PROJECT 001 ? GENOME MAINTENANCE RESEARCH PROGRAM PROJECT SUMMARY/ABSTRACT Members of the Genome Maintenance Research Program (GM) are basic science researchers integrated by the common goal of understanding processes affecting the integrity, expression and duplication of the genome. Research themes within GM include carcinogen metabolism, cell division cycle control, chromatin and epigenetics, DNA replication and repair, DNA damage responses and gene expression. Discovery science that elucidates basic mechanisms, cancer etiology, and opportunities for therapeutic intervention is at the heart of GM. Program leaders foster interactions among GM members and between the Vanderbilt-Ingram Cancer Center (VICC) Research Programs that propel basic discoveries from the bench to clinical practice. In addition, the Program aims to support new research initiatives, build the research infrastructure necessary for discovery, mentor and educate junior members and trainees, and create a dynamic and collaborative environment that advances science faster and further than would be possible as individual laboratories. GM members also participate in two NCI-funded Specialized Programs of Research Excellence (SPOREs) in Gastrointestinal and Breast cancers, and several NIH training grants. GM houses the intellectual resources to support over 75 clinical trials open to accrual at VICC that use drugs that target DNA. In short, GM acts as the organizing entity for all cancer-focused DNA research at Vanderbilt. The GM members' research links to, and has impact for all, of the major cancer types within the VICC catchment area. There are 23 program members from seven departments and two schools, with $9.1M in total peer-reviewed funding and NCI making up 39% ($3.5M). Out of 332 publications, 13% are intra-programmatic and 23% are inter-programmatic. Members also have 106 collaborative publications with investigators at other NCI- designated cancer centers.

Agency
National Institute of Health (NIH)
Institute
National Cancer Institute (NCI)
Type
Center Core Grants (P30)
Project #
2P30CA068485-25
Application #
10024644
Study Section
Subcommittee I - Transistion to Independence (NCI)
Project Start
1998-09-01
Project End
2025-08-31
Budget Start
2020-09-01
Budget End
2021-08-31
Support Year
25
Fiscal Year
2020
Total Cost
Indirect Cost
Name
Vanderbilt University Medical Center
Department
Type
DUNS #
079917897
City
Nashville
State
TN
Country
United States
Zip Code
37232
Maacha, Selma; Hong, Jun; von Lersner, Ariana et al. (2018) AXL Mediates Esophageal Adenocarcinoma Cell Invasion through Regulation of Extracellular Acidification and Lysosome Trafficking. Neoplasia 20:1008-1022
Schulte, Michael L; Fu, Allie; Zhao, Ping et al. (2018) Pharmacological blockade of ASCT2-dependent glutamine transport leads to antitumor efficacy in preclinical models. Nat Med 24:194-202
Petersen, Christine P; Meyer, Anne R; De Salvo, Carlo et al. (2018) A signalling cascade of IL-33 to IL-13 regulates metaplasia in the mouse stomach. Gut 67:805-817
Wang, Jing; Zhao, Yue; Zhou, Xiaofan et al. (2018) Nascent RNA sequencing analysis provides insights into enhancer-mediated gene regulation. BMC Genomics 19:633
Galligan, James J; Wepy, James A; Streeter, Matthew D et al. (2018) Methylglyoxal-derived posttranslational arginine modifications are abundant histone marks. Proc Natl Acad Sci U S A 115:9228-9233
Davenport, James R; Su, Timothy; Zhao, Zhiguo et al. (2018) Modifiable lifestyle factors associated with risk of sessile serrated polyps, conventional adenomas and hyperplastic polyps. Gut 67:456-465
Pannala, Venkat R; Wall, Martha L; Estes, Shanea K et al. (2018) Metabolic network-based predictions of toxicant-induced metabolite changes in the laboratory rat. Sci Rep 8:11678
Zhao, Shilin; Li, Chung-I; Guo, Yan et al. (2018) RnaSeqSampleSize: real data based sample size estimation for RNA sequencing. BMC Bioinformatics 19:191
Croessmann, Sarah; Sheehan, Jonathan H; Lee, Kyung-Min et al. (2018) PIK3CA C2 Domain Deletions Hyperactivate Phosphoinositide 3-kinase (PI3K), Generate Oncogene Dependence, and Are Exquisitely Sensitive to PI3K? Inhibitors. Clin Cancer Res 24:1426-1435
Doxie, Deon B; Greenplate, Allison R; Gandelman, Jocelyn S et al. (2018) BRAF and MEK inhibitor therapy eliminates Nestin-expressing melanoma cells in human tumors. Pigment Cell Melanoma Res 31:708-719

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