The overall objective of the Sphingolipid Animal Cancer Pathobiology (SACP) Shared Resource Core is to provide the Project Leaders with the ability to utilize animal models of carcinogenesis in the execution of their research projects and to maintain genetically engineered mice for the carcinogenesis models. The SACP Shared Resource Core will serve as an essential resource for the use of all animal manipulations needed by the Projects. By centralizing all aspects of in vivo research, the SACP Core will facilitate more rapid and reliable data and minimize the cost of utilizing animal models. The overall aims of the proposal are:
Specific Aim 1 : Ensure proper planning of in vivo research models, provide necessary facilities and expertise for carcinogenesis models and facilitate use of critical Shared Resources. We will a) assist investigators with choosing and/or designing the most appropriate animal model to test hypotheses, including lipid-based transgenic and gene-altered mice: b) provide essential facilities as well as faculty and staff expertise to support research projects in animal models of carcinogenesis;and c) facilitate access to and use of existing shared resources at SBU, including small animal imaging, drug metabolism and pharmacokinetics, tissue biorepository and transgenic and gene knockout generation facilities.
Specific Aim 2 : Enhance and maximize the utility of animal models and provide complementary and alternative approaches. For this Aim we will a) maintain stocks of breeding animals for the Project investigators;b) assist with utilization of carcinogenesis models;and c) provide Project investigators with alternatives to animal research via generation of cell lines from lipid-based genetically engineered mice.
Specific Aim 3 : Provide investigators with assistance and expertise in data collection, interpretation, analysis and management.
In Aim 3 we will a) provide investigators with expertise in pathology, animal model pathobiology and immunohistochemistry;b) assist with data analysis, interpretation and project progression;and c) facilitate sample storage for future studies in animal models of carcinogenesis. Key personel for the SACP Core include an experienced pathologist and a scientific director for Biobanking. Together, these services will provide the necessary expertise in rodent patholgoy and pathobiology associated with carcinogenesis models in additon to biobanking samples generated from animal models of carcinogenesis. These efforts will facilitate the research in this proposal and will provide the expertise to support the Project Leaders. This core is already evolving as a unique and enabling core that is critical for the success of the Program Project.

Public Health Relevance

The SACP Shared Resource Core will serve as a hub of knowledge and resources for the implementation of pre-clinical research in sphingolipids and cancer. This essential resource will facilitate the discovery and determination of novel targets in carcinogenesis, as well as further the development of novel potential therapeutics. The SACP Core will serve as a crucial first step in determining potential mechanisms, interventions and novel therapeutic targets carcinogenesis.

Agency
National Institute of Health (NIH)
Institute
National Cancer Institute (NCI)
Type
Research Program Projects (P01)
Project #
2P01CA097132-11A1
Application #
8742658
Study Section
Special Emphasis Panel (ZCA1-RPRB-J (M1))
Project Start
2002-07-01
Project End
2019-08-31
Budget Start
2014-09-22
Budget End
2015-08-31
Support Year
11
Fiscal Year
2014
Total Cost
$157,052
Indirect Cost
$56,459
Name
State University New York Stony Brook
Department
Type
DUNS #
804878247
City
Stony Brook
State
NY
Country
United States
Zip Code
11794
Lu, Songjian; Cai, Chunhui; Yan, Gonghong et al. (2016) Signal-Oriented Pathway Analyses Reveal a Signaling Complex as a Synthetic Lethal Target for p53 Mutations. Cancer Res 76:6785-6794
Carroll, Brittany L; Pulkoski-Gross, Michael J; Hannun, Yusuf A et al. (2016) CHK1 regulates NF-κB signaling upon DNA damage in p53- deficient cells and associated tumor-derived microvesicles. Oncotarget 7:18159-70
Xu, Ruijuan; Wang, Kai; Mileva, Izolda et al. (2016) Alkaline ceramidase 2 and its bioactive product sphingosine are novel regulators of the DNA damage response. Oncotarget 7:18440-57
García-Barros, Mónica; Coant, Nicolas; Kawamori, Toshihiko et al. (2016) Role of neutral ceramidase in colon cancer. FASEB J 30:4159-4171
McCracken, A N; McMonigle, R J; Tessier, J et al. (2016) Phosphorylation of a constrained azacyclic FTY720 analog enhances anti-leukemic activity without inducing S1P receptor activation. Leukemia :
Adada, Mohamad; Luberto, Chiara; Canals, Daniel (2016) Inhibitors of the sphingomyelin cycle: Sphingomyelin synthases and sphingomyelinases. Chem Phys Lipids 197:45-59
Espaillat, Mel Pilar; Kew, Richard R; Obeid, Lina M (2016) Sphingolipids in neutrophil function and inflammatory responses: Mechanisms and implications for intestinal immunity and inflammation in ulcerative colitis. Adv Biol Regul :
Wang, K; Xu, R; Snider, A J et al. (2016) Alkaline ceramidase 3 deficiency aggravates colitis and colitis-associated tumorigenesis in mice by hyperactivating the innate immune system. Cell Death Dis 7:e2124
Kitatani, K; Usui, T; Sriraman, S K et al. (2016) Ceramide limits phosphatidylinositol-3-kinase C2β-controlled cell motility in ovarian cancer: potential of ceramide as a metastasis-suppressor lipid. Oncogene 35:2801-12
Wu, Song; Powers, Scott; Zhu, Wei et al. (2016) Substantial contribution of extrinsic risk factors to cancer development. Nature 529:43-7

Showing the most recent 10 out of 172 publications