Radiation-induced genomic instability is a modification of the cell genome found in the progeny of irradiated somatic and germ cells but that is not confined on the initial radiation-induced damage and may occur de novo many generations after irradiation. Genomic instability in the germ line does not follow Mendelian segregation and may have unpredictable outcomes in every succeeding generation. This phenomenon, for which there is extensive experimental data and some evidence in human populations exposed to ionising radiation, is not taken into account in health risk assessments. It poses an unknown morbidity/mortality burden. Based on experimental data derived over the last 20 years (up to January 2012) six mechanistic explanations for the phenomenon have been proposed in the peer-reviewed literature. This article compares these hypotheses with the empirical data to test their fitness to explain the phenomenon. As a conclusion, the most convincing explanation of radiation-induced genomic instability attributes it to an irreversible regulatory change in the dynamic interaction network of the cellular gene products, as a response to non-specific molecular damage, thus entailing the rejection of the machine metaphor for the cell in favour of one appropriate to a complex dissipative dynamic system, such as a whirlpool. It is concluded that in order to evaluate the likely morbidity/mortality associated with radiation-induced genomic instability, it will be necessary to study the damage to processes by radiation rather than damage to molecules.
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http://dx.doi.org/10.1007/s00018-012-1148-5 | DOI Listing |
Microorganisms
January 2025
Department of Radiation Oncology, The First Clinical Medical College, Nanjing Medical University, Nanjing 210029, China.
Radiation-induced skin toxicity, resulting from ionizing or nonionizing radiation, is a common skin disorder. However, the underlying relationship between skin microbiota and radiation-induced skin toxicity remains largely unexplored. Herein, we uncover the microbiota-skin interaction based on a genome-wide association study (GWAS) featuring 150 skin microbiota and three types of skin microenvironment.
View Article and Find Full Text PDFGenes (Basel)
January 2025
Department of Oncology, Lombardi Comprehensive Cancer Center, Georgetown University Medical Center, Washington, DC 20057, USA.
Background: Ionizing radiation (IR) is a well-known inducer of cellular senescence and the senescence-associated secretory phenotype (SASP). SASP factors play dual roles in cancer, either promoting or inhibiting its development. This study investigates IR-induced SASP factors specifically secreted by renal cortical epithelial (RCE) cells and their role in promoting renal cell carcinoma (RCC) progression.
View Article and Find Full Text PDFCancer Med
January 2025
Luxembourg Centre for Systems Biomedicine, University of Luxembourg, Belvaux, Luxembourg.
Background: We explored the interaction between the oral microbiome and the development of radiation-induced mucositis in patients with head and neck squamous cell cancer (HNSCC) undergoing chemoradiotherapy (CRT). We prospectively studied the oral microbiome and compared it to healthy controls. Additionally, we compared patients with low-grade (LGM) vs.
View Article and Find Full Text PDFInt J Mol Sci
December 2024
Institute of Biodiversity and Ecosystem Research, Bulgarian Academy of Sciences, 1113 Sofia, Bulgaria.
Classical radiation biology as we understand it clearly identifies genomic DNA as the primary target of ionizing radiation. The evidence appears rock-solid: ionizing radiation typically induces DSBs with a yield of ~30 per cell per Gy, and unrepaired DSBs are a very cytotoxic lesion. We know very well the kinetics of induction and repair of different types of DNA damage in different organisms and cell lines.
View Article and Find Full Text PDFJ Natl Cancer Inst
January 2025
Translational Radiobiology Group, Division of Cancer Sciences, University of Manchester, The Christie NHS Foundation Trust, Manchester, United Kingdom.
Purpose: Overlapping genes are involved with rheumatoid arthritis (RA) and DNA repair pathways. Therefore, we hypothesised that patients with a high polygenic risk score (PRS) for RA will have an increased risk of radiotherapy (RT) toxicity given the involvement of DNA repair.
Methods: Primary analysis was performed on 1494 prostate cancer, 483 lung cancer and 1820 breast cancer patients assessed for development of RT toxicity in the REQUITE study.
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