Associated Papers
Primary exploration of cell-free DNA in the plasma of patients with parathyroid neoplasms using next-generation sequencing.
Zheng Q et al.
Cancer Cell International, 2025
40075389 (PubMed )
Supplement: 12935_2025_3699_MOESM2_ESM.xlsx › Sheet1
CDC73 c.1155-3A>G is a pathogenic variant that causes aberrant splicing, disrupted parafibromin expression, and hyperparathyroidism-jaw tumor syndrome.
Needleman L et al.
Jbmr Plus, 2025
Do Patients With Atypical Parathyroid Adenoma Need Close Follow-up?
Saponaro F et al.
The Journal of Clinical Endocrinology and Metabolism, 2021
The genomic profile of parathyroid carcinoma based on whole-genome sequencing.
Hu Y et al.
International Journal of Cancer, 2020
Molecular genetics of syndromic and non-syndromic forms of parathyroid carcinoma.
Cardoso L et al.
Human Mutation, 2017
Crystal structure of the N-terminal domain of human CDC73 and its implications for the hyperparathyroidism-jaw tumor (HPT-JT) syndrome.
Sun W et al.
Scientific Reports, 2017
29142233 (PubMed )
Supplement: 41598_2017_15715_MOESM1_ESM.pdf
Mutational and large deletion study of genes implicated in hereditary forms of primary hyperparathyroidism and correlation with clinical features.
Pardi E et al.
Plos One, 2017
Utilisation of a cryptic non-canonical donor splice site of the gene encoding PARAFIBROMIN is associated with familial isolated primary hyperparathyroidism.
Bradley KJ et al.
Journal of Medical Genetics, 2005
Genetic analyses of the HRPT2 gene in primary hyperparathyroidism: germline and somatic mutations in familial and sporadic parathyroid tumors.
Cetani F et al.
The Journal of Clinical Endocrinology and Metabolism, 2004
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