Expression of simple mucin type antigens and Lewis type 1 and type 2 chain antigens in the thyroid gland: An immunohistochemical study of normal thyroid tissues, benign lesions, and malignant tumors

1996 ◽  
Vol 7 (4) ◽  
pp. 291-301 ◽  
Author(s):  
Elsa Fonseca ◽  
Salomé Castanhas ◽  
Manuel Sobrinho-Simões
Keyword(s):  
Thyroid Gland ◽  
Immunohistochemical Study ◽  
Malignant Tumors ◽  
Benign Lesions ◽  
Normal Thyroid

scholarly journals Synthesis and Metabolism of Thyroid Hormones Is Preferentially Maintained in Selenium-Deficient Transgenic Mice

Endocrinology ◽  
2006 ◽  
Vol 147 (3) ◽  
pp. 1306-1313 ◽  
Author(s):  
Lutz Schomburg ◽  
Cornelia Riese ◽  
Marten Michaelis ◽  
Emine Griebert ◽  
Marc O. Klein ◽  
...  
Keyword(s):  
Thyroid Gland ◽  
Thyroid Hormones ◽  
Knockout Mice ◽  
Serum Levels ◽  
Mrna Levels ◽  
Normal Range ◽  
Growth Defects ◽  
Low Levels

The thyroid gland is rich in selenium (Se) and expresses a variety of selenoproteins that are involved in antioxidative defense and metabolism of thyroid hormones (TH). Se deficiency impairs regular synthesis of selenoproteins and adequate TH metabolism. We recently generated mice that lack the plasma Se carrier, selenoprotein P (SePP). SePP-knockout mice display decreased serum Se levels and manifest growth defects and neurological abnormalities partly reminiscent of thyroid gland dysfunction or profound hypothyroidism. Thus, we probed the TH axis in developing and adult SePP-knockout mice. Surprisingly, expression of Se-dependent 5′-deiodinase type 1 was only slightly altered in liver, kidney, or thyroid at postnatal d 60, and 5′-deiodinase type 2 activity in brain was normal in SePP-knockout mice. Thyroid gland morphology, thyroid glutathione peroxidase activity, thyroid Se concentration, and serum levels of TSH, T4, or T3 were within normal range. Pituitary TSHβ transcripts and hepatic 5′-deiodinase type 1 mRNA levels were unchanged, indicating regular T3 bioactivity in thyrotropes and hepatocytes. Cerebellar granule cell migration as a sensitive indicator of local T3 action during development was undisturbed. Collectively, these findings demonstrate that low levels of serum Se or SePP in the absence of other challenges do not necessarily interfere with regular functioning of the TH axis. 5′-deiodinase isozymes are preferentially supplied, and Se-dependent enzymes in the thyroid are even less-dependent on serum levels of Se or SePP than in brain. This indicates a top priority of the thyroid gland and its selenoenzymes with respect to the hierarchical Se supply within the organism.

scholarly journals Thyroglobulin Gene Mutations Producing Defective Intracellular Transport of Thyroglobulin Are Associated with Increased Thyroidal Type 2 Iodothyronine Deiodinase Activity

2007 ◽  
Vol 92 (4) ◽  
pp. 1451-1457 ◽  
Author(s):  
Yasuhiko Kanou ◽  
Akira Hishinuma ◽  
Katsuhiko Tsunekawa ◽  
Koji Seki ◽  
Yutaka Mizuno ◽  
...  
Keyword(s):  
Thyroid Gland ◽  
Intracellular Transport ◽  
Mrna Level ◽  
Thyroid Tissue ◽  
Compound Heterozygous ◽  
Free T4 ◽  
Iodothyronine Deiodinase ◽  
Normal Thyroid ◽  
Thyroid Glands

