ABSTRACT
Introduction
The treatment of early-stage triple-negative breast cancer (TNBC) has radically changed in recent years. Response to neoadjuvant treatment has provided prognostic information, and the achievement of a pathological complete response (pCR) is associated with improved prognosis. An exact treatment algorithm that embraces the trade-off of efficacy and toxicity in a risk-adapted manner has, however, not been consolidated.
Areas covered
In this review, we focused on the current treatments used for patients with early triple negative breast cancer, aiming at framing a therapeutic approach toward risk-adapted treatment optimization. We reviewed the clinical trials and other evidence at the foundation of the current clinical practice in early TNBC and identified possible areas of clinical implementation.
Expert opinion
In our opinion, treatment optimization will ensure improved patient-centric outcomes, with less toxicities, better long-term quality of life and risk-adapted treatment modulation. Presently, treatment modulation can be applied in some patients through de-intensification, for small TNBC, informed by novel biomarkers and based on the response to neoadjuvant treatments, especially in the case of pCR. Innovative approaches should incorporate baseline risk and cancer biology, treatment response, and post-surgery biomarkers of prognosis, to deliver risk-adapted treatments for patients with early TNBC.
Article highlights
Novel therapeutic options yielded improved survival outcomes for patients affected by early TNBC.
Treatment de-escalation for clinically or biomarker defined low-risk TNBC could deliver equal survival outcomes with lower toxicity.
The addition of immunotherapy and targeted agents, particularly PARP-i, represent a novel therapeutic option for high risk early TNBC.
Additional biomarkers are required to tailor the use of chemotherapy along with targeted agents for patients both showing residual disease and achieving complete response to neoadjuvant chemotherapy.
Declaration of interest
G Curigliano declares advisory board fees from Seattle Genetics, Roche, Pfizer, Daiichi Sankyo, and Lilly, all outside this work.
The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.
Reviewer disclosures
Peer reviewers on this manuscript have no relevant financial or other relationships to disclose.
Author contribution statement
Conceptualization (EK, GC); methodology and research of the literature (all authors); validation (all authors); first draft (EK, GC, DT), final draft (all the authors), approval of the final draft (all authors), administrative support (GC), leadership and supervising (GC), visualization and graphical display (CS).