98%
921
2 minutes
20
Objective: Endovascular interventions have increasingly replaced open surgery due to their minimally invasive nature and benefits such as faster recovery and fewer wound complications. This shift has led to greater reliance on fluoroscopy, raising concerns about occupational radiation exposure. Ionizing radiation, while essential for guiding procedures, can damage living tissue and potentially induce long-term health effects. Recent guidelines from the European Society for Vascular Surgery and the Cardiovascular and Interventional Radiological Society of Europe emphasize growing radiation risks and advocate for dose optimization and protective strategies. Endovascular specialists-vascular surgeons, interventional cardiologists, and radiologists-are among the most exposed hospital staff. Yet, limited studies have specifically examined the effects of fluoroscopy-induced DNA damage and carcinogenesis in these professionals. The aim of this systematic review is to evaluate the extent to which occupational radiation exposure contributes to DNA damage and cancer risk in endovascular operators.
Methods: A systematic search of the literature from 2000 to April 2025 of PubMed and EMBASE was conducted following PRISMA-guidelines. All experimental studies, observational studies and case reports that examine DNA damage or cancer occurrence in operators performing endovascular procedures due to occupational radiation exposure were included in this review. Studies were categorized into two primary outcomes: cancer and DNA damage. A risk of bias assessment was performed according to Cochrane guidelines.
Results: Twenty-five studies were identified. The findings from these studies suggest that occupational radiation exposure in endovascular operators may lead to early-stage DNA damage shortly after exposure. Additionally, the studies observed chronic DNA damage, including double-strand DNA breaks and chromosomal aberrations, which are hypothesized to be a contributing factor to genomic instability and carcinogenesis. Furthermore, the studies researching carcinogenesis suggests an elevated risk of cancer development in endovascular operators, with particular emphasis on cancer localizations that are more susceptible to radiation, such as leukaemia and thyroid cancer, and in unprotected body areas, such as the skin and the brain.
Conclusions: This systematic review suggests that endovascular operators involved in fluoroscopy-guided interventional procedures may face an increased risk of stochastic health effects, with a particular emphasis on chronic DNA damage and carcinogenesis in localizations more vulnerable to radiation. This review highlights the critical need for enhanced radiation safety measures, awareness, and preventative strategies.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.1016/j.jvs.2025.07.058 | DOI Listing |
Mutat Res Rev Mutat Res
September 2025
Institute of Environmental Medicine, Zhejiang University School of Medicine, Hangzhou 310058, China. Electronic address:
To maintain genomic stability, cells have evolved complex mechanisms collectively known as the DNA damage response (DDR), which includes DNA repair, cell cycle checkpoints, apoptosis, and gene expression regulation. Recent studies have revealed that long non-coding RNAs (lncRNAs) are pivotal regulators of the DDR. Beyond their established roles in recruiting repair proteins and modulating gene expression, emerging evidence highlights two particularly intriguing functions.
View Article and Find Full Text PDFAnnu Rev Pathol
September 2025
3Department of Pathology, Stanford University, Stanford, California, USA;
Clonal hematopoiesis, originally identified as a precursor to hematologic malignancies, has emerged as a significant factor in various nonmalignant diseases. Recent research highlights how somatic mutations in hematopoietic stem cells lead to the expansion of circulating mutated immune cells that exert profound effects on organ function and disease progression. These mutated clones display altered inflammatory profiles and tissue-specific functional consequences, contributing to various diseases including atherosclerotic cardiovascular disease, osteoporosis, heart failure, and neurodegenerative conditions.
View Article and Find Full Text PDFPLoS Comput Biol
September 2025
Department of Genome Sciences, University of Washington, Seattle, Washington, United States of America.
Fanconi Anemia (FA) is a heritable syndrome characterized by DNA damage repair deficits, frequent malformations and a significantly elevated risk of bone marrow failure, leukemia, and mucosal head and neck squamous cell carcinomas (HNSCC). Hematopoietic stem cell gene therapy can prevent marrow failure and lower leukemia risk, but mucosal gene therapy to lower HNSCC risk remains untested. Major knowledge gaps include an incomplete understanding of how rapidly gene-corrected cellular lineages could spread through the oral epithelium, and which delivery parameters are critical for ensuring efficient gene correction.
View Article and Find Full Text PDFProc Natl Acad Sci U S A
September 2025
Cancer Research Center of Marseille: Team DNA Damage and Genome Instability|CNRS, Inserm, Institut Paoli-Calmettes, Aix Marseille Université, Marseille 13009, France.
Following encounter with an unrepaired DNA lesion, replication is halted and can restart downstream of the lesion leading to the formation of a single-stranded DNA (ssDNA) gap. To complete replication, this ssDNA gap is filled in by one of the two lesion tolerance pathways: the error-prone Translesion Synthesis (TLS) or the error-free Homology Directed Gap Repair (HDGR). In the present work, we evidence a role for the RecBC complex distinct from its canonical function in homologous recombination at DNA double strand breaks.
View Article and Find Full Text PDFProc Natl Acad Sci U S A
September 2025
Department of Biology, Massachusetts Institute of Technology, Cambridge, MA 02139.
The mutagenic translesion synthesis (TLS) pathway, which is critically dependent on REV1's ability to recruit inserter TLS polymerases and the POLζ extender polymerase, enables cancer cells to bypass DNA lesions while introducing mutations that likely contribute to the development of chemotherapy resistance and secondary malignancies. Targeting this pathway represents a promising therapeutic strategy. Here, we demonstrate that the expression of the C-terminal domain (CTD) of human REV1, a ca.
View Article and Find Full Text PDF