The DNA Damage and Cellular Defense Program consists of 19 members of the Comprehensive Cancer Center of Wake Forest University, representing 6 Departments. The overall scientific goal within the DNA Damage and Cellular Defense Program is to understand the mechanisms and processes whereby cells sustain-or alternatively, mitigate by prevention or repair-damage to DNA or other critical macromolecular structures.
The Specific Aims of this Program are: 1) To determine mechanisms of damage to DNA by redox-active or electrophilic chemical agents implicated in carcinogenesis. The focus of research in Aim #1 may be divided into two subgroups. One is concerned with mechanisms of DNA damage by redox-active or free radical species, enhancement by metal ions of oxidative damage to DNA, and the role of metal ions in determining the resulting base or sequence specificity of oxidative damage. A second subgroup is interested in electrophilic agents that form cytotoxic and/or mutagenic DNA adducts, often after metabolic activation by phase 1 enzymes such as the cytochrome P450 mixed- function oxidases. 2) To identify and define the significance of phenotype or genotypic factors that determine relative susceptibility to DNA- damaging agents among different cell/tissue types and between organisms. One focus on the mechanisms and relative contribution of specific enzymatic pathways to cellular defenses against DNA damage by electrophiles and reactive oxygen species. A second focus is on cellular regulatory pathways and genetic differences that govern cellular sensitivity to DNA damaging agents. The DDCD Program has a strong funding and productivity record. Total funding of $1.8 M includes 47% NCI funding, and a 88% increase in NCI funding over the past three years. Membership has been reorganized and more narrowly limited to cancer focused investigators; four new faculty recruits have been added since 1997. Members rely heavily on core lab services in support of their research, and have made efficient use of pilot funding mechanisms, many of which have matured into funded grants. Members are highly interactive, with 21 intraprogrammatic publications out of 140 listed since 1996. There are 8 established interactions, and 12 new collaborations begun in the past two years. A number of new and established translational projects a ongoing, with several more pending review.

Agency
National Institute of Health (NIH)
Institute
National Cancer Institute (NCI)
Type
Center Core Grants (P30)
Project #
2P30CA012197-27
Application #
6457412
Study Section
Subcommittee E - Prevention &Control (NCI)
Project Start
1976-03-01
Project End
2006-01-31
Budget Start
Budget End
Support Year
27
Fiscal Year
2001
Total Cost
Indirect Cost
Name
Wake Forest University Health Sciences
Department
Type
DUNS #
041418799
City
Winston-Salem
State
NC
Country
United States
Zip Code
27106
Feliz-Mosquea, Yismeilin R; Christensen, Ashley A; Wilson, Adam S et al. (2018) Combination of anthracyclines and anti-CD47 therapy inhibit invasive breast cancer growth while preventing cardiac toxicity by regulation of autophagy. Breast Cancer Res Treat 172:69-82
Holmila, Reetta J; Vance, Stephen A; Chen, Xiaofei et al. (2018) Mitochondria-targeted Probes for Imaging Protein Sulfenylation. Sci Rep 8:6635
Rego, Stephen L; Harvey, Scott; Simpson, Sean R et al. (2018) TREX1 D18N mice fail to process erythroblast DNA resulting in inflammation and dysfunctional erythropoiesis. Autoimmunity :1-12
Li, X C; Wang, M Y; Yang, M et al. (2018) A mutational signature associated with alcohol consumption and prognostically significantly mutated driver genes in esophageal squamous cell carcinoma. Ann Oncol 29:938-944
Godwin, Ryan C; Macnamara, Lindsay M; Alexander, Rebecca W et al. (2018) Structure and Dynamics of tRNAMet Containing Core Substitutions. ACS Omega 3:10668-10678
Lu, Yong; Wang, Qiang; Xue, Gang et al. (2018) Th9 Cells Represent a Unique Subset of CD4+ T Cells Endowed with the Ability to Eradicate Advanced Tumors. Cancer Cell 33:1048-1060.e7
Akter, Salma; Fu, Ling; Jung, Youngeun et al. (2018) Chemical proteomics reveals new targets of cysteine sulfinic acid reductase. Nat Chem Biol 14:995-1004
Peak, Taylor C; Praharaj, Prakash P; Panigrahi, Gati K et al. (2018) Exosomes secreted by placental stem cells selectively inhibit growth of aggressive prostate cancer cells. Biochem Biophys Res Commun 499:1004-1010
Chmielewski, Jeffrey P; Bowlby, Sarah C; Wheeler, Frances B et al. (2018) CD38 Inhibits Prostate Cancer Metabolism and Proliferation by Reducing Cellular NAD+ Pools. Mol Cancer Res 16:1687-1700
Han, Fei; Li, Chien-Feng; Cai, Zhen et al. (2018) The critical role of AMPK in driving Akt activation under stress, tumorigenesis and drug resistance. Nat Commun 9:4728

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