ESMO Congress 2026

Triple-negative breast cancer (TNBC), lacking ER, PR, and HER2 expression, is not sensitive to endocrine therapy or anti-HER2 treatment; chemotherapy has long been the mainstay systemic therapy in both early and advanced stages, and a standardized regimen is still lacking ^[2][4]. The disease is highly heterogeneous: gene-expression clustering across 21 datasets and 587 TNBC cases defined six subtypes—BL1, BL2, IM, M, MSL, and LAR—with distinct driver pathways, indicating a need for molecular stratification ^[1]. In the neoadjuvant setting, TNBC shows higher pathological complete response (pCR) rates than non-TNBC (22% vs 11%), patients achieving pCR have excellent survival, while those with residual disease fare significantly worse ^[3]; tumour-infiltrating lymphocyte levels also predict neoadjuvant chemotherapy response in TNBC ^[5]. Together this establishes a clear clinical need to identify treatment efficacy earlier, before surgery.

The new readout posted from this meeting comes from the ctDNA kinetics analysis of the B-STRONGER-I study: in stage I–III TNBC, baseline ctDNA detection was 95.1%; by C3D1 (cycle 3 day 1), 80.8% of patients had cleared ctDNA, with a 99.8% median reduction in ctDNA levels—described by the poster as a striking window into early treatment response before surgery. It should be noted that a separate voice appeared under the same meeting tag: a clinician complained that some 'pan-solid tumor' trials exclude breast cancer, calling for non-TOPO-1 ADCs in TNBC and Luminal B breast cancer—this reflects unmet drug-access needs and is a distinct matter from the B-STRONGER-I ctDNA readout.

Relative to existing knowledge, the advance here is moving the efficacy-assessment window from post-surgical pathological pCR ^[3] to a molecular readout at the start of cycle 3, with a 95.1% baseline detection rate indicating that the vast majority of this population is monitorable. In a molecularly heterogeneous disease lacking unified treatment strategies ^[1][4], ctDNA dynamics is complementary to existing predictive tools such as TILs ^[5]; however, the correlation between ctDNA clearance and pCR or long-term survival was not provided in the post.

As for limitations: the study's sample size, specific treatment regimen, follow-up duration, and the association between clearance and pathological response or survival outcomes were not disclosed; the figures above come solely from conference floor posts and should be confirmed against formal reports.