Agency
National Institute of Health (NIH)
Institute
National Cancer Institute (NCI)
Type
Research Project (R01)
Project #
2R01CA055737-04A1
Application #
2096855
Study Section
Radiation Study Section (RAD)
Project Start
1992-04-01
Project End
1998-11-30
Budget Start
1996-03-15
Budget End
1996-11-30
Support Year
4
Fiscal Year
1996
Total Cost
Indirect Cost
Name
Yale University
Department
Radiation-Diagnostic/Oncology
Type
Schools of Medicine
DUNS #
082359691
City
New Haven
State
CT
Country
United States
Zip Code
06520
Rochette, Patrick J; Brash, Douglas E (2010) Human telomeres are hypersensitive to UV-induced DNA Damage and refractory to repair. PLoS Genet 6:e1000926
Rochette, Patrick J; Brash, Douglas E (2008) Progressive apoptosis resistance prior to senescence and control by the anti-apoptotic protein BCL-xL. Mech Ageing Dev 129:207-14
Chao, Dennis L; Eck, J Thomas; Brash, Douglas E et al. (2008) Preneoplastic lesion growth driven by the death of adjacent normal stem cells. Proc Natl Acad Sci U S A 105:15034-9
Knezevic, Dejan; Zhang, Wengeng; Rochette, Patrick J et al. (2007) Bcl-2 is the target of a UV-inducible apoptosis switch and a node for UV signaling. Proc Natl Acad Sci U S A 104:11286-91
Zhang, Wengeng; Hanks, Adrianne N; Boucher, Kenneth et al. (2005) UVB-induced apoptosis drives clonal expansion during skin tumor development. Carcinogenesis 26:249-57
Brash, Douglas E; Zhang, Wengeng; Grossman, Douglas et al. (2005) Colonization of adjacent stem cell compartments by mutant keratinocytes. Semin Cancer Biol 15:97-102
Takeuchi, Seiji; Zhang, Wengeng; Wakamatsu, Kazumasa et al. (2004) Melanin acts as a potent UVB photosensitizer to cause an atypical mode of cell death in murine skin. Proc Natl Acad Sci U S A 101:15076-81
Wikonkal, Norbert M; Remenyik, Eva; Knezevic, Dejan et al. (2003) Inactivating E2f1 reverts apoptosis resistance and cancer sensitivity in Trp53-deficient mice. Nat Cell Biol 5:655-60
Brash, D E; Wikonkal, N M; Remenyik, E et al. (2001) The DNA damage signal for Mdm2 regulation, Trp53 induction, and sunburn cell formation in vivo originates from actively transcribed genes. J Invest Dermatol 117:1234-40
Zhang, W; Remenyik, E; Zelterman, D et al. (2001) Escaping the stem cell compartment: sustained UVB exposure allows p53-mutant keratinocytes to colonize adjacent epidermal proliferating units without incurring additional mutations. Proc Natl Acad Sci U S A 98:13948-53

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