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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Discussion

Authors

Weidong Qin

Danxi Li

Jiawei Zhang

Journals

Frontiers in Oncology

SHILAP Revista de lepidopterología

Actions

Institutions

Nanchang University

Air Force Medical University

Xijing Hospital

References and Citations

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

Key Points

Abstract

Citation Network

Connected Papers

Discussion

Authors

Journals

Actions

Institutions

References and Citations

Citation Network

Connected Papers

Discussion

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