Triple-negative breast cancers (TNBCs) exhibit heightened T cell infiltration, contributing to an enhanced response to immune checkpoint blockade (ICB) compared with other subtypes. An immune-rich immune microenvironment correlates with improved prognosis in early and advanced TNBC. Combination chemotherapy and ICB is now the standard of care in early- and late-stage TNBC. Although programmed death ligand-1 (PD-L1) positivity predicts ICB response in advanced stages, its role in early-stage disease remains uncertain. Despite neoadjuvant ICB becoming common in early-stage TNBC, the necessity of adjuvant ICB after surgery remains unclear. Understanding the molecular basis of the immune response in breast cancer is vital for precise biomarkers for ICB and effective combination therapy strategies.
Competing Interests: Declaration of interests S.L. receives research funding to institution from Novartis, Bristol Myers Squibb, MSD, Puma Biotechnology, Eli Lilly, Nektar Therapeutics, Astra Zeneca/Daiichi Sankyo, and Seattle Genetics. S.L. has acted as consultant (not compensated) to Seattle Genetics, Novartis, Bristol Myers Squibb, MSD, AstraZeneca/Daiichi Sankyo, Eli Lilly, Pfizer, Gilead Therapeutics, Nektar Therapeutics, PUMA Biotechnologies, and Roche-Genentech. S.L. has acted as a consultant (paid to institution) to Novartis, GlaxoSmithKline, Roche-Genentech, Astra Zeneca/Daiichi Sankyo, Pfizer, Gilead Therapeutics, Seattle Genetics, MSD, Tallac Therapeutics, Eli Lilly, and Bristol Myers Squibb. V.C.R. has received honoraria from AstraZeneca and has received travel and education funding from MSD. R.S. serves on an advisory board and/or has a consultancy role for BMS, Roche, and Owkin. R.S. has received research funding by Roche, Puma, and Merck. R.S. has received travel and congress registration support from Roche, Merck, and AstraZeneca.
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