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dc.contributor.authorLI Y.en_GB
dc.contributor.authorSONG E.en_GB
dc.contributor.authorABBAS RIZVI S. M.en_GB
dc.contributor.authorPOWER C. A.en_GB
dc.contributor.authorBERETOV J.en_GB
dc.contributor.authorRAJA C.en_GB
dc.contributor.authorCOZZI P. J.en_GB
dc.contributor.authorMORGENSTERN Alfreden_GB
dc.contributor.authorAPOSTOLIDIS Christosen_GB
dc.contributor.authorALLEN B. J.en_GB
dc.contributor.authorRUSSELL P. J.en_GB
dc.date.accessioned2010-02-25T14:48:53Z-
dc.date.available2009-02-19en_GB
dc.date.available2010-02-25T14:48:53Z-
dc.date.created2009-02-18en_GB
dc.date.issued2009en_GB
dc.date.submitted2009-02-18en_GB
dc.identifier.citationCLINICAL CANCER RESEARCH vol. 15 no. 3 p. 865-875en_GB
dc.identifier.issn1078-0432en_GB
dc.identifier.urihttp://www.aacrjournals.orgen_GB
dc.identifier.urihttp://publications.jrc.ec.europa.eu/repository/handle/JRC50507-
dc.description.abstractPurpose: To investigate the therapeutic potential of 213Bilabeled multiple targeted a-radioimmunoconjugates for treatingprostate cancer (CaP)micrometastases inmousemodels. Experimental Design: PC-3 CaP cells were implanted s.c., in the prostate, and intratibially in NODSCID mice. The expression of multiple tumor ^ associated antigens on tumor xenografts andmicrometastaseswas detected by immunohistochemistry.Targeting vectorswere twomonoclonal antibodies, and a plasminogen activator inhibitor type 2 that binds to cell surface urokinase plasminogen activator, labeledwith 213Bi using standardmethodology. In vivo efficacy ofmultiple a conjugates (MTAT) at different activities was evaluated in these mouse models.Tumor growth was monitored during observations and local regional lymph node metastases were assessed at the end of experiments. Results:The take rate of PC-3 cells was100% for each route of injection.The tumor-associated antigens (MUC1, urokinase plasminogen activator, and BLCA-38) were heterogeneously expressed on primary tumors and metastatic cancer clusters at transit. A single i.p. injection of MTAT (test) at high and low doses caused regression of the growth of primary tumors and prevented local lymph nodemetastases in a concentration-dependent fashion; it also caused cancer cells to undergo necrosis and apoptosis. Conclusions: Our results suggest thatMTATcan impede primary PC-3 CaP growth at three different sites in vivo through induction of apoptosis, and can prevent the spread of cancer cells and target lymph node micrometastases in a concentration-dependent manner. MTAT, by targeting multiple antigens, can overcome heterogeneous antigen expression to kill small CaP cell clusters, thus providing a potent therapy for micrometastases.en_GB
dc.description.sponsorshipJRC.E.5-Nuclear chemistryen_GB
dc.format.mediumPrinteden_GB
dc.languageENGen_GB
dc.publisherAMER ASSOC CANCER RESEARCHen_GB
dc.relation.ispartofseriesJRC50507en_GB
dc.titleInhibition ofMicrometastatic Prostate Cancer Cell Spread in Animal Models By 213BilabeledMultipleTargeted Alpha-Radioimmunoconjugatesen_GB
dc.typeArticles in periodicals and booksen_GB
dc.identifier.doi10.1158/1078-0432.CCR-08-1203en_GB
JRC Directorate:Nuclear Safety and Security

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