Minireview: RET: normal and abnormal functions

Massimo Santoro1, Rosa Marina Melillo, Francesca Carlomagno

  • 1Dipartimento di Biologia e Patologia Cellulare e Molecolare, University Federico II c/o Istituto di Endocrinologia ed Oncologia Sperimentale del Consiglio Nazionale delle Ricerche, Naples, Italy. masantor@unina.it

Endocrinology
|August 28, 2004
PubMed

Insights

The RET gene, a receptor tyrosine kinase, drives thyroid cancers like papillary and medullary thyroid carcinoma. Understanding RET oncogenic conversion and targeting RET are key strategies for thyroid cancer treatment.

Area of Science:

  • Oncology
  • Genetics
  • Molecular Biology

Background:

  • The RET gene encodes a receptor tyrosine kinase involved in cell growth and differentiation.
  • RET alterations are oncogenic, leading to various thyroid cancers, including papillary and medullary thyroid carcinoma.
  • Germline mutations in RET are causative for inherited multiple endocrine neoplasia type 2 syndromes.

Purpose of the Study:

  • To review mechanisms of RET oncogenic conversion.
  • To discuss RET targeting as a therapeutic strategy for thyroid cancer.
  • To provide an overview of RET's role in thyroid tumorigenesis.

Main Methods:

  • Literature review of studies on RET gene function.
  • Analysis of data on RET mutations and their clinical implications.
  • Synthesis of information on RET-targeted therapies.

Main Results:

  • RET oncogenic conversion occurs through various mechanisms, including mutations and fusions.
  • RET alterations are critical drivers in the development of papillary and medullary thyroid carcinomas.
  • Targeting RET signaling pathways shows promise in preclinical and clinical settings.

Conclusions:

  • RET is a pivotal oncogene in thyroid cancer pathogenesis.
  • Targeting RET offers a promising therapeutic avenue for patients with RET-driven thyroid cancers.
  • Further research into RET biology and targeted therapies is warranted.

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