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Immune checkpoint inhibition in breast cancer: targeting PD-1/PD-L1 pathway for therapeutic advances.

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Breast cancer (Tokyo, Japan) 2026 Vol.33(1) p. 25-37
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Shin Y, Shin K, Lee S, Son Y, Rhee I

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Breast cancer (BC) is among the most prevalent and immunogenic malignancies in women, characterized by rapid proliferation and significant immune cell infiltration into the tumor microenvironment (TME

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APA Shin Y, Shin K, et al. (2026). Immune checkpoint inhibition in breast cancer: targeting PD-1/PD-L1 pathway for therapeutic advances.. Breast cancer (Tokyo, Japan), 33(1), 25-37. https://doi.org/10.1007/s12282-025-01793-5
MLA Shin Y, et al.. "Immune checkpoint inhibition in breast cancer: targeting PD-1/PD-L1 pathway for therapeutic advances.." Breast cancer (Tokyo, Japan), vol. 33, no. 1, 2026, pp. 25-37.
PMID 41123812

Abstract

Breast cancer (BC) is among the most prevalent and immunogenic malignancies in women, characterized by rapid proliferation and significant immune cell infiltration into the tumor microenvironment (TME). The programmed cell death protein 1 (PD-1) and its ligand PD-L1 form a critical immune checkpoint axis exploited by tumors to evade immune detection. Targeting this pathway with immune checkpoint inhibitors (ICIs) has shown clinical promise, particularly in triple-negative breast cancer (TNBC). The IMpassion130 trial demonstrated that atezolizumab plus nab-paclitaxel extended progression-free survival (PFS) to 7.5 months compared to 5.0 months with chemotherapy alone. Similarly, the KEYNOTE-522 trial reported a 64.8% pathological complete response (pCR) rate with pembrolizumab-chemotherapy versus 51.2% in the control group. This review summarizes the PD-1/PD-L1 pathway and highlights the therapeutic impact, clinical advances, and future potential of ICIs in BC treatment.

MeSH Terms

Humans; Immune Checkpoint Inhibitors; B7-H1 Antigen; Female; Programmed Cell Death 1 Receptor; Breast Neoplasms; Tumor Microenvironment; Triple Negative Breast Neoplasms; Antineoplastic Combined Chemotherapy Protocols; Signal Transduction; Molecular Targeted Therapy; Antibodies, Monoclonal, Humanized

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