Journal
CONTRAST MEDIA & MOLECULAR IMAGING
Volume -, Issue -, Pages -Publisher
WILEY-HINDAWI
DOI: 10.1155/2017/1686525
Keywords
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Funding
- Department of Defense (DOD) Breast Cancer Research Program (BCRP) [W81XWH-10-1-0558]
- John S. Dunn Foundation
- National Institutes of Health [P30CA016672]
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AXL receptor tyrosine kinase is overexpressed in a number of solid tumor types including triple-negative breast cancer (TNBC). AXL is considered an important regulator of epithelial-to-mesenchymal transition (EMT) and a potential therapeutic target for TNBC. In this work, we used microPET/CT with Cu-64-labeled anti-human AXL antibody (Cu-64-anti-hAXL) to noninvasively interrogate the degradation of AXL in vivo in response to 17-allylamino-17-demethoxygeldanamycin (17-AAG), a potent inhibitor of HSP90. 17-AAG treatment caused significant decline in AXL expression in orthotopic TNBC MDA-MB-231 tumors, inhibited EMT, and delayed tumor growth in vivo, resulting in significant reduction in tumor uptake of Cu-64-anti-hAXL as clearly visualized by microPET/CT. Our data indicate that Cu-64-anti-hAXL can be useful for monitoring anti-AXL therapies and for assessing inhibition of HSP90 molecular chaperone using AXL as a molecular surrogate.
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