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Neuro Endocrinol Lett. 2019 Mar 11;40(1):29-35. [Epub ahead of print]

Dysregulation in IGF-1R, FGFR4 and βKlotho signaling in patients with medullary thyroid cancer.

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Department of Immunoendocrinology, Chair of Endocrinology, Medical University of Lodz, Pomorska 251, 92-213 Lodz, Poland, Poland.
Clinic of Endocrinological and General Surgery, Chair of Endocrinology, Medical University of Lodz, Pabianicka 62, 93-513 Lodz, Poland.
Clinic of Endocrinology, Chair of Endocrinology, Medical University of Lodz, Pomorska 251, Poland.
Department of Neuroendocrinology, Medical University of Lodz, Pomorska 251, 92-213 Lodz, Poland.



Medullary thyroid cancer (MTC) is a relatively rare thyroid neoplasm derived from neuroendocrine C cells which secrete calcitonin. αKlotho (αKL) and βKlotho (βKL) are transmembrane proteins which modulate different signaling systems, such as endocrine FGFs and IGF1 pathways. Dysregulation of the FGF19/FGFR4/βKL and IGF-1/IGF-1R/αKL signaling axes has been implicated in the pathogenesis of several cancers. However, their role in the pathogenesis of MTC has not been determined.


The aim of this study was to assess αKL, βKL, FGF19, IGF-1, FGFR4, and IGF-1R concentrations in a group of 11 patients with medullary thyroid cancer (MTC). The control group consisted of 20 healthy volunteers. Serum concentrations of these factors were measured using specific ELISA methods.


Significantly lower concentrations of βKL and higher concentrations of FGFR4 and IGF-1R were found in patients with MTC as compared to controls.


Our results indicate that a disrupted signaling pathway for βKL, FGFR4 and IGF-1R may play a role in the development of medullary thyroid cancers. However, further studies are required to confirm these findings and to use this knowledge in clinical practice.


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