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Christopher Denny, M.D.
Christopher Denny, M.D.

Specialty:

Pediatric Hematology/Oncology

General Information:

Gender:
Male
Language(s):
English

Affiliation(s):

Professor, Department of Pediatrics
Physician, Department of Pediatrics, Hematology/Oncology
Member, ACCESS Department - Molecular Biology Institute Interdepartmental Ph.D. Program
Member, JCCC Cancer Nanotechnology Program Area

Hospital Affiliation(s):

Mattel Children's Hospital at UCLA
Ronald Reagan UCLA Medical Center

Education:

Fellowship:
Pediatrics, Hematology-Oncology, National Institutes of Health, The Clinical Center, 1983 - 1987
Residency:
Pediatrics, Children's Hospital National Medical Center, 1981 - 1983
Internship:
Pediatrics, Children's Hospital National Medical Center, 1980 - 1981
Medical Degree:
M.D., University of Pennsylvania School of Medicine, 1980

Certification(s):

Medical Board Certification(s):
Pediatric Hematology-Oncology, American Board of Pediatrics, 1990
Pediatrics, American Board of Pediatrics, 1986

Contact Information:

Pediatrics:
(310) 825-6185 Information and referral
(310) 206-5737 Admissions
(310) 825-0867 Outpatient appointments
Pediatric Hematology/Oncology:
(310) 825-6708 Information
(310) 825-0867 Patient appointments
(310) 825-6185 Pediatric physician relations liaison
Phone:
(310) 825-0704 Office
Email:

Scientific Interest(s):

Dr. Christopher Denny's research focuses on genomic mutation as a primary force in the genesis of human malignancy. Molecular isolation of genes involved in tumor-specific rearrangements has identified mechanisms of tumorigenesis and has formed a basis for studying transformation pathways of human cancers.

Denny's lab has focused specifically on the 11:22 translocation that occurs in Ewing's sarcoma and PNET, two lethal and poorly understood pediatric cancers of presumed neural crest origin. This rearrangement fuses a previously unknown gene, termed EWS, to FLI-1, a member of the ETS family of transcription factors. Denny's lab has isolated this chimeric molecule both as genomic and cDNA clones, and has shown that EWS/FLI can transform rodent fibroblast lines. This is consistent with the notion that it plays an active role in Ewing's sarcoma oncogenesis.

Mutation analyses, DNA-binding studies, and subcellular localization experiments have led Denny and his colleagues to hypothesize that EWS/FLI is acting as an aberrant transcription factor that is qualitatively different from normal FLI-1. A novel method for identifying differentially expressed genes has been developed to isolate potential target genes that are modulated by EWS/FLI. This cohort of EWS/FLI regulated genes is now being analyzed with a long-term goal of defining important genetic pathways that are activated during cellular transformation.

Selected Cancer-Related Publications:

Ng KP, Potikyan G, Savene RO, Denny CT, Uversky VN, Lee KA. Multiple aromatic side chains within a disordered structure are critical for transcription and transforming activity of EWS family oncoproteins. Proc Natl Acad Sci U S A. 2007; 104(2): 479-84.

Deneen B, Hamidi H, Denny CT. Functional analysis of the EWS/ETS target gene uridine phosphorylase. Cancer Res. 2003; 63(14): 4268-74.

Deneen B, Welford SM, Ho T, Hernandez F, Kurland I, Denny CT. PIM3 proto-oncogene kinase is a common transcriptional target of divergent EWS/ETS oncoproteins. Mol Cell Biol. 2003; 23(11): 3897-908.