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- W2151637779 abstract "Abstract Despite early benefits seen in cancer patients treated with antivascular endothelial growth factor (VEGF) pathway-targeted drugs, the clinical benefits obtained in terms of progression-free or overall survival have been more modest than expected. This outcome is, at least in part, due to antiangiogenic drug resistance mechanisms that involve pathways mediated largely by the tumor, whether intrinsic or acquired in response to therapy, or by the host, which is either responding directly to therapy or indirectly to tumoral cues. The focus of this review is to distinguish, where possible, between such host and tumor-mediated pathways of resistance and discuss key challenges facing the preclinical and clinical development of antiangiogenic agents, including potential differences in drug efficacies when treating primary tumors or various stages of metastatic disease. (Clin Cancer Res 2009;15(16):5020–5)" @default.
- W2151637779 created "2016-06-24" @default.
- W2151637779 creator A5009195551 @default.
- W2151637779 creator A5010799165 @default.
- W2151637779 creator A5061940667 @default.
- W2151637779 date "2009-08-12" @default.
- W2151637779 modified "2023-10-02" @default.
- W2151637779 title "Tumor and Host-Mediated Pathways of Resistance and Disease Progression in Response to Antiangiogenic Therapy" @default.
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- W2151637779 doi "https://doi.org/10.1158/1078-0432.ccr-09-0095" @default.
- W2151637779 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/2743513" @default.
- W2151637779 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/19671869" @default.
- W2151637779 hasPublicationYear "2009" @default.
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