AN UNUSUAL INITIAL MANIFESTATION OF METASTATIC PAPILLARY THYROID CARCINOMA: RADIOIODINE UPTAKE IN LYMPH NODE METASTATIC LESIONS IN A PATIENT WITH GRAVES' DISEASE

2002 ◽  
Vol 8 (4) ◽  
pp. 304-306 ◽  
Author(s):  
Seth L. Newman ◽  
Annette Y. Griffith ◽  
Allison B. Herbst ◽  
I-Tien Yeh ◽  
John S. Kukora
2008 ◽  
Vol 52 (7) ◽  
pp. 1194-1200 ◽  
Author(s):  
Graciela A. de Cross ◽  
Horacio Suarez ◽  
Fabián Pitoia ◽  
Daniel Moncet ◽  
María Vanegas ◽  
...  

A 29 yrs-old patient was referred to our hospital due to generalized convulsions. She had hyperthyroidism treated with methimazole. Her MRI showed 4 metastatic lesions in the brain. She had a goiter with a "cold" nodule and a palpable ipsilateral lymph node. The FNAB disclosed a papillary thyroid carcinoma. Under 5 mg of MMI treatment, she had a subclinical hyperthyroidism and TRAb were 47.8% (n.v. < 10%). The CT scan also showed lung metastasis. She underwent a total thyroidectomy with a modified neck dissection and she received an accumulated radioiodine dose of 700 mCi during the following two years. She died from the consequences of multiple metastatic lesions. Studies were performed in DNA extracted from paraffin-embedded tissue from the tumor, the metastatic lymph node and the non-tumoral thyroid. The genetic analysis of tumoral DNA revealed point mutations in two different genes: the wild type CAA at codon 61 of N-RAS mutated to CAT, replacing glycine by histidine (G61H) and the normal GCC sequence at codon 623 of the TSHR gene was replaced by TCC, changing the alanine by serine (A623S). In the non-tumoral tissue no mutations were found. In vitro studies showed a constitutive activation of the TSHR. It is very probable that this activating mutation of the TSHR is unable to reach the end point of the PKA cascade in the tumoral tissue. One possibility that could explain this is the presence of a cross-signaling mechanism generating a deviation of the TSH receptor cascade to the more proliferative one involving the MAPKinase, giving perhaps a more aggressive behavior of this papillary thyroid cancer.


2018 ◽  
Vol 91 (3) ◽  
pp. 210-215 ◽  
Author(s):  
Kazuhiro Shimura ◽  
Hironori Shibata ◽  
Yusuke Mizuno ◽  
Naoko Amano ◽  
Ken Hoshino ◽  
...  

Background: The risk factors for rapid growth and early metastasis of papillary thyroid carcinoma (PTC) and the role of coexisting Graves’ disease in the clinical course of PTC remain uncertain in children. Case Description: We report on a Japanese girl, whose PTC rapidly grew and metastasized within 4 years. Graves’ disease was diagnosed by the presence of serum TSH receptor antibodies at 8 years of age when thyroid ultrasonography detected no nodules. After 4 years of effective treatment with thiamazole, multifocal nodules – up to 47 mm in diameter – were detected on thyroid ultrasonography. Chest CT scan revealed multiple metastatic lesions in the lung. After total thyroidectomy, PTC was pathologically diagnosed. The patient underwent two courses of radioactive iodine (RAI) treatment, but the pulmonary metastatic lesions did not take up the RAI. Molecular analyses of the PTC tissue identified a TFG/NTRK1 chimeric gene and disclosed the preserved expression of TSHR and the reduced expression of SLC5A5 compared with non-tumor thyroid tissue. Conclusions: Rapid growth and early metastasis of PTC with coexisting Graves’ disease in this patient can be related to a combination of multiple factors including preserved TSHR expression, reduced SLC5A5 expression, and TFG/NTRK1 rearrangement.


2020 ◽  
Author(s):  
Vanessa Guerreiro ◽  
Cláudia Costa ◽  
Joana Oliveira ◽  
Ana Paula Santos ◽  
Mónica Farinha ◽  
...  

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