The present study is aimed to present the potential role of thyroid hormones (TH) in the pathogenesis of glioblastoma multiforme (GBM). In first part of this presentation the effect of general homeostasis of TH on GBM formation and course was shown. Then the evidence concerning present state of the knowledge about active transport of TH to the brain, the role of iodothyronine deiodinase type 2 and 3 in the setting concentration of T3 in the brain and GBM cells, and finally knowledge about the role of genomic (TH nuclear receptors THRA and THRB) and non-genomic modes (membrane integrin receptor αvβ3) of action of TH and its importance for GBM was outlined. The last part of this presentation was devoted to generally approved signalling pathways leading to the formation and the clinical course of GBM, showing at the same time evidence that each of the pathways is affected by particular TH actions. In conclusion it is suggested that TH is one of the pathogenetic factors for GBM and as such can have practical implications for the formation and course and treatment of this tumour.
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