Pituitary

, Volume 9, Issue 3, pp 179–192

RET and neuroendocrine tumors

Authors

    • Department of PathologyNagoya University Graduate School of Medicine
  • Mayumi Jijiwa
    • Department of PathologyNagoya University Graduate School of Medicine
  • Naoya Asai
    • Department of PathologyNagoya University Graduate School of Medicine
  • Masatoshi Ichihara
    • Department of PathologyNagoya University Graduate School of Medicine
  • Masahide Takahashi
    • Department of PathologyNagoya University Graduate School of Medicine
    • Division of Molecular Pathology, Center for Neurological Disease and CancerNagoya University Graduate School of Medicine
Article

DOI: 10.1007/s11102-006-0263-4

Cite this article as:
Murakumo, Y., Jijiwa, M., Asai, N. et al. Pituitary (2006) 9: 179. doi:10.1007/s11102-006-0263-4

Abstract

The RET proto-oncogene encodes a receptor tyrosine kinase that is a main component of the signaling pathway activated by the glial cell line-derived neurotrophic factor family ligands. Gene targeting studies revealed that signaling through RET plays a crucial role in neuronal and renal organogenesis. It is well-known that germline mutations in RET lead to the human inherited diseases, multiple endocrine neoplasia type 2 (MEN 2) and Hirschsprung’s disease, and that somatic rearrangements of RET cause papillary thyroid carcinoma. Due to marked advances in understanding of the molecular mechanisms of the development of MEN 2, a consensus on MEN 2 management associated with RET status is being reached and currently put into general use as a guideline. In this review, we summarize progress in the study of RET from bench to bedside, focusing on pathophysiology of neuroendocrine tumors.

Keywords

RETTyrosine kinaseSignaling pathwayGermline mutationNeuroendocrine tumorsMEN 2
Download to read the full article text

Copyright information

© Springer Science + Business Media, LLC 2006