Cancer is a genetic disease caused by mutations, chromosomal abnormalities and chromatin changes that alter gene expression and protein function. This simple statement is the foundation of the Genome Maintenance Research Program (GM). GM is a cohesive network of basic science researchers whose collective mission is to understand processes affecting the integrity, expression and duplication of genetic material. This mission consists not only of explaining the etiology of cancer, but also understanding how existing therapeutics work, and identifying opportunities for new therapeutic development. The Program promotes the highest level of scientific discovery by fostering interactions among members, educating members on opportunities for collaborative research with other programs, and serving as a genome-centric resource for the entire Vanderbilt-Ingram Cancer Center (VICC). Research interests of GM members include carcinogen metabolism, DNA metabolism, DNA damage responses, chromatin and gene expression, epigenetics, and the cell division cycle. There are 26 program members of GM from 11 departments and two schools, with $5.4M in NCI funding and $7M in other peer-reviewed cancer-related funding. Out of 399 publications, 15% are intra-programmatic and 21% are inter-programmatic. Members also have 160 collaborative publications with investigators at other institutions.
The Vanderbilt-Ingram Cancer Center (VICC) is a matrix center that integrates all of Vanderbilt University's cancer-related expertise and resources in order to deliver its mission of alleviating cancer death and suffering through pioneering research; innovative patient-centered care; and evidence-based prevention, education and community initiatives. This is accomplished through translation of exceptional cancer research into interventions for the prevention and treatment of cancer. The Cancer Center Support Grant provides infrastructure to facilitate multidisciplinary basic, clinical and population-based research, to advance our discoveries to cancer patients and the community and to educate and train the next generation of cancer investigators.
|Gilchuk, Pavlo; Kuzmina, Natalia; Ilinykh, Philipp A et al. (2018) Multifunctional Pan-ebolavirus Antibody Recognizes a Site of Broad Vulnerability on the Ebolavirus Glycoprotein. Immunity 49:363-374.e10|
|Hebron, Katie E; Li, Elizabeth Y; Arnold Egloff, Shanna A et al. (2018) Alternative splicing of ALCAM enables tunable regulation of cell-cell adhesion through differential proteolysis. Sci Rep 8:3208|
|Bangaru, Sandhya; Zhang, Heng; Gilchuk, Iuliia M et al. (2018) A multifunctional human monoclonal neutralizing antibody that targets a unique conserved epitope on influenza HA. Nat Commun 9:2669|
|Means, Anna L; Freeman, Tanner J; Zhu, Jing et al. (2018) Epithelial Smad4 Deletion Up-Regulates Inflammation and Promotes Inflammation-Associated Cancer. Cell Mol Gastroenterol Hepatol 6:257-276|
|Du, Zhenfang; Lovly, Christine M (2018) Mechanisms of receptor tyrosine kinase activation in cancer. Mol Cancer 17:58|
|Zhang, Qin; Jeppesen, Dennis K; Higginbotham, James N et al. (2018) Mutant KRAS Exosomes Alter the Metabolic State of Recipient Colonic Epithelial Cells. Cell Mol Gastroenterol Hepatol 5:627-629.e6|
|Elion, David L; Cook, Rebecca S (2018) Harnessing RIG-I and intrinsic immunity in the tumor microenvironment for therapeutic cancer treatment. Oncotarget 9:29007-29017|
|Kook, Seunghyi; Qi, Aidong; Wang, Ping et al. (2018) Gene-edited MLE-15 Cells as a Model for the Hermansky-Pudlak Syndromes. Am J Respir Cell Mol Biol 58:566-574|
|Choksi, Yash A; Reddy, Vishruth K; Singh, Kshipra et al. (2018) BVES is required for maintenance of colonic epithelial integrity in experimental colitis by modifying intestinal permeability. Mucosal Immunol 11:1363-1374|
|Cooke, Allison L; Morris, Jamie; Melchior, John T et al. (2018) A thumbwheel mechanism for APOA1 activation of LCAT activity in HDL. J Lipid Res 59:1244-1255|
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