The Johns Hopkins Family Professor in Oncology Research
Professor of Medicine, Cell Biology, Oncology and Pathology
Vice Dean for Research, School of Medicine

Departmental Address:
Ross Research Building
Room 1032
720 Rutland Ave.
Baltimore, MD 21205
Administrative Office:
410-955-2773
410-955-0185 (fax)
Additional Contact:
cvdang@jhmi.edu
COS profile: http://myprofile.cos.com/cvdag
Clinical/Academic Interests
Anemias, Bone Marrow Failure, Myeloproliferative Disorders
Research Interests
My laboratory is studying the mechanisms underlying the neoplastic activities of the MYC oncogene. MYC encodes a transcription factor, c-MYC, that heterodimerizes with Max to bind specific DNA sequences. We have contributed extensively to the identification of functional domains of the c-MYC protein. We, and others, have found that Myc/Max binds to the E-box (CANNTG) sequences to activate transcription and other elements to suppress transcription. We have recently identified thousands putative c-Myc target genes using representational difference analysis and DNA microarray analysis. These genes are part of a growing list of putative c-Myc target genes that are estimated to involve about 10% of genes. We have begun to catalog these genes (www.myc-cancer-gene.org) and are using this database and exploiting phylogenetic footprinting (bioinformatics) to predict in vivo c-Myc binding sequences. The binding regions are validated by a technique we invented, Scanning Chromatin Immunoprecipitation (SChIP). We are currently defining the roles of five selected genes in Myc-mediated phenotypes. Our studies have led to the discovery that c-Myc overexpression activates genes encoding proteins involved in glycolysis and contributes to the Warburg effect or aerobic glycolysis, which is characteristic of essentially all solid tumors. We recently discovered a key role c-Myc in the regulation of mitochondrial homoeostasis. In addition, we discovered that c-Myc overexpression contributes to genomic instability by uncoupling S and M phases of the cell cycle; this effect renders c-Myc overexpressing cycle sensitive to anti-miotics. Our work and those of others have led to the concept that MYC is a central regulator of cell proliferation and cellular metabolism.
Education/Training
- BS, Chemistry (highest honors), University of Michigan
- PhD, Chemistry (distinction), Georgetown University
- MD, (Alpha Omega Alpha), Johns Hopkins University School of Medicine
- Internship, Department of Medicine, Johns Hopkins Hospital
- Residency, Department of Medicine, Johns Hopkins Hospital
- Fellowship, Hematology-Oncology, Cancer Research Institute, UCSF
Academic Positions
- Assistant Professor of Medicine, Johns Hopkins University
- Assistant Professor of Cell Biology & Anatomy, Johns Hopkins University
- Assistant Professor of Oncology, Johns Hopkins University
- Associate Professor of Medicine, Johns Hopkins University
- Director, Division of Hematology, Johns Hopkins University
- Deputy Director of Research, Department of Medicine, Johns Hopkins University,
- Professor of Medicine, Oncology, Pathology, Johns Hopkins University
- Professor of Cell Biology, Johns Hopkins University




