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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.

Author information

1
Department of Immunoendocrinology, Chair of Endocrinology, Medical University of Lodz, Pomorska 251, 92-213 Lodz, Poland, Poland.
2
Clinic of Endocrinological and General Surgery, Chair of Endocrinology, Medical University of Lodz, Pabianicka 62, 93-513 Lodz, Poland.
3
Clinic of Endocrinology, Chair of Endocrinology, Medical University of Lodz, Pomorska 251, Poland.
4
Department of Neuroendocrinology, Medical University of Lodz, Pomorska 251, 92-213 Lodz, Poland.

Abstract

BACKGROUND:

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.

METHODS:

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.

RESULTS:

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

CONCLUSIONS:

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.

PMID:
31184820

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