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dc.contributor.advisorTrawick, Mary-Lynn
dc.contributor.authorWang, Elizabeth
dc.contributor.otherBaylor University.en_US
dc.date.accessioned2013-05-24T22:24:22Z
dc.date.available2013-05-24T22:24:22Z
dc.date.copyright2013-05-01
dc.date.issued2013-05-24
dc.identifier.urihttp://hdl.handle.net/2104/8706
dc.description.abstractCancer is one of the leading causes of mortality in the United States as well as the developing world. Metastasis is responsible for about 90% of cancer deaths, and is a cause of morbidity in those who continue to battle it. Most cancers can be attributed to genetic mutations as well as unhealthy behaviors, but a tumor can metastasize from its primary site into the blood and to distant organs if the tumor microenvironment is supportive. A number of endogenous proteases, embedded in a complex protease network, are shown to be upregulated in cancers and aid in metastasis. This study examines cathepsin B, which is reported to play an important role in tumor progression and metastasis, as a target for drug therapy. It is usually tightly regulated, but in metastasis it cleaves the extracellular matrix of cancer cells to aid in invasion. Inhibition of cathepsin B has been shown to limit metastasis, although ultimately, any attempt to curtail the metastatic process through proteases must consider the relationships of the protease network.en_US
dc.language.isoen_USen_US
dc.rightsBaylor University projects are protected by copyright. They may be viewed from this source for any purpose, but reproduction or distribution in any format is prohibited without written permission. Contact libraryquestions@baylor.edu for inquiries about permission.en_US
dc.titleMetastasis and Cathepsin Ben_US
dc.typeThesisen_US
dc.rights.accessrightsWorldwide accessen_US
dc.contributor.departmentUniversity Scholar.en_US


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