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Triple negative breast cancer (TNBC) is distinguished from other breast cancer subtypes by its lack of therapeutic targets, aggressive biology, and poorest survival rates. In the early breast cancer setting, cytotoxic chemotherapy remains the mainstay of systemic treatment options. Multiple clinical trials and meta-analyses have demonstrated that patients who achieve a pathological complete response (pCR) to neoadjuvant chemotherapy (NAC) have an excellent prognosis [1]. Therefore, NAC is now extensively used for early stage TNBC (and HER2positive breast cancer) to improve prognostic stratification, but also in the setting of residual disease, to enrich for high risk, treatment resistant patients that may benefit from treatment escalation or change of systemic therapy [2]. Reported rates of pathologic complete response (pCR) to neoadjuvant chemotherapy (NAC) regimens in TNBC are typically in the vicinity of 40–60% depending on patient selection and chosen treatment regimen. Higher levels of pre-treatment tumor-infiltrating lymphocytes (TIL) are associated with high rates of pCR suggesting that the presence of robust host immunity contributes to chemotherapy response [3, 4]. This suggests that substantial biological heterogeneity exists within the TNBC subtype. We rationalised that the most clinically relevant heterogeneity exists in patients with tumors that do not achieve a pCR, and that biomarkers that refine prognostic estimates and improve biological understanding in this population might help guide the development of hypothesis-driven clinical trials in the future. We recently reported results from our analysis that combined four data series of patients with TNBC who received NAC and did not achieve pCR, with a key focus on Editorial

Residual disease and immune infiltration as a new surrogate endpoint for TNBC post neoadjuvant chemotherapy