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dc.contributor.advisorVanderah, Todd W.
dc.contributor.authorNikolich-Zugich, Tuana
dc.creatorNikolich-Zugich, Tuanaen_US
dc.date.accessioned2013-08-09T17:41:07Z
dc.date.available2013-08-09T17:41:07Z
dc.date.issued2013
dc.identifier.citationNikolich-Zugich, Tuana. (2013). Multivalent Cathepsin Inhibitor, VBY-825, Attenuates Breast-Induced Bone Cancer Remodelling and Pain (Bachelor's thesis, University of Arizona, Tucson, USA).
dc.identifier.urihttp://hdl.handle.net/10150/297716
dc.description.abstractMetastatic bone cancer originates from breast malignancies causing severe pain and bone destruction in patients. Amongst the novel therapies under clinical development for the treatment of bone metastases are cathepsin inhibitors. Cysteine cathepsins (B, C, F, H, K, L, O, L2/V, W, X/Z) are highly expressed in many human cancers and have been associated with poor patient prognosis. In the RIP1-Tag2 transgenic model of pancreatic cancer, mice treated with VBY-825, reversible inhibitor of cathepsins S, B, V, L, K showed a significant reduction in tumor incidence and growth. In this study, we evaluate the efficacy of the cathepsin inhibitor, VBY-825 as treatment for cancer-induced bone pain. Breast cancer cells, 66.1, were injected within the intramedullary space of the femurs of female mice. After seven days of inoculation, the animals were treated with VBY-825 or vehicle (5% dextrose) subcutaneously for seven days. Spontaneous pain behaviors were significantly attenuated in cancer-induced mice treated with VBY-825, compared to vehicle treated animals. Additionally, cancer-induced animals treated with VBY-825 demonstrated both an improvement in bone integrity and reduction of tumor burden. These results indicate that a cathepsin inhibitor targeting multiple cathepsins, such as VBY-825, could be a novel therapeutic for bone metastases.
dc.language.isoenen_US
dc.publisherThe University of Arizona.en_US
dc.rightsCopyright © is held by the author. Digital access to this material is made possible by the University Libraries, University of Arizona. Further transmission, reproduction or presentation (such as public display or performance) of protected items is prohibited except with permission of the author.en_US
dc.rights.urihttp://rightsstatements.org/vocab/InC/1.0/
dc.titleMultivalent Cathepsin Inhibitor, VBY-825, Attenuates Breast-Induced Bone Cancer Remodelling and Painen_US
dc.typetexten_US
dc.typeElectronic Thesisen_US
thesis.degree.grantorUniversity of Arizonaen_US
thesis.degree.levelbachelorsen_US
thesis.degree.disciplineHonors Collegeen_US
thesis.degree.disciplinePhysiologyen_US
thesis.degree.nameB.S.en_US
refterms.dateFOA2018-07-02T03:34:59Z
html.description.abstractMetastatic bone cancer originates from breast malignancies causing severe pain and bone destruction in patients. Amongst the novel therapies under clinical development for the treatment of bone metastases are cathepsin inhibitors. Cysteine cathepsins (B, C, F, H, K, L, O, L2/V, W, X/Z) are highly expressed in many human cancers and have been associated with poor patient prognosis. In the RIP1-Tag2 transgenic model of pancreatic cancer, mice treated with VBY-825, reversible inhibitor of cathepsins S, B, V, L, K showed a significant reduction in tumor incidence and growth. In this study, we evaluate the efficacy of the cathepsin inhibitor, VBY-825 as treatment for cancer-induced bone pain. Breast cancer cells, 66.1, were injected within the intramedullary space of the femurs of female mice. After seven days of inoculation, the animals were treated with VBY-825 or vehicle (5% dextrose) subcutaneously for seven days. Spontaneous pain behaviors were significantly attenuated in cancer-induced mice treated with VBY-825, compared to vehicle treated animals. Additionally, cancer-induced animals treated with VBY-825 demonstrated both an improvement in bone integrity and reduction of tumor burden. These results indicate that a cathepsin inhibitor targeting multiple cathepsins, such as VBY-825, could be a novel therapeutic for bone metastases.


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