March 3, 2026Open Access

ABCA8-positive lipid-metabolic CAFs mediate immunotherapy resistance in TNBC

Key Points

Immunotherapy resistance is mediated by abca8-positive lipid-metabolic cancer-associated fibroblasts, presenting a critical obstacle in triple-negative breast cancer.
Approximately 70% of patients with TNBC experience reduced responses to immune checkpoint blockade treatment due to an immunosuppressive tumor microenvironment.
Therapeutic intervention targeting the abca8-lipid axis shows promise against immunotherapy resistance, needing further validation for patient outcomes.
Identifying the role of lipid metabolism in tumor microenvironment dynamics may highlight new therapeutic strategies for improving TNBC management.

Abstract

ABCA8+ lpCAFs and APOE+ LAMs contribute to ICB resistance in TNBC through the establishment of an immunosuppressive TME via lipid metabolism reprogramming. Therapeutic intervention targeting the ABCA8-lipid axis presents a promising strategy to enhance ICB efficacy, potentially advancing TNBC treatment outcomes and improving patient survival.

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Cite This Study

Qin et al. (Tue,) studied this question.

synapsesocial.com/papers/69a75b8bc6e9836116a22fe7 https://doi.org/https://doi.org/10.3389/fonc.2025.1729275

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