Residual disease kinetics (BCR-ABL halving and ctDNA slopes)
The speed at which a molecular marker falls during treatment predicts outcome better than a single level: BCR-ABL halving time in chronic myeloid leukaemia and circulating tumour DNA slopes in solid tumours are now used to judge response within weeks.
Overview
Michor and colleagues modelled the biphasic decline of BCR-ABL transcripts on imatinib in 2005 as the death of differentiated then progenitor leukaemic cells, and clinicians adopted the early molecular response and the halving time at three months to predict long-term outcome and switch therapy. In solid tumours, models of circulating tumour DNA clearance predict pathological response and survival in lung, colorectal and breast cancer, and ctDNA kinetics are entering trials as early endpoints and as triggers for treatment change. The models depend on assay sensitivity and on assumptions about shedding.
How it works
Exponential (often biphasic) decline of a tumour-derived marker whose rate constants reflect cell kill in different compartments; early slope predicts depth and durability of response.
- Predicts outcome weeks into treatment
- Standard in chronic myeloid leukaemia
- Emerging early endpoint for trials
- Depends on assay sensitivity and shedding
- Cut-offs vary by disease and assay
- Not yet standard in most solid tumours
Latest papers
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