World Journal of Surgery

, Volume 29, Issue 3, pp 325–333

Molecular Targeting of Pancreatic Disorders

  • Kiichi Tamada
  • Xiao-Ping Wang
  • F. Charles Brunicardi
Article

DOI: 10.1007/s00268-004-7821-6

Cite this article as:
Tamada, K., Wang, XP. & Brunicardi, F.C. World J. Surg. (2005) 29: 325. doi:10.1007/s00268-004-7821-6

Abstract

During the last decade significant advances in gene therapy have made it possible to treat various pancreatic disorders in both animal models and in humans. For example, insulin gene delivery to non-β-cell tissues has been shown to reverse hyperglycemia in diabetic mice, and islet transplantation, based on in vitro differentiation of β cells and concomitant gene targeting to prevent host autoimmune responses, has become more feasible. Additionally, introduction of the glucokinase regulatory protein and protein kinase C-ζ have been shown to improve glucose tolerance in non-insulin-dependent diabetes mellitus animal models. Pancreatic cancer studies utilize several DNA-based strategies for tumor treatment including introduction of tumor suppressor genes, suppression of oncogenes, suicide gene/prodrug therapy, and restricted replication-competent virus therapy. Tumor-specific targeting is an important part of suicide gene therapy, and tumor-specific promoters are used for cell-specific targeting. Tumor-specific suicide gene therapy directed by the rat insulin promoter has been used to eliminate insulinoma tumors in a mouse model. This review compiles a compendium of information related to the treatment of pancreatic disorders using gene therapy.

Copyright information

© Société Internationale de Chirurgie 2005

Authors and Affiliations

  • Kiichi Tamada
    • 1
  • Xiao-Ping Wang
    • 1
  • F. Charles Brunicardi
    • 1
  1. 1.Michael E. DeBakey Department of SurgeryBaylor College of MedicineHoustonUSA