Dennis H. Oh, MD, PhD
Associate Professor in Residence
Department of Dermatology
Contact Information
San Francisco Veterans Affairs Medical Center Department of Dermatology
VAMC 190, 4150 Clement Street, San Francisco, CA 94121
415.750.2091 phone
Training
- MD: Stanford University School of Medicine
- PhD: Biophysics, Stanford University
- Fellowship: Stanford University Department of Biological Sciences
- Residency: Stanford University Department of Dermatology
My laboratory seeks to understand and ultimately to manipulate the response of the skin to DNA damaging agents using biological and physical approaches. Current basic lab research focuses on two areas:
The first project aims to target DNA damage to specific genes and cells, and to understand the detailed mechanisms underlying the damage and repair in systems ranging from single cells to whole skin tissue. We have a particular interest in using triplex-forming oligonucleotides as vehicles to target DNA damage to specific genomic sequences. Recently, we have focused on pathways by which DNA interstrand crosslinks, formed by PUVA therapy and many types of cancer chemotherapeutic agents, are repaired in human cells, and have developed a model that offers insight as to why cells are able to tolerate or succumb to this type of DNA damage. To target DNA damage spatially, we have pioneered multiphoton excitation approaches that may also be useful in targeting photodynamic effects to selected layers and cells of the skin.
Second, the lab studies the cellular mechanisms that regulate DNA repair efficiency in epidermal keratinocytes. Li-Fraumeni syndrome patients are germline heterozygotes for p53 who are predisposed to many internal cancers, but not to non-melanoma skin cancers. As a first step in understanding this clinical phenotype at a cellular level, we have discovered that epidermal keratinocytes differ from other cell types in not exclusively requiring p53 to efficiently repair DNA damage from ultraviolet radiation. Instead, both p53 and one of its homologs, p63, are important in allowing epidermal cells to repair DNA. These results have implications for understanding Li-Fraumeni syndrome as well as general mechanisms of epidermal carcinogenesis.
Finally, I also oversee an asynchronous teledermatology program at the VA Medical Center that serves patients in Northern California and the Pacific Islands, and have an interest in studying the efficacy of telemedicine. Exploiting the VA database and electronic medical record, we have recently measured clinical out comes associated with teledermatology in the management of remotely located skin cancer patients.
Clinical Specialties
- General Dermatology and Dermatologic Surgery
- Teledermatology/Telemedicine
Research Interests
- Photobiology and Photomedicine
- Cutaneous responses to genotoxic stress.
- Manipulation of DNA damage and repair
Publications
- Oh, D.H.; King, B.A.; Boxer; S.G.; Hanawalt, P.C. “Spatially localized generation of nucleotide sequence-specific DNA damage”, Proc. Natl. Acad. Sci. USA2001, 98, 11271-11276.
- King, B.A.; Oh, D.H.“Spatial Control of Reactive Oxygen Species Formation in Fibroblasts Using Two-Photon Excitation, Photochem. Photobiol., 2004, 80(1):1-6.
- Oh, D.H.; Yeh, K. “Differentiating human keratinocytes are deficient in p53 but retain global nucleotide excision repair following ultraviolet radiation”, DNA Repair, 2005, 4:1149-1159.
- Ferguson , B.E.; Oh, D.H. “Proficient global nucleotide excision repair in human keratinocytes but not fibroblasts deficient in p53”, Cancer Res., 2005, 65(19): 8723-8729.
- Mogi, S.; Oh, D.H. “ gamma-H2AX formation in response to interstrand crosslinks requires XPF in human cells”, DNA Repair, 2006, 5:731-740.
- Ferguson , B.E.; Li, H; Dong, T.K.; Hsiao, H.; Oh.D.H. “Impaired repair of cyclobutane pyrmidine dimers in human keratinocytes deficient in p53 and p63”, Carcinogenesis, 2008, 29(1): 70-75.
- Mogi, S.; Butcher, C.E.; Oh, D.H. “DNA polymerase h reduces the g -H2AX response to psoralen interstrand crosslinks in human cells”, Exp. Cell Res., 2008, 314(4):887-895.
- Oh, D.H.; Suzara, V.; Krishnan, R. “Modulation of psoralen DNA crosslinking kinetics associated with a triplex-forming oligonucleotide”, Photochem. Photobiol., 2008, 84:727-733.
- Krishnan, R.; Butcher, C.E.; Oh, D.H. “Real-time observation of DNA repair: 2-aminopurine as a molecular probe”, Proc. SPIE, 2008 , 6867:68670M 1-7.
- Pincus, L.B.; McCalmont, T.H.; Neuhaus, I.M.; Kasper, R.; Oh, D.H. “Basal cell carcinomas arising within multiple trichoepitheliomas”, J. Cutan. Pathol., in press.
- Hsiao, J.L.; Oh, D.H. “Impact of teledermatology on skin cancer diagnosis and treatment”, J. Am. Acad. Dermatol., in press.

