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SOCS2 polymorphisms are not associated with clinical and biochemical phenotypes in acromegalic patients

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Abstract

Purpose

Suppressor of cytokine signaling 2 (SOCS2) is a STAT5b-regulated gene and one of its functions is to influence growth and development through negative regulatory effects on GH/IGF-1 pathway. So, we evaluate the potential influence of SOCS2 single nucleotide polymorphisms (SNPs) on clinical and laboratorial characteristics of a large cohort of Brazilian patients with acromegaly.

Methods

Four SOCS2 SNPs (rs3782415, rs3816997, rs3825199 and rs11107116) were selected and genotyped by real-time PCR using specific Taqman probe assays. A total of 186 patients (116 women, age range 26–88 years) were evaluated.

Results

No association of SOCS2 genotypes was observed with none of the following clinical and laboratorial characteristics: age, sex, body mass index, comorbidities, basal GH, oral glucose tolerance test GH nadir, IGF-I, ULNR-IGF-I.

Conclusion

Despite of the key role of SOCS2 in the regulation of GH receptor signaling, we did not find any significant association between SOCS2 polymorphisms and acromegaly.

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Acknowledgements

We thanks to Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP) for the financial support.

Funding

This study was funded in part by Fundação de Amparo à Pesquisa do Estado de São Paulo – FAPESP (Grant Number 2010/11718-1).

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Correspondence to Ericka B. Trarbach.

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The authors declare that they have no conflict of interest.

Ethical approval

All procedures performed in studies involving human participants were in accordance with the ethical standards of the institutional and/or national research committee and with the 1964 Helsinki declaration and its later amendments or comparable ethical standards.

Informed consent

Informed consent was obtained from all individual participants included in the study.

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Trarbach, E.B., Jorge, A.A., Duarte, F.H. et al. SOCS2 polymorphisms are not associated with clinical and biochemical phenotypes in acromegalic patients. Pituitary 20, 319–324 (2017). https://doi.org/10.1007/s11102-016-0779-1

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  • DOI: https://doi.org/10.1007/s11102-016-0779-1

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