Christopher T. Denny, MD

Christopher Denny, MD

Professor, Department of Pediatrics
Physician, Department of Pediatrics, Hematology/Oncology




Pediatric Hematology/Oncology

Institutional Affiliation

UCLA Mattel Children's Hospital
Ronald Reagan UCLA Medical Center



Pediatrics, Hematology-Oncology, National Institutes of Health, The Clinical Center, 1983 - 1987


Pediatrics, Children's Hospital National Medical Center, 1980 - 1981


MD, University of Pennsylvania School of Medicine, 1980


Pediatrics, Children's Hospital National Medical Center, 1981 - 1983

Board Certifications

Pediatric Hematology-Oncology, American Board of Pediatrics, 1990
Pediatrics, American Board of Pediatrics, 1986

Contact Information


(310) 825-0704 - Office
(310) 825-6185 - Pediatrics information, referral and physician relations liaison
(310) 206-5737 - Pediatrics admissions
(310) 825-0867 - Pediatrics outpatient appointments
(310) 825-6708 - Pediatric Hematology/Oncology information
(310) 825-0867 - Pediatric Hematology/Oncology patient appointments

Scientific Interests

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.

Highlighted 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.