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dc.contributor.authorStylianopoulos, T.en
dc.contributor.authorJain, R. K.en
dc.creatorStylianopoulos, T.en
dc.creatorJain, R. K.en
dc.date.accessioned2019-05-06T12:24:40Z
dc.date.available2019-05-06T12:24:40Z
dc.date.issued2013
dc.identifier.urihttp://gnosis.library.ucy.ac.cy/handle/7/48859
dc.description.abstractBlood perfusion in tumors can be significantly lower than that in the surrounding normal tissue owing to the leakiness and/or compression of tumor blood vessels. Impaired perfusion reduces oxygen supply and results in a hypoxic microenvironment. Hypoxia promotes tumor progression and immunosuppression, and enhances the invasive and metastatic potential of cancer cells. Furthermore, poor perfusion lowers the delivery of systemically administered drugs. Therapeutic strategies to improve perfusion include reduction in vascular permeability by vascular normalization and vascular decompression by alleviating physical forces (solid stress) inside tumors. Both strategies have shown promise, but guidelines on how to use these strategies optimally are lacking. To this end, we developed a mathematical model to guide the optimal use of these strategies. The model accounts for vascular, transvascular, and interstitial fluid and drug transport as well as the diameter and permeability of tumor vessels. Model simulations reveal an optimal perfusion region when vessels are uncompressed, but not very leaky. Within this region, intratumoral distribution of drugs is optimized, particularly for drugs 10 nm in diameter or smaller and of low binding affinity. Therefore, treatments should modify vessel diameter and/or permeability such that perfusion is optimal. Vascular normalization is more effective for hyperpermeable but largely uncompressed vessels (e.g., glioblastomas), whereas solid stress alleviation is more beneficial for compressed but less-permeable vessels (e.g., pancreatic ductal adenocarcinomas). In the case of tumors with hyperpermeable and compressed vessels (e.g., subset of mammary carcinomas), the two strategies need to be combined for improved treatment outcomes.en
dc.language.isoengen
dc.sourceProceedings of the National Academy of Sciences of the United States of Americaen
dc.subject2':4
dc.subjectModelsen
dc.subjectComputer Simulationen
dc.subjectarticleen
dc.subjectdoxorubicinen
dc.subjecthumanen
dc.subjectNeoplasmsen
dc.subjectHumansen
dc.subjectcontrolled studyen
dc.subjectcancer survivalen
dc.subjectpriority journalen
dc.subjecttaxane derivativeen
dc.subjecttreatment outcomeen
dc.subjectsolid tumoren
dc.subjectbreast carcinomaen
dc.subjectupregulationen
dc.subjectbevacizumaben
dc.subjectsunitiniben
dc.subjectBiologicalen
dc.subjectpancreas adenocarcinomaen
dc.subjecthuman cellen
dc.subjectovary carcinomaen
dc.subjectregulatory mechanismen
dc.subjectnelfinaviren
dc.subjectsurgical techniqueen
dc.subjectdrug delivery systemen
dc.subjectDrug Delivery Systemsen
dc.subjectglioblastomaen
dc.subjectBiomechanical Phenomenaen
dc.subjectMathematical modelingen
dc.subjectRegional Blood Flowen
dc.subjectextracellular matrixen
dc.subjectlosartanen
dc.subjectTumor microenvironmenten
dc.subjectmonoclonal antibody DC101en
dc.subjectblood vessel permeabilityen
dc.subjectvascular normalizationen
dc.subjectcediraniben
dc.subjectsaridegiben
dc.subjecttissue perfusionen
dc.subjectdrug transporten
dc.subjecthydraulic conductivityen
dc.subject2 (4 hydroxyphenyl) 4 morpholinopyrido[3'en
dc.subject2 d]pyrimidineen
dc.subject5]furo[3en
dc.subjectblood vessel diameteren
dc.subjectCapillary Permeabilityen
dc.subjectdiphtheria toxinen
dc.subjectdrug bindingen
dc.subjectMechanical forcesen
dc.subjectneutralizing antibodyen
dc.subjectprocollagen proline 2 oxoglutarate 4 dioxygenaseen
dc.subjectprotein farnesyltransferase inhibitoren
dc.subjectprotein tyrosine phosphataseen
dc.subjectsemaxaniben
dc.subjectvasculotropin antibodyen
dc.subjectVessel decompressionen
dc.subjectVessel permeabilityen
dc.titleCombining two strategies to improve perfusion and drug delivery in solid tumorsen
dc.typeinfo:eu-repo/semantics/article
dc.identifier.doi10.1073/pnas.1318415110
dc.description.volume110
dc.description.startingpage18632
dc.description.endingpage18637
dc.author.facultyΠολυτεχνική Σχολή / Faculty of Engineering
dc.author.departmentΤμήμα Μηχανικών Μηχανολογίας και Κατασκευαστικής / Department of Mechanical and Manufacturing Engineering
dc.type.uhtypeArticleen
dc.contributor.orcidStylianopoulos, T. [0000-0002-3093-1696]
dc.description.totalnumpages18632-18637
dc.gnosis.orcid0000-0002-3093-1696


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