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.

Public Health Relevance

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.

Agency
National Institute of Health (NIH)
Institute
National Cancer Institute (NCI)
Type
Center Core Grants (P30)
Project #
5P30CA068485-24
Application #
9783497
Study Section
Subcommittee I - Transistion to Independence (NCI)
Program Officer
Roberson, Sonya
Project Start
1997-09-17
Project End
2020-08-31
Budget Start
2019-09-01
Budget End
2020-08-31
Support Year
24
Fiscal Year
2019
Total Cost
Indirect Cost
Name
Vanderbilt University Medical Center
Department
Type
DUNS #
079917897
City
Nashville
State
TN
Country
United States
Zip Code
37232
Bloodworth, Melissa H; Rusznak, Mark; Pfister, Connor C et al. (2018) Glucagon-like peptide 1 receptor signaling attenuates respiratory syncytial virus-induced type 2 responses and immunopathology. J Allergy Clin Immunol 142:683-687.e12
Saito-Diaz, Kenyi; Benchabane, Hassina; Tiwari, Ajit et al. (2018) APC Inhibits Ligand-Independent Wnt Signaling by the Clathrin Endocytic Pathway. Dev Cell 44:566-581.e8
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Rojas, Juan D; Lin, Fanglue; Chiang, Yun-Chen et al. (2018) Ultrasound Molecular Imaging of VEGFR-2 in Clear-Cell Renal Cell Carcinoma Tracks Disease Response to Antiangiogenic and Notch-Inhibition Therapy. Theranostics 8:141-155
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Vierra, Nicholas C; Dickerson, Matthew T; Jordan, Kelli L et al. (2018) TALK-1 reduces delta-cell endoplasmic reticulum and cytoplasmic calcium levels limiting somatostatin secretion. Mol Metab 9:84-97
Schlegel, Cameron; Weis, Victoria G; Knowles, Byron C et al. (2018) Apical Membrane Alterations in Non-intestinal Organs in Microvillus Inclusion Disease. Dig Dis Sci 63:356-365
Lewis Jr, James S; Shelton, Jeremy; Kuhs, Krystle Lang et al. (2018) p16 Immunohistochemistry in Oropharyngeal Squamous Cell Carcinoma Using the E6H4 Antibody Clone: A Technical Method Study for Optimal Dilution. Head Neck Pathol 12:440-447
Werfel, Thomas A; Wang, Shan; Jackson, Meredith A et al. (2018) Selective mTORC2 Inhibitor Therapeutically Blocks Breast Cancer Cell Growth and Survival. Cancer Res 78:1845-1858

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