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Contrast Media & Molecular Imaging
Volume 2017, Article ID 1686525, 11 pages
Research Article

MicroPET/CT Imaging of AXL Downregulation by HSP90 Inhibition in Triple-Negative Breast Cancer

1Department of Cancer Systems Imaging, The University of Texas MD Anderson Cancer Center, Houston, TX, USA
2Department of Radiology, The 1st Affiliated Hospital of Anhui Medical University, Hefei, Anhui, China
3Department of Systems Biology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA

Correspondence should be addressed to Yongqiang Yu; moc.361.piv@gnaiqgnoyuy.rjc, Shiaw-Yih Lin; gro.nosrednadm@nilys, and Chun Li; gro.nosrednadm@ilc

Received 7 February 2017; Accepted 2 April 2017; Published 14 May 2017

Academic Editor: Kai Yang

Copyright © 2017 Wanqin Wang et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


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 64Cu-labeled anti-human AXL antibody (64Cu-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 64Cu-anti-hAXL as clearly visualized by microPET/CT. Our data indicate that 64Cu-anti-hAXL can be useful for monitoring anti-AXL therapies and for assessing inhibition of HSP90 molecular chaperone using AXL as a molecular surrogate.