ArticleScientific reports2016
Transient appearance of circulating tumor DNA associated with de novo treatment.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- The Role of ctDNA in the Management of Non-Small-Cell Lung Cancer in the AI and NGS Era.International journal of molecular sciences · 2024Review
- The Correlation between Plasma Circulating Tumor DNA and Radiographic Tumor Burden.The Journal of molecular diagnostics : JMD · 2024Review
- Modeling the Effect of Spatial Structure on Solid Tumor Evolution and Circulating Tumor DNA Composition.Cancers · 2024Article
- Modeling the effect of spatial structure on solid tumor evolution and ctDNA composition.bioRxiv : the preprint server for biology · 2023Article
- Blood, toil, and taxoteres: Biological determinants of treatment-induced ctDNA dynamics for interpreting tumor response.Pathology oncology research : POR · 2022Review
- Targeted Liquid Biopsy Using Irradiation to Facilitate the Release of Cell-Free DNA from a Spatially Aimed Tumor Tissue.Cancer research and treatment · 2022Article
- How to Obtain a High Quality ctDNA in Lymphoma Patients: Preanalytical Tips and Tricks.Pharmaceuticals (Basel, Switzerland) · 2021Review
- Plasma ctDNA Response Is an Early Marker of Treatment Effect in Advanced NSCLC.JCO precision oncology · 2021Article
- Early circulating tumour DNA kinetics measured by ultra-deep next-generation sequencing during radical radiotherapy for non-small cell lung cancer: a feasibility study.Radiation oncology (London, England) · 2020Observational
- Circulating free tumor DNA in non-small cell lung cancer (NSCLC): clinical application and future perspectives.Journal of thoracic disease · 2019Review
Corrections and comments
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The limitation of circulating tumor DNA (ctDNA) is its inability to detect cancer cell subpopulations with few or no dying cells. Lung cancer patients subjected to the EGFR tyrosine kinase inhibitor (EGFR-TKI) treatment were prospectively collected, and ctDNA levels represented by the activating and T790M mutations were measured. The first data set (21 patients) consisting of samples collected in the period from before initiation of EGFR-TKI to at least 2 weeks after initiation: the ctDNA dynamics generally exhibited a rapid decrease and/or a transient increase. In 4 patients, we detected a transient increase of ctDNA bearing activating mutations not identified in biopsy samples. ctDNA with the same genotypical pattern was identified in 7 out of the 39 patients of the second data set intended to include samples until the onset of disease progression. In 6 of the 7 patients, this unique ctDNA appeared in the early period after treatment initiation, and did not reappear even after disease progression or chemotherapy. In another patient, similar ctDNA appeared upon radiation therapy. The identification of ctDNA with a unique genotype indicates the presence of cancer cell subpopulations that normally contain few or no dying cells, but generate dead cells because of the treatment.
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