Agency
National Institute of Health (NIH)
Institute
National Institute of Environmental Health Sciences (NIEHS)
Type
Research Project (R01)
Project #
7R01ES006501-03
Application #
2155351
Study Section
Metabolic Pathology Study Section (MEP)
Project Start
1994-05-01
Project End
1997-04-30
Budget Start
1996-01-01
Budget End
1996-04-30
Support Year
3
Fiscal Year
1995
Total Cost
Indirect Cost
Name
Wake Forest University Health Sciences
Department
Biology
Type
Schools of Medicine
DUNS #
041418799
City
Winston-Salem
State
NC
Country
United States
Zip Code
27106
Govindarajan, Baskaran; Mizesko, Melissa C; Miller, Mark Steven et al. (2003) Tuberous sclerosis-associated neoplasms express activated p42/44 mitogen-activated protein (MAP) kinase, and inhibition of MAP kinase signaling results in decreased in vivo tumor growth. Clin Cancer Res 9:3469-75
Govindarajan, Baskaran; Klafter, Robert; Miller, Mark Steven et al. (2002) Reactive oxygen-induced carcinogenesis causes hypermethylation of p16(Ink4a) and activation of MAP kinase. Mol Med 8:1-8
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Leone-Kabler, S; Wessner, L L; McEntee, M F et al. (1997) Ki-ras mutations are an early event and correlate with tumor stage in transplacentally-induced murine lung tumors. Carcinogenesis 18:1163-8
Wessner, L L; Fan, M; Schaeffer, D O et al. (1996) Mouse lung tumors exhibit specific Ki-ras mutations following transplacental exposure to 3-methylcholanthrene. Carcinogenesis 17:1519-26