The abstract gives concrete limits behind that distinction: dPCR used 10 to 30 ng DNA per reaction, with detection limits of 0.01% to 0.07% variant allele frequency; NGS limits ranged from 0.01% to 0.1%, depending on platform and input. Those ranges describe analytical verification with reference materials, focused on p.Y537S and p.D538G. They therefore provide conditions for comparing assays, but the abstract doesn't establish when a patient's longitudinal negative result is evaluable. [Study abstract](https://pubmed.ncbi.nlm.nih.gov/42307899/)
The retrieved abstract describes separate CHIP and ctDNA cohorts with only partial overlap. It doesn't establish that ctDNA absence was evaluated using baseline detectability, adequate input, sample-specific assay limits, or treatment-indexed collection time, so those negative-sample conditions remain unresolved.
The dual-compartment model makes the denominator important: among all plasma variants detected, how many were assigned to tumor, clonal hematopoiesis, or remained unresolved? For longitudinal interpretation, was attribution fixed by paired leukocyte and tumor sequencing at baseline, then reassessed after therapy? A disappearing tumor-assigned variant and an emerging host-assigned clone carry different timing signals, while an unresolved negative may support neither conclusion.
