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Tumors, nanomedicine

Greish, K. (2007) Enhanced permeability and retention of macromolecular drags in solid tumors a royal gate for targeted anticancer nanomedicines. Journal of Drug Targeting 15 457-464. [Pg.26]

Rhyner MN et al. (2006) Quantum dots and multifunctional nanoparticles New contrast agents for tumor imaging. Nanomedicine. 1 209-217. [Pg.84]

Two major steps in drug delivery are commonly considered first step is the tissue vascular level (organ), accomplished by EPR effect for polymer therapeutics (nanomedicine) which can traverse the vascular wall to the tumor interstitium, where EPR effect plays the single most important role [69]. [Pg.108]

Lu D, Wientjes MG, Lu Z, Au JL, Tumor priming enhances delivery and efficacy of nanomedicines. J Pharmacol Exp Ther 2007 322 80-88. [Pg.244]

Hampel S, Kunze D, Haase D, et al. Carbon nanotubes filled with a chemotherapeutic agent a nanocarrier mediates inhibition of tumor cell growth. Nanomedicine 2008 3 175-182. [Pg.266]

Hainfeld, J., Smilowitz, H., O Connor, M., Dihnanian, F., Slatkin, D. Gold nanoparticle imaging and radiotherapy of brain tumors in mice. Nanomedicine 8(10), 1601-1609 (2013)... [Pg.87]

Active targeting can also enhance the distribution of nanomedicine within the tumor interstitium (Drummond et al. 1999). Active targeting has been explored to deliver drugs into resistant cancer cells (Sapra and AUen 2003). [Pg.412]

Elbayoumi TA, Torchilin VP (2009) Tumor-targeted nanomedicines enhanced antitumor efficacy in vivo of doxorubicin loaded, long-circulating liposomes modified with cancer specific monoclonal antibody. Clin Cancer Res 15 1973-1980... [Pg.48]

L. Balogh, S. S. Nigavekar and B. M. Nair, et al. Significant effect of size on the in vivo biodistribution of gold composite nanodevices in mouse tumor models. Nanomedicine Nanotechnology, Biology, and Medicine, 3(4), 281-296 (2007). [Pg.283]

Figure 11.1 Journey of a stimulus-targeted nanomedicine After intravenous administration, both stimuli-targeted and un-targeted nanomedicines rely on the EPR effect for primary tumor targeting. Then, activatable nanocarriers are converted in active forms by tumor stimuli, either acidosis, hypoxia or overexpressed proteases. This conversion leads to exposure of internalization moieties of pharmaceutical agent delivery systems or signal emission of enrichment nanoprobes. EPR enhanced permeabihty and retention effect, F fluorophore, Q quencher, MMP matrix metaUoproteases. Figure 11.1 Journey of a stimulus-targeted nanomedicine After intravenous administration, both stimuli-targeted and un-targeted nanomedicines rely on the EPR effect for primary tumor targeting. Then, activatable nanocarriers are converted in active forms by tumor stimuli, either acidosis, hypoxia or overexpressed proteases. This conversion leads to exposure of internalization moieties of pharmaceutical agent delivery systems or signal emission of enrichment nanoprobes. EPR enhanced permeabihty and retention effect, F fluorophore, Q quencher, MMP matrix metaUoproteases.
The use of broader targeting motifs exposed only after nanocarrier activation by a tumor-stimulus has been proposed to address both the reduced internalization produced by PEGylation and the treatment of most tumors from a minimal nanomedicine library [30]. In this approach, tumor-stimuli-sensitive formulations are administered as precursors which stay inactive imtil endocytosis or diagnostic functions are switched on after localized activation by a tumor stimulus. The main physiological tumor stimuli... [Pg.313]


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See also in sourсe #XX -- [ Pg.231 , Pg.232 ]




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