RAS proto-oncogene in medullary thyroid carcinoma

  1. Valeriano Leite1,2,3
  1. 1 Unidade de Investigação em Patobiologia Molecular (UIPM) , Instituto Português de Oncologia de Lisboa Francisco Gentil E.P.E., Rua Prof. Lima Basto, 1099-023 Lisboa, Portugal
    2 Serviço de Endocrinologia , Instituto Português de Oncologia de Lisboa Francisco Gentil E.P.E., Rua Prof. Lima Basto, 1099-023 Lisboa, Portugal
    3 Clínica Universitária de Endocrinologia , Faculdade de Ciências Médicas, Universidade Nova de Lisboa, Campo Mártires da Pátria 130, 1150-228 Lisboa, Portugal
  1. Correspondence should be addressed to M M Moura; Email: mmoura{at}ipolisboa.min-saude.pt
  1. Figure 1

    Summary of the most frequently mutated genes in MTC. The graph represents the genes that are mutated in at least two samples, or only in a single sample but after being tested in more than 100 MTC. The data relate to the COSMIC v68 release, at http://sanger.ac.uk/cosmic (accessed May 2014).

  2. Figure 2

    Signaling pathways implicated in thyroid carcinogenesis. RAS/RAF/MEK/ERK and PI3K/AKT/mTOR pathways are involved in propagation of signals from cell membrane tyrosine kinase receptors into the nucleus and regulate multiple cellular processes, including proliferation, survival, growth, migration, and differentiation. The main therapeutic agents and their targets are shown. CYS, cysteine-rich domain; GDNF, glial cell-derived neurotrophic factor; PIP3, phosphatidylinositol (3,4,5)-trisphosphate; TD, transmembrane domain; TK, tyrosine kinase domain.

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