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Background The addition of adjuvant capecitabine to standard chemotherapy of early-stage triple-negative breast cancer (TNBC) patients has improved survival in a few randomised trials and in meta-analyses. However, many patients did not benefit. We evaluated the  BRCA1 -like DNA copy number signature, indicative of homologous recombination deficiency, as a predictive biomarker for capecitabine benefit in the TNBC subgroup of the FinXX trial. Methods Early-stage TNBC patients were randomised between adjuvant capecitabine-containing (TX + CEX: capecitabine-docetaxel, followed by cyclophosphamide-epirubicin-capecitabine) and conventional chemotherapy (T + CEF: docetaxel, followed by cyclophosphamide-epirubicin-fluorouracil). Tumour  BRCA1 -like status was determined on low-coverage, whole genome next-generation sequencing data using an established DNA comparative genomic hybridisation algorithm. Results For 129/202 (63.9%) patients the  BRCA1 -like status could be determined, mostly due to lack of tissue. During a median follow-up of 10.7 years, 35 recurrences and 32 deaths occurred. Addition of capecitabine appears to improve recurrence-free survival more among 61 (47.3%) patients with non- BRCA1 -like tumours (HR 0.23, 95% CI 0.08–0.70) compared to 68 (52.7%) patients with  BRCA1 -like tumours (HR 0.66, 95% CI 0.24–1.81) (P-interaction = 0.17). Conclusion Based on our data, patients with non- BRCA1 -like TNBC appear to benefit from the addition of capecitabine to adjuvant chemotherapy. Patients with  BRCA1 -like TNBC may also benefit. Additional research is needed to define the subgroup within  BRCA1 -like TNBC patients who may not benefit from adjuvant capecitabine.

Adjuvant capecitabine-containing chemotherapy benefit and homologous recombination deficiency in early-stage triple-negative breast cancer patients