 1008210
- Report Number(s):
- PNNL-SA-74577; KP1602020
- Journal Information:
- International Journal of Radiation Biology, 87(2):171-191, Journal Name: International Journal of Radiation Biology, 87(2):171-191 Journal Issue: 2 Vol. 87; ISSN 0955-3002
- Country of Publication:
- United States
- Language:
- English
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Related Subjects
59 BASIC BIOLOGICAL SCIENCES
99 GENERAL AND MISCELLANEOUS
BIOLOGY
CARCINOGENESIS
DNA
DNA METHYLATION CHANGES
DNA methylation
DOUBLE-STRAND BREAKS
GENE-EXPRESSION CHANGES
HYPOTHESIS
INDUCED CHROMOSOMAL INSTABILITY
INFLAMMATORY-TYPE RESPONSES
INSTABILITY
IONIZING-RADIATION
METHYLATION
MUTATIONS
MicroRNA
NON-CPG METHYLATION
PERSISTENT OXIDATIVE STRESS
PROGENY
RADIATIONS
UNSTABLE CELL-LINES
X-RAY- IRRADIATION
chromatin remodelling
epigenetics
genomic instability
ionising radiation
99 GENERAL AND MISCELLANEOUS
BIOLOGY
CARCINOGENESIS
DNA
DNA METHYLATION CHANGES
DNA methylation
DOUBLE-STRAND BREAKS
GENE-EXPRESSION CHANGES
HYPOTHESIS
INDUCED CHROMOSOMAL INSTABILITY
INFLAMMATORY-TYPE RESPONSES
INSTABILITY
IONIZING-RADIATION
METHYLATION
MUTATIONS
MicroRNA
NON-CPG METHYLATION
PERSISTENT OXIDATIVE STRESS
PROGENY
RADIATIONS
UNSTABLE CELL-LINES
X-RAY- IRRADIATION
chromatin remodelling
epigenetics
genomic instability
ionising radiation