Figure 1.
Figure 1. Longitudinal disease monitoring with plasma BRAFV600E-mutant ctDNA and FDG-PET/CT during treatment with vinblastine-prednisone (VB-PRED) and dabrafenib-trametinib (DAB-TRA). (A) Longitudinal disease monitoring by quantitative assessment of the copy number of BRAFV600E-mutant ctDNA within the plasma. BRAFV600E-mutant DNA becomes undetectable during treatment with DAB-TRA but is detectable when treatment is interrupted. When treatment is resumed, BRAFV600E-mutant DNA copy numbers decrease and become undetectable after 6 weeks of treatment. (B) FDG-PET maximal intensity projection imaging. Sites of disease activity are revealed by more intense (black color) FDG focal uptake in the skeleton. Upon treatment with dabrafenib-trametinib, FDG uptake is normalized but recurs discreetly after interruption of therapy.

Longitudinal disease monitoring with plasmaBRAFV600E-mutant ctDNA and FDG-PET/CT during treatment with vinblastine-prednisone (VB-PRED) and dabrafenib-trametinib (DAB-TRA). (A) Longitudinal disease monitoring by quantitative assessment of the copy number of BRAFV600E-mutant ctDNA within the plasma. BRAFV600E-mutant DNA becomes undetectable during treatment with DAB-TRA but is detectable when treatment is interrupted. When treatment is resumed, BRAFV600E-mutant DNA copy numbers decrease and become undetectable after 6 weeks of treatment. (B) FDG-PET maximal intensity projection imaging. Sites of disease activity are revealed by more intense (black color) FDG focal uptake in the skeleton. Upon treatment with dabrafenib-trametinib, FDG uptake is normalized but recurs discreetly after interruption of therapy.

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