ArticleOncotarget2018
Circulating tumor DNA as a marker of treatment response in BRAF V600E mutated non-melanoma solid tumors.
Article in Oncotarget, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 16 citations in OpenAlex.
- Trial
- Similar genetic profile in early and late stage urothelial tract cancer.Journal of cancer research and clinical oncology · 2024Article
- Liquid Biopsy for Disease Monitoring in Non-Small Cell Lung Cancer: The Link between Biology and the Clinic.Cells · 2021Article
- Advances in anti-BRAF therapies for lung cancer.Investigational new drugs · 2021Review
- Correlating Radiomic Features of Heterogeneity on CT with Circulating Tumor DNA in Metastatic Melanoma.Cancers · 2020Article
- Harmonizing Cell-Free DNA Collection and Processing Practices through Evidence-Based Guidance.Clinical cancer research : an official journal of the American Association for Cancer Research · 2020Review
- Quantitative analysis of the BRAF V595E mutation in plasma cell-free DNA from dogs with urothelial carcinoma.PloS one · 2020Article
- Translational Application of Circulating DNA in Oncology: Review of the Last Decades Achievements.Cells · 2019Review
- Cell-free DNA in newly diagnosed patients with glioblastoma - a clinical prospective feasibility study.Oncotarget · 2019Article
- The emerging role of cell-free DNA as a molecular marker for cancer management.Biomolecular detection and quantification · 2019Review
- Article
- Clinical application of cfDNA: moving in the right direction, but still a long way to go.Oncotarget · 2018Article
- The Neurogenome study: Comprehensive molecular profiling to optimize treatment for Danish glioblastoma patients.Neuro-oncology advancesArticle
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Authors and funding
12 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeWe evaluated longitudinal tracking of BRAF V600E in circulating cell-free DNA (cfDNA) as a marker of treatment response to BRAF inhibitor (BRAFi) combination therapies in non-melanoma solid tumors included in the Copenhagen Prospective Personalized Oncology (CoPPO) program. EXPERIMENTAL
designPatients with BRAF V600E-mutated tumors were treated with combination therapies including BRAFi. Quantification of mutant cfDNA from plasma was determined and correlated to clinical outcomes. Exome sequencing was performed to identify possible resistance mutations.
resultsTwenty-three patients had BRAF-mutated tumors out of 455 patients included in CoPPO and 17 started BRAFi combination (EGFRi/MEKi) therapy. Tumor responses were achieved in 8 out of 16 evaluable patients and the median overall- and progression-free survival (OS and PFS) was 15 and 4.8 months, respectively. Longitudinal measurements of BRAF V600E-mutant cfDNA indicated disease progression prior to radiological evaluation and a reduction in the mutant fraction of more than 50% after 4 and 12 weeks of therapy was associated with a significantly longer PFS (p=0.003 and p=0.029) and OS (p=0.029 and p=0.017). Furthermore, the baseline mutant fraction and total level of cfDNA positively correlated with tumor burden (p=0.026 and p=0.024). Finally, analysis of cfDNA at progression revealed novel mutations potentially affecting the MAPK pathway.
conclusionBRAFi combination therapies showed a response rate of 50% in BRAF V600E-mutated non-melanoma tumors. The fraction of BRAF-mutant cfDNA represent a sensitive indicator for clinical outcomes with plasma collected at week 4 and 12 as crucial time points for monitoring response and disease progression.
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