Display Settings:

Format

Send to:

Choose Destination
See comment in PubMed Commons below
Cancer Lett. 2006 Jan 28;232(1):90-8. Epub 2005 Oct 20.

Oncogenic rearrangements of the NTRK1/NGF receptor.

Author information

  • 1Department of Experimental Oncology and Labs Operative Unit 3, Istituto Nazionale Tumori, Via G. Venezian, 1 20133 Milan, Italy. marco.peirotti@istitutotumori.mi.it

Abstract

The NTRK1 gene encodes the high affinity receptor for Nerve Growth Factor, and its action regulates neural development and differentiation. Deregulation of NTRK1 activity is associated with several human disorders. Loss of function mutations causes the genetic disease congenital insensitivity to pain with anhidrosis (CIPA). Constitutive activation of NTRK1 has been detected in several tumor types. An autocrine loop involving NTRK1 and NGF is associated with tumor progression in prostate carcinoma and in breast cancer. A novel alternative splicing variant with constitutive oncogenic potential has been recently described in neuroblastoma. Somatic rearrangements of NTRK1, producing chimeric oncogenes with constitutive tyrosine kinase activity, have been detected in a consistent fraction of papillary thyroid tumors. The topic of this review is a detailed analysis of the thyroid TRK oncogenes. The modalities of their activation, their mechanism of action, the contribution of activating sequences, and the molecular mechanisms underlying their generation will be discussed.

PMID:
16242838
[PubMed - indexed for MEDLINE]
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Elsevier Science
    Loading ...
    Write to the Help Desk