简介：AIM:Toinvestigatethebiologicaleffectsofinternalirradiation,andthetherapeuticeffectivenesswasassessedof131I-labeledanti-epidermalgrowthfactorreceptor（EGFR）liposomes,derivedfromcetuximab,whenusedasatumor-targetingcarrierinacolorectalcancermousemodel.METHODS:WedescribedtheliposomesandcharacterizedtheirEGFR-targetedbindingandcellularuptakeinEGFR-overexpressingLS180colorectalcancercells.Afterintra-tumorinjectionsof74MBq（740MBq/mL）131I-antiEGFR-BSA-PCL,weinvestigatedthebiologicaleffectsofinternalirradiationandthetherapeuticefficacyof131I-antiEGFR-BSA-PCLoncolorectalcancerinamaleBALB/cmousemodel.Tumorsize,bodyweight,histopathology,andSPECTimagingweremonitoredfor33dpost-therapy.RESULTS:Therapidradioiodineuptakeof131I-antiEGFR-BSA-PCLand131I-BSA-PCLreachedmaximumlevelsat4hafterincubation,andthe131Iuptakeof131I-antiEGFR-BSA-PCLwashigherthanthatof131I-BSAPCLinvitro.The131Itissuedistributionassayrevealedthat131I-antiEGFR-BSA-PCLwasmarkedlytakenupbythetumor.Furthermore,atissuedistributionassayrevealedthat131I-antiEGFR-BSA-PCLwasmarkedlytakenupbythetumorandreacheditsmaximaluptakevalueof21.0±1.01%ID/g（%ID/gisthepercentageinjecteddosepergramoftissue）at72hfollowingtherapy;thedrugconcentrationinthetumorwashigherthanthatintheliver,heart,colon,orspleen.Tumorsizemeasurementsshowedthattumordevelopmentwassignificantlyinhibitedbytreatmentswith131I-antiEGFR-BSA-PCLand131I-BSA-PCL.Thevolumeoftumorincreased,andtreatmentratewith131I-antiEGFR-BSA-PCLwas124%±7%,lowerthanthatwith131I-BSA-PCL（127%±9%）,131I（143%±7%）,andnormalsaline（146%±10%）.Thepercentagelossesinoriginalbodyweightswere39%±3%,41%±4%,49%±5%,and55%±13%,respectively.Thebestsurvivalandcurerateswereobtainedinthegrouptreatedwith131I-antiEGFR-BSA-PCL.Theanimalsinjec