Director, Molecular Carcinogenesis Laboratory
Professor of Pathology
Douglas_Hixson@brown.edu
T: 401 444-8058
F: 401 444-8141
Rhode Island Hospital
Department of Medicine/Medical Oncology
593 Eddy Street George 362
Providence, RI 02903
Medical education/Graduate education:
Purdue University, W. LaFayette, IN, B.S. 1969- M.S. 1971
Ph.D. University of Texas Graduate School of Biomedical Sciences, Houston, TX, 1975
Fellowship:
Rosalie B. Hite Predoctoral Fellow in Virology, M.D. The Univ. of Texas, Anderson Hospital and Tumor Institute, Houston, Texas
Board certification:
Anatomic Pathology and Clinical Pathology
Research interests:
Molecular Carcinogenesis, Cell adhesion, Stem Cells
Current approved research grants:
NIH RO1 CA 42715 09/30/85-03/31/03 Cellular Origins of Liver Cancer. The first aim of this proposal will focus on efforts to clone cDNAs for monoclonal antibody defined antigens; aim 2 will assess the role of these antigens in bile duct morphogeneis and aim 3 will explore the role of OV6+ periportal hepatocytes in liver carinogenesis.
NIH RO1 CA 42714 Douglas Hixson, 05/03/99-01/31/04 Molecular Determinants of Multicellular Organization.The major goals of this project are to identify accessory proteins associated with C-CAM 1, an Ig like adhesion molecule and the role of the tumor suppressive activity of this protein in liver carcinogenesis.
NIH R01 CA73611-01A1, 04/01/99-03/31/04. Expression & Role of TA1, Oncofetal Gene in Liver Cancer. This proposal will examine the regulation and function of TA1/E16 in hepatic cells, focusing on its role as a putative amino acid transporter in conferring growth and survival advantage to tumor cells which have lost regulation of this molecule.
NIH RO1CA93840-01, 12/01/01-11/30/06. Genesis of Liver CA with Oval Cell Traits. Aims of this study: determine if continuous lines of oval cells are able to differentiate into hepatocytes capable of progression to HCC: determine if isolated oval cells initiated in situ by treatment with chemical carcinogens are capable of progression ad to determine if the loss of BD.1 inducibility by oval cells and high passage BDEC during arrest is associated with early events in cholangiocarcinogenesis.
1P20RR17695 09/30/02-08/31/07. COBRE Center for Cancer Research Development. The mission of the Center is to coalesce and foster outstanding, interactive, lab-based cancer research centered on the Molecular and Cellular Pathogenesis of Cancer. The goal will be to develop program projects with different but related themes, into interactive research groups composed of junior investigators supported by peer reviewed grants.
Most recent significant publications:
Hixson, D.C., Brown, J., McBride, A.C., Affigne, S. Differentiation status of rat ductal cells and ethionine-induced hepatic carcinomas defined with surface-reactive monoclonal antibodies. Exper Molec Path 68:152-169, 2000.
Estrera, V.T., Chen, D-T, Luo, W., Hixson, D.C., and Lin, S-H. Signal transduction by the CEACAM1 tumor suppressor. J Bio Chem 276:15547-15553, 2001.
Makarovskiy, A. N., Siryaporn, E., Hixson, D. C., Akerley, W., Survival of docetaxel-resistant prostate cancer cells in vitro depends on phenotype alterations and continuity of drug exposure, Cell Mol Life Sci, 59: 1198-1211, 2002.
