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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.
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.
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.
It reframes the blood test from a yes-or-no residual disease result into a measure of how well chemotherapy is working and how fast a relapse is coming, which is what an escalation trial would need.
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