Radiation-Induced Synchronous Parathyroid Carcinoma and Papillary Thyroid Carcinoma Clinical, Morphological, and Genetic Insights /

The clinicopathological and molecular features of synchronous parathyroid carcinoma (PC) and thyroid carcinoma in a male patient are presented. At 11, he received mantle field radiotherapy for Hodgkin lymphoma. He had a 26-year adulthood history of recurrent nephrolithiasis treated five times with l...

Teljes leírás

Elmentve itt :
Bibliográfiai részletek
Szerzők: Iványi Gábor
Christofi Alexandros
Sipka Gábor
Zombori Tamás
Kuthi Levente
Simon Andrea Beáta
Dobi Deján
Lázár György ifj
Valkusz Zsuzsanna
Iványi Béla
Dokumentumtípus: Cikk
Megjelent: 2025
Sorozat:INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES 26 No. 9
Tárgyszavak:
doi:10.3390/ijms26094441

mtmt:36124343
Online Access:http://publicatio.bibl.u-szeged.hu/36678
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520 3 |a The clinicopathological and molecular features of synchronous parathyroid carcinoma (PC) and thyroid carcinoma in a male patient are presented. At 11, he received mantle field radiotherapy for Hodgkin lymphoma. He had a 26-year adulthood history of recurrent nephrolithiasis treated five times with lithotripsy. At 52, he was referred to our clinic for hypercalcemia. Primary hyperparathyroidism was diagnosed (calcium: 3.46 mmol/L, parathormone: 150 pmol/L, preserved renal function, nephrolithiasis, and osteoporosis). Neck ultrasound revealed a 41 × 31 × 37 mm nodule in the left thyroid and smaller nodules in the right thyroid. Enlarged cervical lymph nodes were not observed. The large nodule was interpreted as parathyroid adenoma on 99Tc-pertechnetate scintigraphy/99Tc-MIBI scintigraphy with SPECT/CT. Total left-sided and subtotal right-sided thyroidectomy were performed. Histopathology confirmed locally invasive, low-grade PC (pT2; positive for parafibromin and E-cadherin, negative for galectin-3 and PGP9.5; wild-type expression for p53 and retinoblastoma protein; Ki-67 index 10%) and incidental papillary thyroid carcinoma (pT1b). Genetic profiling revealed no loss in CDC73, MEN1, CCND1, PIK3CA, CDH1, RB1, and TP53 genes. Deletions in CDKN2A, LATS1, ARID1A, ARID1B, RAD54L, and MUTYH genes and monosomies in nine chromosomes were identified. The tumor mutational burden and genomic instability score were low, and the tumor was microsatellite-stable. The thyroid carcinoma exhibited a TRIM24::BRAF fusion. Following surgery, the parathormone and calcium levels had normalized, and the patient underwent radioiodine treatment for thyroid cancer. The follow-up of 14 months was eventless. In summary, the clinical, laboratory, and imaging features of hyperparathyroidism taken together could have suggested malignancy, then confirmed histologically. The synchronous carcinomas were most likely caused by irradiation treatment diagnosed 41 years after exposure. It seems that the radiation injury initially induced parathyroid adenoma in young adulthood, which underwent a malignant transformation around age fifty. 
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700 0 1 |a Christofi Alexandros  |e aut 
700 0 1 |a Sipka Gábor  |e aut 
700 0 1 |a Zombori Tamás  |e aut 
700 0 1 |a Kuthi Levente  |e aut 
700 0 1 |a Simon Andrea Beáta  |e aut 
700 0 1 |a Dobi Deján  |e aut 
700 0 1 |a Lázár György ifj  |e aut 
700 0 1 |a Valkusz Zsuzsanna  |e aut 
700 0 1 |a Iványi Béla  |e aut 
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