The goal of the University of Louisville Molecular Targets COBRE Core D is to facilitate the rapid translation of novel approaches to cancer prevention, diagnosis and treatment through the use of transgenic mouse models of cancer. In particular. Core D will facilitate the translational objectives of University of Louisville COBRE-related investigators by developing coordinated resources, techniques, expertise and several colonies of transgenic mice for the safety and efficacy testing of novel anti-cancer approaches. The initial goal will be to establish colonies of the transgenic mice and to develop methods for longitudinal monitoring of tumor progression or regression without the need to euthanize the animals. Once the core is established, the long-term objectives will be to provide access of transgenic mouse models of cancer to junior and senior cancer researchers at the University of Louisville, including past and present COBRE investigators, in order to facilitate the testing of novel anti-cancer compounds and strategies. The specific objectives are to: (i) Maintain, distribute and provide pre-clinical toxicity and efficacy support for transgenic mouse models of melanoma, childhood neuroblastoma, lung, breast, prostate, colon, pancreatic and hematological cancers;(ii) Provide technical support for transgenic mouse genotyping, specimen collection and processing, and PK analyses of novel anti-cancer agents;and (iii) Conduct state-of-the-art diagnostic imaging services for the detection of tumors and response to novel therapeutic agents. In summary, we propose a core facility that will procure and breed transgenic mouse models of several common cancer types and that will provide technical services to facilitate the testing of novel strategies and drugs developed at the University of Louisville.
Core E will support pre-clinical safety and efficacy trials of novel compounds and strategies to detect, prevent and treat cancer so that our COBRE investigators can rapidly move these agents and strategies from laboratory benches into cages and then phase I trials of human subjects suffering with cancer.
|Zhao, Guoping; Neely, Aaron M; Schwarzer, Christian et al. (2016) N-(3-oxo-acyl) homoserine lactone inhibits tumor growth independent of Bcl-2 proteins. Oncotarget 7:5924-42|
|Smith, Colin A; Ban, David; Pratihar, Supriya et al. (2016) Allosteric switch regulates protein-protein binding through collective motion. Proc Natl Acad Sci U S A 113:3269-74|
|Garbett, Nichola C; Brock, Guy N (2016) Differential scanning calorimetry as a complementary diagnostic tool for the evaluation of biological samples. Biochim Biophys Acta 1860:981-9|
|Waigel, Sabine; Rendon, Beatriz E; Lamont, Gwyneth et al. (2016) MIF inhibition reverts the gene expression profile of human melanoma cell line-induced MDSCs to normal monocytes. Genom Data 7:240-2|
|Yaddanapudi, Kavitha; Rendon, Beatriz E; Lamont, Gwyneth et al. (2016) MIF Is Necessary for Late-Stage Melanoma Patient MDSC Immune Suppression and Differentiation. Cancer Immunol Res 4:101-12|
|Sabo, T Michael; Trent, John O; Lee, Donghan (2015) Population shuffling between ground and high energy excited states. Protein Sci 24:1714-9|
|England, Christopher G; Miller, M Clarke; Kuttan, Ashani et al. (2015) Release kinetics of paclitaxel and cisplatin from two and three layered gold nanoparticles. Eur J Pharm Biopharm 92:120-9|
|Miller, M Clarke; Ohrenberg, Carl J; Kuttan, Ashani et al. (2015) Separation of Quadruplex Polymorphism in DNA Sequences by Reversed-Phase Chromatography. Curr Protoc Nucleic Acid Chem 61:17.7.1-18|
|Satpathy, Shuchismita R; Jala, Venkatakrishna R; Bodduluri, Sobha R et al. (2015) Crystalline silica-induced leukotriene B4-dependent inflammation promotes lung tumour growth. Nat Commun 6:7064|
|Andreeva, Kalina; Soliman, Maha M; Cooper, Nigel G F (2015) Regulatory networks in retinal ischemia-reperfusion injury. BMC Genet 16:43|
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