Eric J. Sorscher, MD

Division: Hematology & Oncology

Campus Address: MCLM 798

Phone: (205) 934-9640


Departmental Affiliation(s):
Primary: Medicine
Secondary: Physiology & Biophysics

Dr. Sorscher is originally from Flint, MI and graduated summa cum laude with honors in biology from Yale University in 1979. He completed his medical degree from Harvard University in 1984 following a one year leave of absence to study cystic fibrosis. He trained as a resident at Massachusetts General Hospital, and completed two postdoctoral fellowships, one at Massachusetts General, the other at UAB. In 1989, Dr. Sorscher was recruited to UAB to the position of Assistant Professor of Medicine and Physiology and Biophysics, and Associate Scientist at the Gregory Fleming James Cystic Fibrosis Center. In 1994, Dr. Sorscher was appointed to the position of Associate Professor of Medicine and Physiology and Biophysics as well as Director of the UAB Cystic Fibrosis Research Center. In 1998, Dr. Sorscher was promoted to the position of Professor in the Departments of Medicine and Physiology and Biophysics. In 2003 he became the recipient of the Gwaltney Endowed Chair for cystic fibrosis research at UAB.

Research Description:
Cystic Fibrosis and Molecular Genetics; Patient Oriented Research

Dr. Sorscher has two major research interests. He directs the UAB Cystic Fibrosis Research Center that performs respected studies concerning molecular pathogenesis of this disease. His own laboratory investigates the structure and function of the gene product responsible for cystic fibrosis (i.e., the cystic fibrosis transmembrane conductance regulator, CFTR), and also evaluates new approaches to therapy, including the activation of alternate chloride secretory pathways in cystic fibrosis epithelia, molecular correction of mutant CFTR, and gene transfer-related aspects of cystic fibrosis using both viral and non-viral vectors. The other major interest in Dr. Sorscher's laboratory involves the characterization of a novel mechanism for tumor sensitization using the E. coli PNP gene. In this approach, tumors are rendered hundreds or thousands of times more sensitive to conventional chemotherapy by expression of a prokaryotic enzyme that cleaves nontoxic nucleoside prodrugs to a very toxic form. The research involves analysis of the crystal structure of E. coli PNP, and structure-based drug design of novel compounds that would be effectively cleaved in vitro and in vivo. Gene transfer vectors that might be important in the treatment of human cancers are also developed and characterized.

Selected Publications:
  • Cormet-Boyaka E, Hong JS, Berdiev BK, Fortenberry JA, Rennolds J, Clancy JP, Benos DJ, Boyaka PN, Sorscher EJ.A truncated CFTR protein rescues endogenous DeltaF508-CFTR and corrects chloride transport in mice. FASEB J. 2009 Nov;23(11):3743-51. Epub 2009 Jul 20.
  • Rowe SM, Clancy JP, Sorscher EJ. A breath of fresh air. Sci Am. 2011 Aug;305(2):68-73.
  • Hill, AE, JS Hong, H Wen, L Teng, DT McPherson, SA McPherson, DN Levasseur, EJ Sorscher. Micro-RNA-like effects of complete intronic sequences. Frontiers in Bioscience 11:1998-2006, 2006.
  • Rowe SM, SM Miller and EJ Sorscher. Mechanisms underlying cystic fibrosis. New England Journal of Medicine352(19):1992-2001, 2005.
  • Hill A and EJ Sorscher. Common structural patterns in human genes. Bioinformatics 10: 1093, 2004.
  • Hong, JS, WR Waud, DN Levasseur, TM Townes, H Wen, SA McPherson, BA Moore, Z, Bebok, PW Allan, JA Secrist 3rd, WB Parker, EJ Sorscher. Excellent in vivo bystander activity of fludarabine phosphate against human glioma xenografts that express the escherichia coli purine nucleoside phosphorylase gene. Cancer Research 64(18):6610-5, 2004.
  • Naren AP, B Cobb, C Li, K Roy, D Nelson, GD Heda, J Liao, KL Kirk, EJ Sorscher, J Hanrahan, JP Clancy. A macromolecular complex of â2 adrenergic receptor, CFTR, and ezrin/radixin/moesin-binding phosphoprotein 50 is regulated by PKA. Proceedings of the National Academy of Sciences USA 100:342-346, 2003.
  • Ruiz FE, JP Clancy, MA Perricone, Z Bebok, J Hong, SH Cheng, DP Meeker, KR Young, R Schoumacher, M Weatherly, JE Morris, L Sindel, M Rosenberg, FW van Ginkel, JR McGhee, D Kelly, RK Lyrene, EJ Sorscher. A clinical inflammatory syndrome attributable to aerosolized lipid/DNA administration in cystic fibrosis. Human Gene Therapy 12(7):751-761, 2001.
  • Hughes, B.W., S.A. King, P.W. Allan, W.B. Parker, and E.J. Sorscher. Cell to cell contact is not required for bystander cell killing by Escherichia coli purine nucleoside phosphorylase. Journal of Biological Chemistry 273: 2322-2328, 1998.
  • Bebok, Z., C. Mazzochi, S.A. King, J.S. Hong, and E.J. Sorscher. The mechanism underlying cystic fibrosis transmembrane conductance regulator transport from the endoplasmic reticulum to the proteasome includes Sec61beta and a cytosolic, deglycosylated intermediary. Journal of Biological Chemistry 273: 29873-29878, 1998.
  • Bedwell DM, A Kaenjak, DJ Benos, Z Bebok, JK Bubien, J Hong, A Tousson, JP Clancy, EJ Sorscher. Suppression of a CFTR premature stop mutation in a bronchial epithelial cell line. Nature Medicine 3: 1280-1284, 1997.
  • Parker, W.B., S.A. King, P.W. Allan, L.L. Bennett, Jr., J.A. Secrist, III, J.A. Montgomery, K.S. Gilbert, W.R. Waud, A.H. Wells, G.Y. Gillespie, and E.J. Sorscher. In vivo gene therapy of cancer with E. coli purine nucleoside phosphorylase. Human Gene Therapy 8: 1637-1644, 1997.
  • Logan, J., D. Hiestand, P. Daram, Z. Huang, D.D. Muccio, J. Hartman, B. Haley, W.J. Cook, and E.J. Sorscher. Cystic fibrosis transmembrane conductance regulator mutations that disrupt nucleotide binding. Journal of Clinical Investigation 94: 228-236, 1994.
  • Hartman J, Z Huang, TA Rado, S Peng, T Jilling, DD Muccio, EJ Sorscher. Recombinant synthesis, purification, and nucleotide binding characteristics of the first nucleotide binding domain of the cystic fibrosis gene product. Journal of Biological Chemistry 267: 6455-6458, 1992.
  • Sorscher, E.J., K.L. Kirk, M.L. Weaver, T. Jilling, J.E. Blalock, and R.D. LeBoeuf. Antisense oligodeoxynucleotide to the cystic fibrosis gene inhibits anion transport in normal cultured sweat duct cells. Proceedings of the National Academy of Sciences of the United States of America 88: 7759-7762, 1991.