Dysfunction of the RET receptor in human cancer

Cell Mol Life Sci. 2004 Dec;61(23):2954-64. doi: 10.1007/s00018-004-4276-8.

Abstract

RET is the receptor for glial-derived neurotrophic factor growth factors. It is a paradigm of a single gene that causes different types of human cancer when targeted by different genetic alterations. Like other receptor tyrosine kinases, once activated, RET recruits a variety of signaling molecules that mediate biological responses. Here we review data on the signaling pathways that lead to RET-mediated cell transformation and recent evidence that manipulation of RET holds promise for thyroid cancer treatment.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Carcinoma, Papillary / metabolism
  • Cell Transformation, Neoplastic
  • Humans
  • Ligands
  • Models, Biological
  • Models, Genetic
  • Neoplasms / metabolism*
  • Phosphorylation
  • Protein Structure, Tertiary
  • Proto-Oncogene Proteins / physiology*
  • Proto-Oncogene Proteins c-ret
  • Receptor Protein-Tyrosine Kinases / physiology*
  • Signal Transduction
  • Thyroid Neoplasms / metabolism

Substances

  • Ligands
  • Proto-Oncogene Proteins
  • Proto-Oncogene Proteins c-ret
  • Receptor Protein-Tyrosine Kinases