The Tumor Development Program focuses on understanding the genetic, epigenetic and developmental processes that take place in tumor-initiating cells and tumor-susceptible tissues during tumor development. The Program was established in 2007 by combining the Oncodevelopmental Biology Program with the Cancer Genetics &Epigenetics Program. This merger logically combines expertise in developmental aspects of cancer with genetic and epigenetic mechanisms underiying cancer development. Drs. Robert Oshima and Manuel Perucho are co-Leaders of the Program, which consists of 14 full members and 2 adjunct members. The Program comprises three overarching themes, which benefit from highly interdisciplinary program membership, including expertise in genetic and epigenetic pathways, stem cell biology, mouse models of cancer and medicinal chemistry: 1- Genetic and epigenetic changes in cancer. Program members continue to lead the field of the "mutator phenotype" and carcinogenesis, with additional strengths in the areas of chromatin modifications, cell cycle regulation and checkpoint signaling, and RNA biology;2- Stem cell biology, with focus of Notch and Wnt signaling, and mouse models of cancer, with focus on mammary gland and colon models. The Program is a resource for all CCSG Programs due to its expertise in mouse tumor models;and 3- Novel targets in cancer treatment, with focus on nuclear receptors and retinoic acids. Notably, members of the Program have developed a retinoid-like drug, Targretin?, which is FDA-approved for the treatment cutaneous T cell lymphoma. Members of this collaborative and multidisciplinary Program interact at a number of levels, including monthly faculty meetings and through collaborative grants. Program funding is currently at $12.9MM in annual total costs ($7.0MM direct). Program members participate in two POIs (1 from NCI), three U54/U19 grants, and 15 additional collaborative peer-reviewed federal and state grants. Program members also have 17 NIH ROIs (7 from NCI). The Program's productivity is further reflected by 345 publications since last review, and by 58 Program publications in 2008, which represent 14% of intra- and 21% of inter-programmatic collaborations, respectively.

Public Health Relevance

The Tumor Development Program tackles the fundamental causes underlying tumor inifiafion and development. Understanding the eariy genefic, epigenefic and developmental changes and defects that occur in tumor-initiating cells and tumor-susceptible tissues is expected to lead into novel therapies that target eariy stages of cancer, or key cell populations that continue to drive malignancy of late stage tumors.

Agency
National Institute of Health (NIH)
Institute
National Cancer Institute (NCI)
Type
Center Core Grants (P30)
Project #
5P30CA030199-33
Application #
8669926
Study Section
Subcommittee G - Education (NCI)
Project Start
Project End
Budget Start
2014-05-01
Budget End
2015-04-30
Support Year
33
Fiscal Year
2014
Total Cost
$108,876
Indirect Cost
$100,216
Name
Sanford-Burnham Medical Research Institute
Department
Type
DUNS #
020520466
City
La Jolla
State
CA
Country
United States
Zip Code
92037
Lechtenberg, Bernhard C; Rajput, Akhil; Sanishvili, Ruslan et al. (2016) Structure of a HOIP/E2~ubiquitin complex reveals RBR E3 ligase mechanism and regulation. Nature 529:546-50
Zhong, Zhenyu; Umemura, Atsushi; Sanchez-Lopez, Elsa et al. (2016) NF-κB Restricts Inflammasome Activation via Elimination of Damaged Mitochondria. Cell 164:896-910
Olson, Erika J; Lechtenberg, Bernhard C; Zhao, Chunxia et al. (2016) Modifications of a Nanomolar Cyclic Peptide Antagonist for the EphA4 Receptor To Achieve High Plasma Stability. ACS Med Chem Lett 7:841-6
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Zhao, Wei; Mazar, Joseph; Lee, Bongyong et al. (2016) The Long Noncoding RNA SPRIGHTLY Regulates Cell Proliferation in Primary Human Melanocytes. J Invest Dermatol 136:819-28
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McQuary, Philip R; Liao, Chen-Yu; Chang, Jessica T et al. (2016) C. elegans S6K Mutants Require a Creatine-Kinase-like Effector for Lifespan Extension. Cell Rep 14:2059-67
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Koh, Mei Yee; Gagea, Mihai; Sargis, Timothy et al. (2016) A new HIF-1α/RANTES-driven pathway to hepatocellular carcinoma mediated by germline haploinsufficiency of SART1/HAF in mice. Hepatology 63:1576-91

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