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. 2017 Mar 2;1(4):313-316.
doi: 10.1210/js.2017-00031. eCollection 2017 Apr 1.

Mutational Analysis of ZFY in Sporadic Parathyroid Adenomas

Robert Romano  1 , La Shondra Ellis  1 , Nick Yu  1 , Justin Bellizzi  1 , Taylor C Brown  2 , Reju Korah  2 , Tobias Carling  2 , Jessica Costa-Guda  1   3 , Andrew Arnold  1   4
Affiliations

Mutational Analysis of ZFY in Sporadic Parathyroid Adenomas

Robert Romano et al. J Endocr Soc. .

Abstract

Context: The molecular pathogenesis of sporadic parathyroid adenomas is incompletely understood, with alterations in cyclin D1/PRAD1 and MEN1 most firmly established as genetic drivers. The gene encoding the X-linked zinc finger protein (ZFX) has recently been implicated in the pathogenesis of a subset of parathyroid adenomas after recurrent, hotspot-focused somatic mutations were identified. ZFX escapes X inactivation and is transcribed from both alleles in women, and a highly homologous gene encoding the Y-linked zinc finger protein (ZFY) provides dosage compensation in males.

Objective: We sought to investigate the role of ZFY mutation in sporadic parathyroid adenoma.

Intervention: Polymerase chain reaction and Sanger sequencing were used to examine DNA from typically presenting, sporadic (nonfamilial, nonsyndromic) parathyroid adenomas from male patients for mutations within the ZFY gene.

Results: No mutations were identified among 117 adenomas.

Conclusions: The absence of ZFY mutations in this series suggests that ZFY rarely, if ever, acts as a driver oncogene in sporadic parathyroid adenomas. The apparent differences in tumorigenic capabilities between the closely related zinc finger proteins ZFX and ZFY suggest that structure-function studies could represent an opportunity to gain insight into neoplastic processes in the parathyroid glands.

Keywords: ZFX; ZFY; oncogene; parathyroid.

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