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- W1915663515 abstract "Vascular endothelial growth factor-A (VEGF) signals vascular development and angiogenesis mainly by binding to VEGF receptor family member 2 (VEGFR-2). Adaptor proteins mediate many VEGFR-2's functions in the development of blood vessels. Cancer cells secrete VEGF to activate VEGFR-2 pathway in their neighboring endothelial cells in the process of cancer-related angiogenesis. Interestingly, activation of VEGFR-2 signaling is found in breast cancer cells, but its role and regulation are not clear. We highlighted research advances of VEGFR-2, with a focus on VEGFR-2's regulation by mutant p53 in breast cancer. In addition, we reviewed recent Food and Drug Administration-approved tyrosine kinase inhibitor drugs that can inhibit the function of VEGFR-2. Ongoing preclinical and clinical studies might prove that pharmaceutically targeting VEGFR-2 could be an effective therapeutic strategy in treating triple-negative breast cancer." @default.
- W1915663515 created "2016-06-24" @default.
- W1915663515 creator A5005085624 @default.
- W1915663515 creator A5084743296 @default.
- W1915663515 date "2015-10-09" @default.
- W1915663515 modified "2023-09-30" @default.
- W1915663515 title "The Emerging Regulation of VEGFR-2 in Triple-Negative Breast Cancer" @default.
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- W1915663515 doi "https://doi.org/10.3389/fendo.2015.00159" @default.
- W1915663515 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4598588" @default.
- W1915663515 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/26500608" @default.
- W1915663515 hasPublicationYear "2015" @default.
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