Professor, Pediatrics, UCLA School of Medicine
Pediatric Hematology & Oncology
Dr. Christopher T. Denny, MD
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Christopher Denny is an expert in the field of Pediatric Hematology & Oncology. He researched medicine at Perelman School of Medicine at the University of Pennsylvania. He has 2 awards "Elected Member" and "Super Doctor". Christopher Denny is a published doctor as well. He has 51 publications published. The latest was: EWS/FLI1 up regulates mE2-C, a cyclin-selective ubiquitin conjugating enzyme involved in cyclin B destruction.
Publications
- Phosphoproteomic Profiling Reveals IL6-Mediated Paracrine Signaling within the Ewing Sarcoma Family of Tumors.
- An engineered anti-CA19-9 cys-diabody for positron emission tomography imaging of pancreatic Cancer and targeting of polymerized liposomal nanoparticles.
- Enhanced growth inhibition of Osteosarcoma by cytotoxic polymerized liposomal nanoparticles targeting the alcam cell surface receptor.
- Pediatric Sarcomas: Translating Molecular Pathogenesis of Disease to Novel Therapeutic Possibilities.
- Oncogenic fusion protein EWS/FLI1 down regulates gene expression by both transcriptional and post-transcriptional mechanisms.
- Targeting liposomes toward novel pediatric antiCancer therapeutics.
- ABT-869 inhibits the proliferation of Ewing Sarcoma cells and suppresses platelet-derived growth factor receptor beta and c-KIT signaling pathways.
- Genetically defined EWS/FLI1 model System suggests mesenchymal origin of Ewing's family tumors.
- EWS/FLI1 regulates tumor angiogenesis in Ewing's Sarcoma via suppression of thrombospondins.
- Multiple aromatic side chains within a disordered structure are critical for transcription and transforming activity of EWS family oncoproteins.
- Oncogenic MITF dysregulation in clear cell sarcoma: defining the MiT family of human Cancers.
- Cooperative DNA binding with AP-1 proteins is required for transformation by EWS-Ets fusion proteins.
- Functional analysis of the EWS/ETS target gene uridine phosphorylase.
- PIM3 proto-oncogene kinase is a common transcriptional target of divergent EWS/ETS oncoproteins.
- Focus on embryonal malignancies.
- Molecular mechanisms of Cancer.
- Alternatively spliced exons encode the Tissue-specific 5' termini of leukocyte pp52 and stromal cell S37 mRNA isoforms.
- Localization of preferential sites of rearrangement within the BCR gene in Philadelphia chromosome-positive Acute lymphoblastic leukemia.
- Gene rearrangements in Ewing's Sarcoma.
- Burkitt lymphoma cell line carrying a variant translocation creates new DNA at the breakpoint and violates the hierarchy of immunoglobulin gene rearrangement.
- Cross-contamination limits the use of recycled anion exchange resins for preparing plasmid DNA.
- Leukemia and the disruption of normal hematopoiesis.
- The clonal nature of mediastinal germ cell tumors and Acute myelogenous leukemia. A case report and review of the literature.
- Human lymphocyte-specific pp52 gene is a member of a highly conserved dispersed family.
- Structural basis for the interaction of the free SH2 domain EAT-2 with SLAM receptors in hematopoietic cells.
- Streamlined approach to creating yeast artificial chromosome libraries from specialized cell sources.
- A variant Ewing''s Sarcoma translocation (7;22) fuses the EWS gene to the ETS gene ETV1.
- Characterization of transformation related genes in oral Cancer cells.
- Biology of EWS/FLI and related fusion genes in Ewing''s Sarcoma and primitive neuroectodermal tumor.
- Ewing's Sarcoma--a clinical enigma coming into focus.
- TCL1 oncogene expression in AIDS-related lymphomas and lymphoid Tissues.
- Chronic myelomonocytic Leukemia: Tel-a-kinase what Ets all about.
- Characterization of the BCR promoter in Philadelphia chromosome-positive and -negative cell lines.
- A second Ewing's Sarcoma translocation, t(21;22), fuses the EWS gene to another ETS-family transcription factor, ERG.
- EWS/FLI1-induced manic fringe renders NIH 3T3 cells tumorigenic.
- Biology of EWS/ETS fusions in Ewing''s family tumors.
- Promoters containing ATF-binding sites are de-regulated in cells that express the EWS/ATF1 oncogene.
- Detection of differentially expressed genes in primary tumor Tissues using representational differences analysis coupled to microarray hybridization.
- EAT-2 is a novel SH2 domain containing protein that is up regulated by Ewing''s Sarcoma EWS/FLI1 fusion gene.
- Divergent Ewing''s Sarcoma EWS/ETS fusions confer a common tumorigenic phenotype on NIH3T3 cells.
- Loss of p16 pathways stabilizes EWS/FLI1 expression and complements EWS/FLI1 mediated transformation.
- EWS-FLI1, EWS-ERG, and EWS-ETV1 oncoproteins of Ewing tumor family all suppress transcription of transforming growth factor beta type II receptor gene.
- Multiple domains mediate transformation by the Ewing''s Sarcoma EWS/FLI-1 fusion gene.
- EWS/FLI1 up regulates mE2-C, a cyclin-selective ubiquitin conjugating enzyme involved in cyclin B destruction.
- EWS/ETS fusion genes induce epithelial and neuroectodermal differentiation in NIH 3T3 fibroblasts.
- DNA binding domain-independent pathways are involved in EWS/FLI1-mediated oncogenesis.
- The COOH-terminal domain of FLI-1 is necessary for full tumorigenesis and transcriptional modulation by EWS/FLI-1.
- Ewing Sarcoma 11;22 translocation produces a chimeric transcription factor that requires the DNA-binding domain encoded by FLI1 for transformation.
- The Ewing's Sarcoma EWS/FLI-1 fusion gene encodes a more potent transcriptional activator and is a more powerful transforming gene than FLI-1.
- Identification of target genes for the Ewing's Sarcoma EWS/FLI fusion protein by representational difference analysis.
Schools
University Of Pennsylvania School Of Medicine
Chldns Hospital National Med Center
National Cancer Institute
Conditions Treated
- Acute Leukemia
- Adrenal Gland Cancer
- Brain and Nervous System Cancer (incl. Gliomas, Astrocytoma, Schwannoma, Medulloblastoma, Chordoma)
- Brain Cancer
- View All
Doctors Specialties
- Pediatric Hematology
- Oncology
Accepted Insurances
Awards
- Elected Member
- Super Doctor
Education
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National Institutes of Health Clinical Center -
Children's National Medical Center - George Washington University -
Perelman School of Medicine at the University of Pennsylvania
Hospital
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Mattel Children's Hospital UCLA -
Ronald Reagan UCLA Medical Center -
Santa Monica-UCLA Medical Center and Orthopaedic Hospital
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