Studies of the molecular changes that are a consequence of various disease states may ultimately lead to an understanding of the process of disease development and possible prevention of the progression of disease. We are developing cDNA microarray technology and intend to use this technology to determine mechanisms of apoptosis. Advances in genomics has allowed for the development of technology where gene expression of thousands of genes may be monitored simultaneously in biological samples. We are currently conducting studies examining the gene expression changes in a variety of cells exposed to apoptotic agents. These basic studies will contribute information that may be useful in the treatment and understanding of some diseases including AIDS and cancer where apoptosis is a significant contributing component. Microarrays may be used to identify toxic effects of drugs, to improve the current testing models, and to also understand the mechanism of action of these agents. This should also lead to the identification of new genes/targets involved in environmental, viral or genetic-linked diseases including cancer and diseases of the immune, nervous, and pulmonary/respiratory systems. - Microarray, apoptosis, RNA, oxidant stress, NFk-B, p53

Agency
National Institute of Health (NIH)
Institute
National Institute of Environmental Health Sciences (NIEHS)
Type
Intramural Research (Z01)
Project #
1Z01ES023027-01
Application #
6227936
Study Section
Special Emphasis Panel (LMC)
Project Start
Project End
Budget Start
Budget End
Support Year
1
Fiscal Year
1999
Total Cost
Indirect Cost
City
State
Country
United States
Zip Code
Liu, Jie; Xie, Yaxiong; Merrick, B Alex et al. (2006) Transplacental arsenic plus postnatal 12-O-teradecanoyl phorbol-13-acetate exposures associated with hepatocarcinogenesis induce similar aberrant gene expression patterns in male and female mouse liver. Toxicol Appl Pharmacol 213:216-23
Innes, Cynthia L; Heinloth, Alexandra N; Flores, Kristina G et al. (2006) ATM requirement in gene expression responses to ionizing radiation in human lymphoblasts and fibroblasts. Mol Cancer Res 4:197-207
Liu, Jie; Xie, Yaxiong; Ducharme, Danica M K et al. (2006) Global gene expression associated with hepatocarcinogenesis in adult male mice induced by in utero arsenic exposure. Environ Health Perspect 114:404-11
Malarkey, David E; Parker, Joel S; Turman, Coral A et al. (2005) Microarray data analysis of mouse neoplasia. Toxicol Pathol 33:127-35
Annereau, Jean-Philippe; Szakacs, Gergely; Tucker, Charles J et al. (2004) Analysis of ATP-binding cassette transporter expression in drug-selected cell lines by a microarray dedicated to multidrug resistance. Mol Pharmacol 66:1397-405
Hodges, Leslie C; Cook, Jennifer D; Lobenhofer, Edward K et al. (2003) Tamoxifen functions as a molecular agonist inducing cell cycle-associated genes in breast cancer cells. Mol Cancer Res 1:300-11
Bottone Jr, Frank G; Martinez, Jeanelle M; Collins, Jennifer B et al. (2003) Gene modulation by the cyclooxygenase inhibitor, sulindac sulfide, in human colorectal carcinoma cells: possible link to apoptosis. J Biol Chem 278:25790-801
Heinloth, Alexandra N; Shackelford, Rodney E; Innes, Cynthia L et al. (2003) Identification of distinct and common gene expression changes after oxidative stress and gamma and ultraviolet radiation. Mol Carcinog 37:65-82
Heinloth, Alexandra N; Shackelford, Rodney E; Innes, Cynthia L et al. (2003) ATM-dependent and -independent gene expression changes in response to oxidative stress, gamma irradiation, and UV irradiation. Radiat Res 160:273-90
Rojas, E; Shi, Z-Z; Valverde, M et al. (2003) Cell survival and changes in gene expression in cells unable to synthesize glutathione. Biofactors 17:13-9

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