Akademik Veri Yönetim Sistemi
Gene, cilt.1001, 2026 (SCI-Expanded, Scopus)
Triple-negative breast cancer (TNBC) remains one of the most aggressive and therapeutically challenging subtypes of breast cancer due to the absence of estrogen receptor, progesterone receptor, and HER2 expression. As a result, treatment options remain limited, and patient outcomes are often poor. Increasing evidence suggests that tumor angiogenesis plays a critical role in TNBC progression, highlighting the vascular endothelial growth factor receptor (VEGFR) pathway as a potential therapeutic target. This review critically examines the biological role of VEGFR signaling in TNBC and evaluates current therapeutic strategies targeting this pathway. Preclinical studies demonstrate that VEGFR inhibition can suppress tumor growth, angiogenesis, and metastasis. However, clinical trials of anti-angiogenic therapies have produced inconsistent results, raising essential questions regarding patient selection, resistance mechanisms, and therapeutic combinations. We summarize current preclinical and clinical evidence, discuss mechanisms underlying treatment resistance, and evaluate emerging strategies combining VEGFR inhibition with immunotherapy, chemotherapy, and DNA-damage–targeting agents. In addition, we highlight the importance of molecular stratification and biomarker-driven approaches to identify patients most likely to benefit from anti-angiogenic therapy. Overall, while VEGFR-targeted therapy alone has shown limited success, rational combination strategies and improved patient selection may significantly enhance its clinical utility in TNBC.