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10.1158/1535-7163.MCT-14-0774-T http://scihub22266oqcxt.onion/10.1158/1535-7163.MCT-14-0774-T C4571491!4571491 !25824336     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=25824336 &cmd=llinks): Failed to open stream: HTTP request failed! 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Small Molecule MYC Inhibitor Conjugated to Integrin-Targeted Nanoparticles Extends Survival in a Mouse Model of Disseminated Multiple Myeloma |pdf=|usr=}}{{25824336 }} gab.com Text Small Molecule MYC Inhibitor Conjugated to Integrin-Targeted Nanoparticles Extends Survival in a Mouse Model of Disseminated Multiple Myeloma JO: Mol Cancer Ther http://www.kidney.de/pget.php?&tw=1&pmid=25824336 #FOAvip Multiple myeloma pathogenesis is driven by the MYC oncoprotein, its dimerization with MAX, and the binding of this heterodimer to E-Boxes in the vicinity of target genes. The systemic utility of potent small molecule inhibitors of MYC-MAX dimerization was limited by poor bioavailability, rapid metabolism, and inadequate target site penetration. We hypothesized that new lipid-based MYC-MAX dimerization inhibitor prodrugs delivered via integrin-targeted nanoparticles (NP) would overcome prior shortcomings of MYC inhibitor approaches and prolong survival in a mouse model of cancer. An Sn 2 lipase-labile prodrug inhibitor of MYC-MAX dimerization (MI1-PD) was developed which decreased cell proliferation and induced apoptosis in cultured multiple myeloma cell lines alone (P < 0.05) and when incorporated into integrin-targeted lipid-encapsulated NPs (P < 0.05). Binding and efficacy of NPs closely correlated with integrin expression of the target multiple myeloma cells. Using a KaLwRij metastatic multiple myeloma mouse model, VLA-4-targeted NPs (20 nm and 200 nm) incorporating MI1-PD (D) NPs conferred significant survival benefits compared with respective NP controls, targeted (T) no-drug (ND), and untargeted (NT) control NPs (T/D 200: 46 days vs. NT/ND: 28 days, P < 0.05 and T/D 20: 52 days vs. NT/ND: 29 days, P = 0.001). The smaller particles performed better of the two sizes. Neither MI1 nor MI1-PD provided survival benefit when administered systemically as free compounds. These results demonstrate for the first time that a small molecule inhibitor of the MYC transcription factor can be an effective anticancer agent when delivered using a targeted nanotherapy approach. Twit Text FOAVip Small Molecule MYC Inhibitor Conjugated to Integrin-Targeted Nanoparticles Extends Survival in a Mouse Model of Disseminated Multiple Myeloma ????Mol Cancer Ther http://www.kidney.de/pget.php?&tw=1&pmid=25824336 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25824336 #FOAvip English Wikipedia <ref>{{Cite pmid|25824336 }}</ref> Small Molecule MYC Inhibitor Conjugated to Integrin-Targeted Nanoparticles Extends Survival in a Mouse Model of Disseminated Multiple Myeloma #MMPMID25824336 Soodgupta D ; Pan D ; Cui G ; Senpan A ; Yang X ; Lu L ; Weilbaecher KN ; Prochownik EV ; Lanza GM ; Tomasson MH Mol Cancer Ther 2015[Jun]; 14 (6 ): 1286-1294 PMID25824336 show ga Multiple myeloma pathogenesis is driven by the MYC oncoprotein, its dimerization with MAX, and the binding of this heterodimer to E-Boxes in the vicinity of target genes. The systemic utility of potent small molecule inhibitors of MYC-MAX dimerization was limited by poor bioavailability, rapid metabolism, and inadequate target site penetration. We hypothesized that new lipid-based MYC-MAX dimerization inhibitor prodrugs delivered via integrin-targeted nanoparticles (NP) would overcome prior shortcomings of MYC inhibitor approaches and prolong survival in a mouse model of cancer. An Sn 2 lipase-labile prodrug inhibitor of MYC-MAX dimerization (MI1-PD) was developed which decreased cell proliferation and induced apoptosis in cultured multiple myeloma cell lines alone (P < 0.05) and when incorporated into integrin-targeted lipid-encapsulated NPs (P < 0.05). Binding and efficacy of NPs closely correlated with integrin expression of the target multiple myeloma cells. Using a KaLwRij metastatic multiple myeloma mouse model, VLA-4-targeted NPs (20 nm and 200 nm) incorporating MI1-PD (D) NPs conferred significant survival benefits compared with respective NP controls, targeted (T) no-drug (ND), and untargeted (NT) control NPs (T/D 200: 46 days vs. NT/ND: 28 days, P < 0.05 and T/D 20: 52 days vs. NT/ND: 29 days, P = 0.001). The smaller particles performed better of the two sizes. Neither MI1 nor MI1-PD provided survival benefit when administered systemically as free compounds. These results demonstrate for the first time that a small molecule inhibitor of the MYC transcription factor can be an effective anticancer agent when delivered using a targeted nanotherapy approach. |Animals [MESH] |Apoptosis/drug effects [MESH] |Basic Helix-Loop-Helix Leucine Zipper Transcription Factors/chemistry/metabolism [MESH] |Blotting, Western [MESH] |Cell Line, Tumor [MESH] |Cell Survival/drug effects [MESH] |Disease Models, Animal [MESH] |Dose-Response Relationship, Drug [MESH] |Humans [MESH] |Integrin alpha4beta1/*antagonists & inhibitors/metabolism [MESH] |Integrin alphaVbeta3/*antagonists & inhibitors/metabolism [MESH] |Mice [MESH] |Multiple Myeloma/*drug therapy/pathology [MESH] |Nanoparticles/*chemistry [MESH] |Prodrugs/pharmacology [MESH] |Protein Multimerization/drug effects [MESH] |Proto-Oncogene Proteins c-myc/*antagonists & inhibitors/chemistry/metabolism [MESH] |Small Molecule Libraries/chemistry/metabolism/*pharmacology [MESH] |Survival Analysis [MESH]Small Molecule MYC Inhibitor Conjugated to Integrin-Targeted Nanoparti(epmc).pdf DeepDyve Pubget Overpricing