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McNamara, Megan E; Loyfer, Netanel; Kiliti, Amber J; Schmidt, Marcel O; Shabi-Porat, Sapir; Jain, Sidharth S; Martinez Roth, Sarah; McDeed, 4th, A Patrick; Shahrour, Nesreen; Ballew, Elizabeth; Lin, Yun-Tien; Li, Heng-Hong; Deslattes Mays, Anne; Rudra, Sonali; Riegel, Anna T; Unger, Keith; Kaplan, Tommy; Wellstein, Anton
JCI insight, 07/2023, Letnik: 8, Številka: 14Journal Article
Radiation therapy is an effective cancer treatment, although damage to healthy tissues is common. Here we analyzed cell-free, methylated DNA released from dying cells into the circulation to evaluate radiation-induced cellular damage in different tissues. To map the circulating DNA fragments to human and mouse tissues, we established sequencing-based, cell-type-specific reference DNA methylation atlases. We found that cell-type-specific DNA blocks were mostly hypomethylated and located within signature genes of cellular identity. Cell-free DNA fragments were captured from serum samples by hybridization to CpG-rich DNA panels and mapped to the DNA methylation atlases. In a mouse model, thoracic radiation-induced tissue damage was reflected by dose-dependent increases in lung endothelial and cardiomyocyte methylated DNA in serum. The analysis of serum samples from patients with breast cancer undergoing radiation treatment revealed distinct dose-dependent and tissue-specific epithelial and endothelial responses to radiation across multiple organs. Strikingly, patients treated for right-sided breast cancers also showed increased hepatocyte and liver endothelial DNA in the circulation, indicating the impact on liver tissues. Thus, changes in cell-free methylated DNA can uncover cell-type-specific effects of radiation and provide a readout of the biologically effective radiation dose received by healthy tissues.
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JCR | SNIP | JCR | SNIP | JCR | SNIP | JCR | SNIP |
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in: SICRIS
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