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
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
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
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
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
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)
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
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