EvidenceBreast cancer (all types)

This is what the NHS R208 pathway yields in practice: a one-in-seven positive rate among the eligible, at the cost of clinician time spent on eligibility scoring.

An argument for universal rather than criteria-based germline testing at diagnosis, with turnaround fast enough to inform surgery; for TNBC patients, who are already eligible, the lesson is timing.

For TNBC, which is diagnosed young and is the PARP inhibitor-eligible subtype, the guideline makes germline testing part of the diagnostic workup rather than a referral decision.

ctDNA clearance may refine pCR as a surrogate: a patient with residual disease but no ctDNA may not need escalation, the hypothesis behind ctDNA-guided post-neoadjuvant trials.

TMB-high is uncommon but not negligible in TNBC, rises at relapse, and the tumour-agnostic pembrolizumab indication makes it worth measuring on a metastatic biopsy.

For TNBC, where brain metastases are common, the blind spot matters: a negative ctDNA test does not exclude intracranial relapse.

West Africa carries the highest germline burden reported for an unselected breast cancer population, and the genes are the same ones that predispose to TNBC elsewhere, so limited genetic services there should start with these families.

It fixes the lymphocyte-predominant share of TNBC at about 30% and shows TILs predict chemotherapy response before immunotherapy enters the picture.

The excess of triple-negative disease in women of African ancestry is substantially genetic in origin rather than only social, which supports ancestry-aware risk models and trial enrolment.

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 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.

This is the breast-cancer pivotal behind the 2013 EU authorisation of Lonquex, establishing lipegfilgrastim as an alternative once-per-cycle growth factor to pegfilgrastim. The confidence interval for lambda belongs to a Poisson-model effect estimate and is not a hazard ratio.

This is the reference frequency table for basal-like disease: it explains why PARP inhibitors and platinum, borrowed from ovarian cancer, work in TNBC, and why the PI3K pathway is broken by copy number rather than the hotspot mutations that drugs were designed against.

Founder-mutation screening of every breast cancer patient is justified in the Bahamas, and the finding explains part of the early-onset, BRCA1-driven triple-negative burden across Afro-Caribbean populations.

Functional RB1 loss is part of basal-like biology, which explains why CDK4/6 inhibitors have not worked in TNBC and why the cell-cycle vulnerability there lies downstream of RB.

Founder mutations make population-level testing feasible because a three-variant panel finds most carriers; the BRCA1 founder variants in particular predispose to basal-like, triple-negative tumours, so ancestry shapes who gets this disease and who is eligible for PARP inhibitors.