- Medical School - Vanderbilt University School of Medicine (1994-1999)
- Internship - Johns Hopkins Hospital (1999-2000), Internal Medicine
- Residency - Johns Hopkins Hospital (2000-2002), Internal Medicine
- Fellowship - Johns Hopkins Hospital (2002-2004), Medical Oncology
- Fellowship - Johns Hopkins Hospital (2004-2009), Oncology
- Graduate School - Johns Hopkins University School of Medicine (2003-2009)
- Other Post Graduate Training - Johns Hopkins University School of Medicine (2003-2009)
David Wang, M.D., Ph.D.
- Internal Medicine - Hematology/Oncology
Dr. Wang received his B.A. degree from Asbury College and his M.D. degree from Vanderbilt University. During medical school, he spent a year at the National Cancer Institute as an HHMI-NIH Research Scholar working in the laboratory of Dr. Robert Lechleider and Dr. Anita Roberts, where he investigated TGF-beta and BMP signal transduction. Dr. Wang then completed residency training on the Osler Medical Service of the Johns Hopkins Hospital and fellowship training in medical oncology at the Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins. At the conclusion of his postdoctoral training in the laboratory of Dr. D. Neil Watkins, he received his Ph.D. degree in Cellular and Molecular Medicine from the Johns Hopkins University. His dissertation research examined the role of Hedgehog signaling in Barrett’s esophagus and esophageal adenocarcinoma. Dr. Wang’s laboratory is focused on understanding the role of aberrant developmental pathway signaling in esophageal cancer and precursor lesions. In his clinic, Dr. Wang sees patients with esophageal cancer, gastric cancer, and other gastrointestinal malignancies.
- American Association for Cancer Research
- American Gastroenterological Association
- American Society of Clinical Oncology
- NCI 2006, National Research Service Award
- American Society of Clinical Oncology 2005, Young Investigator Award
- The Endocrine Society 1999, Medical Student Achievement Award
- Howard Hughes Medical Institute 1998, Continued Fellowship for Medical Studies
Malignant transformation of non-neoplastic Barrett’s epithelial cells through well-defined genetic manipulations.
X Zhang, C Yu, K Wilson, HY Zhang, SD Melton, X Huo, DH Wang, RM Genta, SJ Spechler, RF Souza PLOS One September 2010 5 (9) e13093
Tumor suppressor HIC1 directly regulates SIRT1 to modulate p53 dependent DNA damage responses.
WY Chen, DH Wang, RC Yen, J Luo, W Gu, SB Baylin Cell November 2005 123 (3) 437-48
Aberrant epithelial-mesenchymal hedgehog signaling characterizes Barrett’s metaplasia.
DH Wang, NJ Clemons, T Miyashita, AJ Dupuy, W Zhang, A Szczepny, IM Corcoran-Schwartz, DL Wilburn, EA Montgomery, JS Wang, NA Jenkins, NA Copeland, JW Harmon, WA Phillips, DN Watkins Gastroenterology May 2010 138(5) 1810-22
Acid and bile salt-induced CDX2 expression differs in esophageal squamous cells from patients with and without Barrett’s Esophagus.
X Huo, HY Zhang, XI Zhang, JP Lynch, ED Strauch, JY Wang, SD Melton, RM Genta, DH Wang, SJ Spechler, RF Souza Gastroenterology July 2010 139 (1) 194-203
A novel Smad nuclear interacting protein, SNIP1, suppresses p300-dependent TGF-β signal transduction.
RH Kim, D Wang, M Tsang, J Martin, C Huff, MP de Caestecker, WT Parks, X Meng, RJ Lechleider, T Wang, AB Roberts Genes and Development July 2000 14 (13) 1605-16
Biology of Barrett’s esophagus and esophageal adenocarcinoma.
DH Wang, RF Souza Gastrointestinal Endoscopy Clinics of North America January 2011 21 (1) 25-38
The Smad4 activation domain (SAD) is a proline-rich, p300-dependent transcriptional activation domain.
MP de Caestecker, T Yahata, D Wang, WT Parks, S Huang, CS Hill, T Shioda, AB Roberts, RJ Lechleider The Journal of Biological Chemistry January 2000 275 (3) 2115-22
Epigenetic inactivation of the canonical Wnt antagonist Sry-box containing gene 17 in colorectal cancer.
W Zhang, SC Glockner, M Guo, EO Machida, DH Wang, H Easwaran, L Van Neste, JG Herman, KE Schuebel, DN Watkins, N Ahuja, SB Baylin Cancer Research April 2008 68 (8) 2764-72
Cancer-related inflammation and Barrett’s carcinogenesis: Interleukin-6 and STAT3 mediate apoptotic resistance in transformed Barrett’s cells.
HY Zhang, Q Zhang, X Zhang, C Yu, X Huo, E Cheng, DH Wang, SJ Spechler, RF Souza American Journal of Physiology. Gastrointestinal and Liver Physiology. 2011 (In press)
- Malignant transformation of non-neoplastic Barrett’s epithelial cells through well-defined genetic manipulations.
- Barrett's esophagus
- Esophageal cancer
- Gastric cancer
- Hedgehog signaling
- Molecularly targeted therapy