Arterial Embolization Hyperthermia Using As2O3 Nanoparticles in VX2 Carcinoma–Induced Liver Tumors 英文参考文献.docVIP
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Arterial Embolization Hyperthermia Using As2O3 Nanoparticles in VX2 Carcinoma–Induced Liver Tumors 英文参考文献
ArterialEmbolizationHyperthermiaUsingAs2O3
NanoparticlesinVX2Carcinoma–InducedLiverTumors
HuiYu1,Guang-YuZhu1,Rui-ZhiXu2,Huan-ZhangNiu1,QinLu1,Guo-ZhaoLi1,Zi-YuWang3,
Dong-ShengZhang3,NingGu2,Gao-JunTeng1*
1JiangsuKeyLaboratoryofMolecularImagingandFunctionalImaging,DepartmentofRadiology,Zhong-DaHospital,MedicalSchoolofSoutheastUniversity,Nanjing,
China, 2Jiangsu Laboratory for Biomaterials and Devices, State Key Laboratory of BioElectronics, School of Biological Science and Medical Engineering, Southeast
University,Nanjing,China,3DepartmentofPathologyandPathophysiology,MedicalSchoolofSoutheastUniversity,Nanjing,China
Abstract
Background:Combinationtherapyforarterialembolizationhyperthermia(AEH)witharsenictrioxide(As2O3 )nanoparticles
(ATONs)isanoveltreatmentforsolidmalignancies.Thisstudywasperformedtoevaluatethefeasibilityandtherapeutic
effectofAEHwithAs2O3nanoparticlesinarabbitlivercancermodel.Theprotocolwasapprovedbyourinstitutionalanimal
usecommittee.
Methodology/Principal Findings: In total, 60 VX2 liver-tumor-bearing rabbits were randomly assigned to five groups
(n=12/group)andreceivedAEHwithATONs(Group1),hepaticarterialembolizationwithATONs(Group2),lipiodol(Group
3),orsaline(Group4),onday14aftertumorimplantation.TwelverabbitsthatreceivedAEHwithATONswerepreparedfor
temperature measurements, and were defined as Group 5. Computed tomography was used to measure the tumors’
longestdimension,andevaluationwasperformedaccordingtotheResponseEvaluationCriteriainSolidTumors.Hepatic
toxicity, tumornecrosis rate,vascular endothelialgrowthfactor level,and microvesseldensity weredetermined.Survival
rates were measured using the Kaplan-Meier method. The therapeutic temperature (42.5uC) was obtained in Group 5.
Hepatotoxicityreactionsoccurredbutweretransientinallgroups.Tumorgrowthwasdelayedandsurvivalwasprolonged
inGroup1(treatedwithAEHandATONs).Plasmaandtumorvascularendothelialgrowthfactorandmicrovesseldensity
weresignificantlyinhibitedinGroup1,whiletumornecrosisrateswerem
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