ArticleGastrointestinal disorders (Basel, Switzerland)2021
Cardiomyocyte-specific circulating cell-free methylated DNA in esophageal cancer patients treated with chemoradiation.
Article in Gastrointestinal disorders (Basel, Switzerland), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 4 citations in OpenAlex.
- DNA damage and repair in cardiomyopathy: mechanisms and therapeutic opportunities.American journal of physiology. Heart and circulatory physiology · 2026Review
- Circulating cell-free DNA methylation patterns indicate cellular sources of allograft injury after liver transplant.Nature communications · 2025Article
- Circulating, cell-free methylated DNA indicates cellular sources of allograft injury after liver transplant.bioRxiv : the preprint server for biology · 2024Article
- Modeling Susceptibility to Cardiotoxicity in Cancer Therapy Using Human iPSC-Derived Cardiac Cells and Systems Biology.Heart failure clinics · 2022Review
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Authors and funding
12 authors at 1 institution in 1 country.
Funding
Abstract
Thoracic high dose radiation therapy (RT) for cancer has been associated with early and late cardiac toxicity. To assess altered rates of cardiomyocyte cell death due to RT we monitored changes in cardiomyocyte-specific, cell-free methylated DNA (cfDNA) shed into the circulation. Eleven patients with distal esophageal cancer treated with neoadjuvant chemoradiation to 50.4 Gy (RT) and concurrent carboplatin and paclitaxel were enrolled. Subjects underwent fasting blood draws prior to the initiation and after completion of RT as well as 4-6 months following RT. An island of six unmethylated CpGs in the FAM101A locus was used to identify cardiomyocyte-specific cfDNA in serum. After bisulfite treatment this specific cfDNA was quantified by amplicon sequencing at a depth of >35,000 reads/molecule. Cardiomyocyte-specific cfDNA was detectable before RT in the majority of patient samples and showed some distinct changes during the course of treatment and recovery. We propose that patient-specific cardiac damages in response to the treatment are indicated by these changes although co-morbidities may obscure treatment-specific events.
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Registered trials
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