Skip to main content

Inhibitors of the Hedgehog Signal Transduction Pathway

Buy Article:

$63.00 plus tax (Refund Policy)

Abstract:

Aberrant Hedgehog (Hh) signaling plays an important role in the pathogenesis and maintenance of many cancers. The mechanisms by which this pathway contributes to tumor progression are only now being unraveled. There appear to be two distinct ways by which Hh signaling becomes constitutively activated in tumors: by over expression of the ligand itself, or by acquisition of mutations in Hh signaling components at or downstream of the Hh receptor. The goal of this review is to briefly present the key components of the Hh pathway, and then discuss the known inhibitors of this pathway. We will describe how each inhibitor was identified, what is known of its mechanism of action, and its potential as a therapeutic agent against tumors dependent on Hh signaling.

Keywords: cancer; cyclopamine; hedgehog; inhibitors; review

Document Type: Review Article

DOI: https://doi.org/10.2174/157339405774574243

Affiliations: Department of Pharmacology and Toxicology, Dartmouth Medical School, Hanover, NH 03755, USA.

Publication date: 2005-11-01

More about this publication?
  • Current Cancer Therapy Reviews publishes frontier reviews on all the latest advances in clinical oncology, cancer therapy and pharmacology. The journal's aim is to publish the highest quality review articles dedicated to clinical research in the field. The journal is essential reading for all researchers and clinicians in cancer therapy.
  • Access Key
  • Free ContentFree content
  • Partial Free ContentPartial Free content
  • New ContentNew content
  • Open Access ContentOpen access content
  • Partial Open Access ContentPartial Open access content
  • Subscribed ContentSubscribed content
  • Partial Subscribed ContentPartial Subscribed content
  • Free Trial ContentFree trial content
Cookie Policy
X
Cookie Policy
Ingenta Connect website makes use of cookies so as to keep track of data that you have filled in. I am Happy with this Find out more