Science Translational Medicine

One technology page on OnCo cites this paper by its DOI; this record gives the citation a page of its own so a reader can follow it without leaving OnCo. Read the abstract above alongside the citing page listed under Related; the record was created automatically from the Europe PMC entry and its figures have not been checked by hand.

The field's standing explanation for its own poor clinical record is that it has been tested in the wrong patients: people with widely metastatic, heavily pretreated disease and exhausted immune systems. This paper is the preclinical case for testing it in the opposite situation, in early disease before surgery, where an immune response can still be built.

Minimal residual disease became measurable in solid tumours, and the DYNAMIC and CIRCULATE trials that followed turned the measurement into a treatment decision.

The paper that established lymphoma as the solid-tumour field where circulating tumour DNA works best, because the mutations are many and the tumour sheds. It underpins the response-adapted trial designs now being built on molecular rather than radiographic response.

The proof-of-principle paper for molecular residual disease in breast cancer, and the origin of the personalised digital PCR approach that c-TRAK TN later tested prospectively in TNBC.

The case for re-biopsy at progression, for treating resistance as a diagnosis rather than an endpoint, and for the idea of a drug holiday. It is also the origin of resistance-directed sequencing: what you give next should depend on what the tumour became.

A GNAS mutation in cyst fluid says the cyst is an IPMN, and in a cancer it says the cancer came from one, which is the molecular basis of cyst triage.

It was the first therapeutically tractable alteration found in squamous lung cancer, and in the decade since it has become the standard example of amplification not equalling dependence, because copy number alone has selected patients poorly in trials.

One technology page on OnCo cites this paper by its DOI; this record gives the citation a page of its own so a reader can follow it without leaving OnCo. Read the abstract above alongside the citing page listed under Related; the record was created automatically from the Europe PMC entry and its figures have not been checked by hand.

The field's standing explanation for its own poor clinical record is that it has been tested in the wrong patients: people with widely metastatic, heavily pretreated disease and exhausted immune systems. This paper is the preclinical case for testing it in the opposite situation, in early disease before surgery, where an immune response can still be built.

Minimal residual disease became measurable in solid tumours, and the DYNAMIC and CIRCULATE trials that followed turned the measurement into a treatment decision.

The paper that established lymphoma as the solid-tumour field where circulating tumour DNA works best, because the mutations are many and the tumour sheds. It underpins the response-adapted trial designs now being built on molecular rather than radiographic response.

The proof-of-principle paper for molecular residual disease in breast cancer, and the origin of the personalised digital PCR approach that c-TRAK TN later tested prospectively in TNBC.

The case for re-biopsy at progression, for treating resistance as a diagnosis rather than an endpoint, and for the idea of a drug holiday. It is also the origin of resistance-directed sequencing: what you give next should depend on what the tumour became.

A GNAS mutation in cyst fluid says the cyst is an IPMN, and in a cancer it says the cancer came from one, which is the molecular basis of cyst triage.

It was the first therapeutically tractable alteration found in squamous lung cancer, and in the decade since it has become the standard example of amplification not equalling dependence, because copy number alone has selected patients poorly in trials.