ArticleRadiation and environmental biophysics2026
Assessment of radiotherapy effect and toxicity using tissue-associated DNA methylation markers in cell-free DNA: a study on prostate cancer.
Article in Radiation and environmental biophysics, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 1 paper.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
- Circulating Cell-free DNA as a biomarker for radiation-induced injury: From mechanistic insights to clinical translation.Cancer metastasis reviews · 2026Review
Corrections and comments
- Erratum issued
Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
This study aimed to evaluate tissue-associated circulating cell-free DNA (cfDNA) as indicators of radiotherapy-related effects and treatment-associated toxicity in prostate cancer. In addition, inter-individual variability in these markers and their responses to radiotherapy-induced cystitis and rectitis were investigated. The DNA methylation status of six tissue-associated genes representing the prostate (KLK3, TGM4), colon (MUC2, MS4A12), and bladder (UPK2, DHRS2) was analyzed in serum-derived cfDNA using methylation-sensitive melting curve analysis (MS-MCA). Five of the six analyzed genes demonstrated significantly higher relative DNA levels in patients with prostate cancer compared with controls. Radiotherapy did not significantly alter the relative DNA levels of these tissue-associated genes. However, cfDNA fragmentation was significantly increased in the post-treatment group compared to the pre-treatment group. Notably, 79-bp DNA fragments were significantly more abundant than 230-bp fragments. In the post-treatment group, no significant correlations were observed between cfDNA fragmentation and the relative DNA levels of most targets, except for an association between the 230-bp fragment and TGM4 relative DNA levels. These findings suggest limited coupling between cfDNA fragmentation patterns and tissue-associated cfDNA release. Marked inter-individual variability in cfDNA methylation signatures was observed across all examined CpG-containing regions except UPK2. This variability did not change significantly following radiotherapy and may therefore limit the utility of these assay regions for monitoring individual radiation-induced tissue damage. Furthermore, no significant changes in methylation profiles of colon- or bladder-associated genes were detected in patients who developed radiotherapy-induced rectitis or cystitis. Overall, increased cfDNA fragmentation following radiotherapy and substantial inter-individual variability in methylation profiles across tissue-associated regions may mask tissue-associated cfDNA signals, thereby complicating the assessment of radiation-induced tissue damage.
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