Cellular and Molecular Life Sciences CMLS

, Volume 61, Issue 23, pp 2954–2964

Oncogenic protein tyrosine kinases

Dysfunction of the RET receptor in human cancer
  • M. Santoro
  • F. Carlomagno
  • R. M. Melillo
  • A. Fusco
Multi-author Review

DOI: 10.1007/s00018-004-4276-8

Cite this article as:
Santoro, M., Carlomagno, F., Melillo, R.M. et al. CMLS, Cell. Mol. Life Sci. (2004) 61: 2954. 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.

Key words.

Thyroid tyrosine kinase inhibitors RET MEN2 papillary thyroid carcinoma 

Copyright information

© Birkhäuser Verlag, Basel 2004

Authors and Affiliations

  • M. Santoro
    • 1
  • F. Carlomagno
    • 1
  • R. M. Melillo
    • 1
  • A. Fusco
    • 1
  1. 1.Dipartimento di Biologia e Patologia Cellulare e MolecolareUniversity ‘Federico II’NaplesItaly

Personalised recommendations