Histopathology, immunohistochemistry, confocal laser scanning microscopy, and in situ hybridization are techniques that are integral to cancer at the applicant site the Arkansas Cancer Research Center (ACRC) at the University of Arkansas for Medical Sciences (UAMS). The Experimental Pathology hared Resource Laboratory (EPSRL) will provide high-quality, reliable experimental pathology facilities; save costs for investigators and the institution; increase efficiency of sample processing and evaluation; and eliminate duplication of services, equipment, and material. In addition, the EPSRL will implement stringent standards of quality control to ensure that the techniques offered provide optimum results to all investigators using the shared resource. The current facility offers confocal laser scanning results to all investigators using the shared resource. The current facility offers confocal laser scanning microscopy, immunohistochemistry, and histopathology services to more than 60 investigators in more than 13 departments. Funding is sought to expand current services, to establish a formal support mechanism for key personnel; to add in situ hybridization capabilities; and to develop a more extensive armamentarium of special stains, immunohistochemistry, and antigen retrieval techniques. The PI and the co-investigators for this proposal have ample experience in pathology, confocal microscopy cell biology, and molecular biology. Each has previously directed a shared 4resource facility, with successful attention to equipment maintenance, control materials, quality control and quality assurance procedures, and expertise in protocol development. This proposal outlines the following Specific Aims: 1. Maintain an active centralize laboratory for providing state-of-the- art immunohistochemistry, histopathology, and confocal laser scanning microscopy for cancer center investigators. 2. Ensure rigorous quality control and quality assurance on all samples evaluated in the EPSRL 3. Develop new in situ hybridization capabiliti4es for use by cancer center investigators. The EPSRL will be pivotal in improving the research infrastructure at the ACRC and UAMS, provide a model for the development of additional shared resource, and significantly enhance the institutional positional for future funding by a P30 NCI Cancer Center Support Grant.

Agency
National Institute of Health (NIH)
Institute
National Cancer Institute (NCI)
Type
Resource-Related Research Projects (R24)
Project #
1R24CA082899-01
Application #
2902221
Study Section
Special Emphasis Panel (ZCA1-SRRB-C (M1))
Program Officer
Berman, Jules J
Project Start
1999-07-15
Project End
2004-06-30
Budget Start
1999-07-15
Budget End
2000-06-30
Support Year
1
Fiscal Year
1999
Total Cost
Indirect Cost
Name
University of Arkansas for Medical Sciences
Department
Pathology
Type
Schools of Medicine
DUNS #
City
Little Rock
State
AR
Country
United States
Zip Code
72205
Reid, Angela B; Kurten, Richard C; McCullough, Sandra S et al. (2005) Mechanisms of acetaminophen-induced hepatotoxicity: role of oxidative stress and mitochondrial permeability transition in freshly isolated mouse hepatocytes. J Pharmacol Exp Ther 312:509-16
Kurten, Richard C; Chowdhury, Parag; Sanders Jr, Ronald C et al. (2005) Coordinating epidermal growth factor-induced motility promotes efficient wound closure. Am J Physiol Cell Physiol 288:C109-21
James, Laura P; Kurten, Richard C; Lamps, Laura W et al. (2005) Tumour necrosis factor receptor 1 and hepatocyte regeneration in acetaminophen toxicity: a kinetic study of proliferating cell nuclear antigen and cytokine expression. Basic Clin Pharmacol Toxicol 97:8-14
Bene, Anca; Kurten, Richard C; Chambers, Timothy C (2004) Subcellular localization as a limiting factor for utilization of decoy oligonucleotides. Nucleic Acids Res 32:e142
Zent, Clive S; Chen, James B; Kurten, Richard C et al. (2004) Alemtuzumab (CAMPATH 1H) does not kill chronic lymphocytic leukemia cells in serum free medium. Leuk Res 28:495-507
Jones, Stacie M; Hiller, F Charles; Jacobi, Sandie E et al. (2003) Enhanced beta2-adrenergic receptor (beta2AR) signaling by adeno-associated viral (AAV)-mediated gene transfer. BMC Pharmacol 3:15