Document Detail


Antiangiogenic cancer therapy: monitoring with molecular US and a clinically translatable contrast agent (BR55).
MedLine Citation:
PMID:  20515975     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
PURPOSE: To develop and test human kinase insert domain receptor (KDR)-targeted microbubbles (MBs) (MB(KDR)) for imaging KDR at the molecular level and for monitoring antiangiogenic therapy in a human colon cancer xenograft tumor model in mice.
MATERIALS AND METHODS: Animal studies were approved by the Institutional Administrative Panel on Laboratory Animal Care. A heterodimeric peptide that binds to human KDR with low nanomolar affinity (K(D) = 0.5 nmol/L) was coupled onto the surface of perfluorobutane-containing lipid-shelled MBs (MB(KDR)). Binding specificity of MB(KDR) to human KDR and cross-reactivity with murine vascular endothelial growth factor (VEGF) receptor 2 (VEGFR2) were tested in cell culture under flow shear stress conditions (at 100 sec(-1)). In vivo binding specificity of MB(KDR) to VEGFR2 was tested in human LS174T colon cancer xenografts in mice with a 40-MHz ultrasonographic (US) transducer. Targeted contrast material-enhanced US imaging signal by using MB(KDR) was longitudinally measured during 6 days in tumors with (n = 6) and without (n = 6) antiangiogenic treatment (anti-VEGF antibody). Ex vivo VEGFR2 staining and microvessel density analysis were performed. Significant differences were evaluated (t, Mann-Whitney, or Wilcoxon test).
RESULTS: Cell culture experiments showed four times greater binding specificity of MB(KDR) to human KDR and cross-reactivity to murine VEGFR2 (P < or = .01). In vivo imaging signal was more than three times higher (P = .01) with MB(KDR) compared with control MBs and decreased significantly (approximately fourfold lower, P = .03) following in vivo receptor blocking with anti-VEGFR2 antibody. One day after initiation of antiangiogenic therapy, imaging signal was significantly decreased (approximately 46% lower, P = .02) in treated versus untreated tumors; it remained significantly lower (range, 46%-84% decreased; P = .038) during the following 5 days. Microvessel density was significantly reduced (P = .04) in treated (mean, 7.3 microvessels per square millimeter +/- 4.7 [standard deviation]) versus untreated tumors (mean, 22.0 microvessels per square millimeter +/- 9.4); VEGFR2 expression was significantly decreased (>50% lower, P = .03) in treated tumors.
CONCLUSION: Human MB(KDR) allow in vivo imaging and longitudinal monitoring of VEGFR2 expression in human colon cancer xenografts.
Authors:
Marybeth A Pysz; Kira Foygel; Jarrett Rosenberg; Sanjiv S Gambhir; Michel Schneider; Jürgen K Willmann
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2010-06-01
Journal Detail:
Title:  Radiology     Volume:  256     ISSN:  1527-1315     ISO Abbreviation:  Radiology     Publication Date:  2010 Aug 
Date Detail:
Created Date:  2010-07-26     Completed Date:  2010-09-24     Revised Date:  2011-08-03    
Medline Journal Info:
Nlm Unique ID:  0401260     Medline TA:  Radiology     Country:  United States    
Other Details:
Languages:  eng     Pagination:  519-27     Citation Subset:  AIM; IM    
Affiliation:
Department of Radiology, Molecular Imaging Program at Stanford, Stanford University School of Medicine, 300 Pasteur Dr, Room H1307, Stanford, CA 94305, USA.
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MeSH Terms
Descriptor/Qualifier:
Angiogenesis Inhibitors / administration & dosage*
Animals
Cell Line, Tumor
Colonic Neoplasms / drug therapy*,  ultrasonography*
Contrast Media
Drug Delivery Systems / methods
Humans
Mice
Microbubbles
Molecular Probe Techniques*
Peptides / diagnostic use*
Reproducibility of Results
Sensitivity and Specificity
Ultrasonography / methods*
Grant Support
ID/Acronym/Agency:
CA114747 P50/CA/NCI NIH HHS; R21 CA139279/CA/NCI NIH HHS; R21 CA139279-01A1/CA/NCI NIH HHS
Chemical
Reg. No./Substance:
0/Angiogenesis Inhibitors; 0/Contrast Media; 0/Peptides
Comments/Corrections
Comment In:
Radiology. 2010 Aug;256(2):331-3   [PMID:  20656826 ]

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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