There is increasing evidence that oxidative damage and free radicals, with sequelae of altered cellular energetics and protein alterations, are important in the initiation, promotion, invasion, metastasis, and treatment of cancers. Moreover, oxidative damage and free radicals also are implicated in the side effects of normal tissue injury following cancer therapy, including chemotherapy, radiafion, and biological modifiers. The Free Radical Biology in Cancer Shared Resource Facility (FRBC SRF) was established to provide expertise in and analyses of free radicals, cellular energetics, and reactive species, as well as proteomics in cancer and cancer biology for Markey Cancer Center (MCC) investigators who perform basic, pre-clinical, and clinical research. The four basic services provided by the FRBC SRF are: 1) Analysis of markers of oxidative and nitrosative stress;2) Molecular biological manipulation of biological systems with which to investigate redox signals, including measurements of mitochondrial function by Seahorse technology;3) Proteomics identification of differentially expressed, differentially oxidized, or differentially covalently modified proteins in various cancer-related systems;4) Electron paramagnetic resonance (EPR) detection of free radicals. Development of new applications and methodology for better understanding of the roles of free radicals in cancer and cancer chemotherapy and technical assistance with grant and manuscript preparation by MCC investigators will also be provided. Included in these functions of the considerable expertise of the FRBC SRF Technical Advisory Committee to educate MCC investigators on proper sample handling and preparation methods so that reliable, precise, and artifact-free assay results are obtained. Multiple investigators from all four research programs of the MCC (Redox Injury and Repair [RR];Cancer Cell Biology and Signaling [CS];Cancer Prevention and Control [CP];and Drug Discovery, Delivery and Translational Therapeutics [DT]) have used one or more services of the FRBC SRF. Indeed, even as a relatively new shared resource, the FRBC SRF still had usage by 26% of MCC investigators.

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Damaging free radicals are produced by cancers and with various cancer treatments. When cells are damaged, evidence of free radical-induced oxidative or nitrosative stress becomes apparent. The Free Radical Biology in Cancer Shared Resource Facility addresses these issues for members of the MCC by determining markers of oxidative stress, measuring oxidative stress-mediated mitochondrial dysfunction using Seahorse technology, and identifying aberrant cellular proteins using proteomics.

National Institute of Health (NIH)
National Cancer Institute (NCI)
Center Core Grants (P30)
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Subcommittee G - Education (NCI)
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Shi, Jian; Wang, Yifan; Zeng, Lei et al. (2014) Disrupting the interaction of BRD4 with diacetylated Twist suppresses tumorigenesis in basal-like breast cancer. Cancer Cell 25:210-25
Tuna, Halide; Avdiushko, Rita G; Sindhava, Vishal J et al. (2014) Regulation of the mucosal phenotype in dendritic cells by PPAR?: role of tissue microenvironment. J Leukoc Biol 95:471-85
Huang, Yan; Hu, Yin; Liu, Jinze (2014) Piecing the puzzle together: a revisit to transcript reconstruction problem in RNA-seq. BMC Bioinformatics 15 Suppl 9:S3
Chen, Li; Voronovich, Zoya; Clark, Kenneth et al. (2014) Predicting the likelihood of an isocitrate dehydrogenase 1 or 2 mutation in diagnoses of infiltrative glioma. Neuro Oncol 16:1478-83
Barone, Eugenio; Di Domenico, Fabio; Butterfield, D Allan (2014) Statins more than cholesterol lowering agents in Alzheimer disease: their pleiotropic functions as potential therapeutic targets. Biochem Pharmacol 88:605-16
Förster, Sarah; Welleford, Andrew S; Triplett, Judy C et al. (2014) Increased O-GlcNAc levels correlate with decreased O-GlcNAcase levels in Alzheimer disease brain. Biochim Biophys Acta 1842:1333-9
Gilbert, Misty R; Liu, Yinxing; Neltner, Janna et al. (2014) Autophagy and oxidative stress in gliomas with IDH1 mutations. Acta Neuropathol 127:221-33
Farr, Susan A; Ripley, Jessica L; Sultana, Rukhsana et al. (2014) Antisense oligonucleotide against GSK-3? in brain of SAMP8 mice improves learning and memory and decreases oxidative stress: Involvement of transcription factor Nrf2 and implications for Alzheimer disease. Free Radic Biol Med 67:387-95
Cenini, Giovanna; Fiorini, Ada; Sultana, Rukhsana et al. (2014) An investigation of the molecular mechanisms engaged before and after the development of Alzheimer disease neuropathology in Down syndrome: a proteomics approach. Free Radic Biol Med 76:89-95
Liu, Yinxing; Gilbert, Misty R; Kyprianou, Natasha et al. (2014) The tumor suppressor prostate apoptosis response-4 (Par-4) is regulated by mutant IDH1 and kills glioma stem cells. Acta Neuropathol 128:723-32

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