[Molecular mechanism of thyroid carcinogenesis]

Nihon Rinsho. 2007 Nov;65(11):1959-65.
[Article in Japanese]

Abstract

Molecular mechanism of thyroid carcinogenesis has been well studied through the discovery of genetic abnormalities such as RET/PTC rearrangement and BRAF mutation, both of which constitutively activate MAP kinase pathway and are frequently found in papillary thyroid cancer. The TP53 mutation is thought to play a critical role in transformation of differentiated thyroid cancer into anaplastic thyroid cancer. Besides these genetic alterations, cancer stem cell theory has recently been applied to thyroid field. A better understanding of thyroid cancer stem cell may not only ameliorate our comprehension of thyroid cancer biology, but also open the possibility of innovative diagnostic procedures and development of novel targeted therapies. In this article, we mainly review thyroid carcinogenesis based on the evidence of radiation-induced cancer and cancer stem cell hypothesis.

Publication types

  • English Abstract
  • Review

MeSH terms

  • Adenocarcinoma, Papillary / genetics*
  • Adenocarcinoma, Papillary / pathology
  • Cell Transformation, Neoplastic / genetics
  • Extracellular Signal-Regulated MAP Kinases / physiology
  • Gene Rearrangement
  • Humans
  • Mutation
  • Neoplastic Stem Cells / pathology
  • Proto-Oncogene Proteins B-raf / genetics
  • Proto-Oncogene Proteins c-ret / genetics
  • Receptors, G-Protein-Coupled / genetics
  • Thyroid Neoplasms / genetics*
  • Thyroid Neoplasms / pathology
  • Tumor Suppressor Protein p53 / genetics

Substances

  • Receptors, G-Protein-Coupled
  • TP53 protein, human
  • Tumor Suppressor Protein p53
  • taste receptors, type 2
  • Proto-Oncogene Proteins c-ret
  • RET protein, human
  • BRAF protein, human
  • Proto-Oncogene Proteins B-raf
  • Extracellular Signal-Regulated MAP Kinases