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dc.contributor.authorGevertz, Jana L.
dc.date.accessioned2017-09-23T15:12:28Z
dc.date.available2017-09-23T15:12:28Z
dc.date.issued2016
dc.identifier.citationJ.L. Gevertz, 2016. Microenvironment-Mediated Modeling of Tumor Response to Vascular-Targeting Drugs. Advances in Experimental Medicine and Biology 936: 191-208.en_US
dc.identifier.urihttps://dx.doi.org/10.1007/978-3-319-42023-3_10
dc.descriptionThe final version is available at link.springer.com.en_US
dc.description.abstractThe tumor-associated microvasculature is one of the key elements of the microenvironment that helps shape, and is shaped by, tumor progression. Given the important role of the vasculature in tumor progression, and the fact that tumor and normal vasculature are physiologically and molecularly distinct, much effort has gone into the development of vascular-targeting drugs that in theory should target tumors without significant risk to normal tissue. In this chapter, a multiscale hybrid mathematical model of tumor-vascular interactions is presented to provide a theoretical basis for assessing tumor response to vascular-targeting drugs. Model performance is calibrated to quantitative clinical data on tumor response to angiogenesis inhibitors (AIs), preclinical data on response to a cytotoxic chemotherapy, and qualitative preclinical data on response to vascular disrupting agents (VDAs). The calibrated model is then used to explore two questions of clinical interest. First, the hypothesis that AIs and VDAs are complementary treatments, rather than redundant, is explored. The model predicts a minimal increase in antitumor activity as a result of adding a VDA to an AI treatment regimen, and in fact at times the combination can exert less antitumor activity than stand-alone AI treatment. Second, the question of identifying an optimal dosing strategy for treating with an AI and a cytotoxic agent is addressed. Using a stochastic optimization scheme, an intermittent schedule for both chemotherapy and AI administration is identified that can eradicate the simulated tumors. We propose that this schedule may have increased clinical antitumor activity compared to currently used treatment protocols.en_US
dc.language.isoen_USen_US
dc.publisherKiuweren_US
dc.subjectAngiogenesis inhibitorsen_US
dc.subjectCytotoxic chemotherapyen_US
dc.subjectHybrid cellular automaton modelen_US
dc.subjectTumor-vasculature interactionsen_US
dc.subjectVascular disrupting agentsen_US
dc.titleMicroenvironment-Mediated Modeling of Tumor Response to Vascular-Targeting Drugsen_US
dc.typeArticleen_US
dc.typeTexten_US
dc.typePostprinten_US
dc.typePostprinten_US
prism.publicationNameAdvances in Experimental Medicine and Biology
prism.volume936
prism.publicationDate2016
prism.startingPage191
prism.endingPage208
dc.identifier.handlehttps://dr.tcnj.edu/handle/2900/1420


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