[Molecular pathogenesis of thyroid tumors]

Dtsch Med Wochenschr. 2015 Apr;140(8):578-82. doi: 10.1055/s-0041-101491. Epub 2015 Apr 7.
[Article in German]

Abstract

The molecular pathogenesis of thyroid tumors has been an evolving field in the past years. The constitutive activation of intracellular tyrosine kinases has been identified as a hallmark of thyroid cancer. The activation of MAPK and PI3K pathways through somatic gene mutations or gene rearrangements seem to play a pivotal role in the pathogenesis of follicular-cell-derived tumors. In poorly differentiated tumors and anaplastic tumors often an accumulation of genetic alterations from differentiated thyroid cancer but also novel gene mutations can be observed. The C-cell-derived medullary thyroid cancer evolves through the constitutive activation of the RET kinase, either through germline RET mutations or somatic RET and RAS mutations. The better knowledge of the molecular pathogenesis allowed the development of targeted therapies in thyroid cancer patients. The identification of molecular response markers to tyrosine kinase inhibitor therapy is desirable.

Publication types

  • English Abstract

MeSH terms

  • Animals
  • Carcinogenesis / metabolism*
  • Gene Expression Regulation, Neoplastic
  • Humans
  • Mitogen-Activated Protein Kinase Kinases / metabolism*
  • Models, Biological
  • Pathology, Molecular / methods
  • Phosphatidylinositol 3-Kinases / metabolism*
  • Proto-Oncogene Proteins c-ret / metabolism*
  • Signal Transduction
  • Thyroid Neoplasms / diagnosis
  • Thyroid Neoplasms / metabolism*
  • ras Proteins / metabolism*

Substances

  • Phosphatidylinositol 3-Kinases
  • Proto-Oncogene Proteins c-ret
  • RET protein, human
  • Mitogen-Activated Protein Kinase Kinases
  • ras Proteins