Programmed death ligand 1 and the tumor microenvironment shape immune checkpoint combination therapy in triple-negative breast cancer

Triple-negative breast cancer (TNBC) is a clinically aggressive and molecularly heterogeneous subtype in which immune checkpoint blockade produces meaningful but inconsistent benefit. Programmed death-ligand 1 (PD-L1), expressed across malignant and immune-cell compartments, functions through programmed cell death protein 1 (PD-1) within a tumor microenvironment that can either sustain antitumor immunity or promote immune escape. This review critically integrates TNBC molecular heterogeneity, PD-1/PD-L1 signaling, microenvironmental regulation, resistance mechanisms, predictive biomarkers, safety, and clinical evidence for PD-L1-directed therapy. Unlike drug-centered summaries, it links divergent clinical outcomes to chemotherapy backbone, disease setting, biomarker assay, and immune context. Comparative analysis of the IMpassion trials indicates that efficacy cannot be attributed to the antibody alone. Tumor-infiltrating lymphocytes, cancer-associated fibroblasts, tumor-associated macrophages, tumor-associated neutrophils, and myeloid-derived suppressor cells form interacting networks that shape PD-L1 expression, immune exclusion, and adaptive resistance. Emerging strategies include bispecific antibodies targeting cytotoxic T-lymphocyte-associated protein 4 (CTLA-4) or lymphocyte activation gene 3 (LAG-3) alongside PD-L1; co-blockade of T-cell immunoglobulin and mucin domain-containing protein 3 (TIM-3) or T-cell immunoreceptor with immunoglobulin and ITIM domains (TIGIT); sialic acid-binding immunoglobulin-like lectin 9 (Siglec-9)-directed macrophage approaches; and cellular therapies. Current evidence favors integrated biomarkers rather than PD-L1 staining alone, combining assay-defined PD-L1 status with immune-cell composition, molecular subtype, and dynamic markers such as circulating tumor DNA. The central clinical challenge is to identify the patients, disease settings, and combinations in which therapeutic benefit outweighs toxicity and resistance.

Authors

Institutions

Publication Details

Journal
Discover Oncology
Published
2026-10-28
DOI
https://doi.org/10.1007/s12672-026-06209-0
Primary Topic
Cancer Immunotherapy and Biomarkers
Type
article
Field-Weighted Citation Impact
0.00
Controls
|||
ALL TIME
JAN
FEB
MAR
APR
MAY
JUN
JUL
AUG
SEP
OCT
article

Programmed death ligand 1 and the tumor microenvironment shape immune checkpoint combination therapy in triple-negative breast cancer

Ronak Ahmadi, Fatemeh Malekinejad, Mehrdad Nourizadeh, Razieh Nabizadeh et al.
1 links
Discover Oncology
Cancer Immunotherapy and Biomarkers
article

Programmed death ligand 1 and the tumor microenvironment shape immune checkpoint combination therapy in triple-negative breast cancer

Ronak Ahmadi, Fatemeh Malekinejad, Mehrdad Nourizadeh, Razieh Nabizadeh, Kimia Azami
article en

Abstract

Triple-negative breast cancer (TNBC) is a clinically aggressive and molecularly heterogeneous subtype in which immune checkpoint blockade produces meaningful but inconsistent benefit. Programmed death-ligand 1 (PD-L1), expressed across malignant and immune-cell compartments, functions through programmed cell death protein 1 (PD-1) within a tumor microenvironment that can either sustain antitumor immunity or promote immune escape. This review critically integrates TNBC molecular heterogeneity, PD-1/PD-L1 signaling, microenvironmental regulation, resistance mechanisms, predictive biomarkers, safety, and clinical evidence for PD-L1-directed therapy. Unlike drug-centered summaries, it links divergent clinical outcomes to chemotherapy backbone, disease setting, biomarker assay, and immune context. Comparative analysis of the IMpassion trials indicates that efficacy cannot be attributed to the antibody alone. Tumor-infiltrating lymphocytes, cancer-associated fibroblasts, tumor-associated macrophages, tumor-associated neutrophils, and myeloid-derived suppressor cells form interacting networks that shape PD-L1 expression, immune exclusion, and adaptive resistance. Emerging strategies include bispecific antibodies targeting cytotoxic T-lymphocyte-associated protein 4 (CTLA-4) or lymphocyte activation gene 3 (LAG-3) alongside PD-L1; co-blockade of T-cell immunoglobulin and mucin domain-containing protein 3 (TIM-3) or T-cell immunoreceptor with immunoglobulin and ITIM domains (TIGIT); sialic acid-binding immunoglobulin-like lectin 9 (Siglec-9)-directed macrophage approaches; and cellular therapies. Current evidence favors integrated biomarkers rather than PD-L1 staining alone, combining assay-defined PD-L1 status with immune-cell composition, molecular subtype, and dynamic markers such as circulating tumor DNA. The central clinical challenge is to identify the patients, disease settings, and combinations in which therapeutic benefit outweighs toxicity and resistance.

Discover Oncology
Islamic Azad University of Tabriz (IR), Tabriz University of Medical Sciences (IR), Islamic Azad University Kazeron (IR)
Good health and well-being
Openalex Percentile: Top 16%
Cancer Immunotherapy and Biomarkers
AI Navigator

Ask Laika to Summarize, Analyze, and Connect papers live on the map.

Summarize Papers & Methodologies

Extract key findings, datasets, and comparative methods across publications.

Benchmark Rankings & Visual Analytics

Rank top research institutions, authors, funders, topics, and journals by Field-Weighted Citation Impact (FWCI) and paper volume with instant charts.

Connect Distant Disciplines

Bridge topological clusters on the map to find hidden collaborative intersections.

Laika access coming soon