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.
Original language | English |
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Pages (from-to) | 313-316 |
Number of pages | 4 |
Journal | Journal of the Endocrine Society |
Volume | 1 |
Issue number | 4 |
DOIs | |
State | Published - Apr 2017 |
Keywords
- Oncogene
- Parathyroid
- ZFX
- ZFY