Abstract Context: Most patients with defective synthesis and/or secretion of thyroglobulin (Tg) present relatively high serum free T3 (FT3) concentrations with disproportionately low free T4 (FT4) resulting in a high FT3/FT4 ratio. The mechanism of this change in FT3/FT4 ratio remains unknown. Objective: We hypothesize that increased type 2 iodothyronine deiodinase (D2) activity in the thyroid gland may explain the higher FT3/FT4 ratio that is frequently observed in patients with abnormal Tg synthesis. Design: We recently identified a compound heterozygous patient (patient A) with a Tg G2356R mutation and one previously described (C1245R) that is known to cause a defect in intracellular transport of Tg. In the current study, after determining the abnormality caused by G2356R, we measured D2 activity as well as its mRNA level in the thyroid gland. We also measured the thyroidal D2 activity in three patients with Tg transport defect and in normal thyroid tissue. Results: Morphological and biochemical analysis of the thyroid gland from patient A, complemented by a pulse-chase experiment, revealed that G2356R produces a defect in intracellular Tg transport. D2 activity but not type 1 deiodinase in thyroid glands of patients with abnormal Tg transport was significantly higher than in normal thyroid glands, whereas D2 mRNA level in patient A was comparable with that in normal thyroid glands. Furthermore, there was a positive correlation between D2 activity and FT3/FT4 ratios. Conclusion: Increased thyroidal D2 activity in the thyroid gland is responsible for the higher FT3/FT4 ratios in patients with defective intracellular Tg transport.

scholarly journals CNS Tumors in Neurofibromatosis

2017 ◽  
Vol 35 (21) ◽  
pp. 2378-2385 ◽  
Author(s):  
Jian Campian ◽  
David H. Gutmann
Keyword(s):  
Protein Function ◽  
Malignant Tumors ◽  
Genetic Disorders ◽  
Treatment Options ◽  
Cranial Nerves ◽  
Cns Tumors ◽  
Low Grade ◽  
Precision Oncology

Neurofibromatosis (NF) encompasses a group of distinct genetic disorders in which affected children and adults are prone to the development of benign and malignant tumors of the nervous system. The purpose of this review is to discuss the spectrum of CNS tumors arising in individuals with NF type 1 (NF1) and NF type 2 (NF2), their pathogenic etiologies, and the rational treatment options for people with these neoplasms. This article is a review of preclinical and clinical data focused on the treatment of the most common CNS tumors encountered in children and adults with NF1 and NF2. Although children with NF1 are at risk for developing low-grade gliomas of the optic pathway and brainstem, individuals with NF2 typically manifest low-grade tumors affecting the cranial nerves (vestibular schwannomas), meninges (meningiomas), and spinal cord (ependymomas). With the identification of the NF1 and NF2 genes, molecularly targeted therapies are beginning to emerge, as a result of a deeper understanding of the mechanisms underlying NF1 and NF2 protein function. As we enter into an era of precision oncology, a more comprehensive awareness of the factors that increase the risk of developing CNS cancers in affected individuals, coupled with a greater appreciation of the cellular and molecular determinants that maintain tumor growth, will undoubtedly yield more effective therapies for these cancer predisposition syndromes.

scholarly journals Type 1 and type 2 iodothyronine deiodinases in the thyroid gland of patients with 3,5,3′-triiodothyronine-predominant Graves' disease

2011 ◽  
Vol 164 (1) ◽  
pp. 95-100 ◽  
Author(s):  
Mitsuru Ito ◽  
Nagaoki Toyoda ◽  
Emiko Nomura ◽  
Yuuki Takamura ◽  
Nobuyuki Amino ◽  
...  
Keyword(s):  
Thyroid Gland ◽  
Mrna Level ◽  
Antithyroid Drug ◽  
High Serum ◽  
Graves Disease ◽  
Iodothyronine Deiodinase ◽  
Iodothyronine Deiodinases ◽  
Antithyroid Drug Therapy

Objective3,5,3′-triiodothyronine-predominant Graves' disease (T3-P-GD) is characterized by a persistently high serum T3 level and normal or even lower serum thyroxine (T4) level during antithyroid drug therapy. The source of this high serum T3 level has not been clarified. Our objective was to evaluate the contribution of type 1 and type 2 iodothyronine deiodinase (D1 (or DIO1) and D2 (or DIO2) respectively) in the thyroid gland to the high serum T3 level in T3-P-GD.MethodsWe measured the activity and mRNA level of both D1 and D2 in the thyroid tissues of patients with T3-P-GD (n=13) and common-type GD (CT-GD) (n=18) who had been treated with methimazole up until thyroidectomy.ResultsThyroidal D1 activity in patients with T3-P-GD (492.7±201.3 pmol/mg prot per h) was significantly higher (P<0.05) than that in patients with CT-GD (320.7±151.9 pmol/mg prot per h). On the other hand, thyroidal D2 activity in patients with T3-P-GD (823.9±596.4 fmol/mg prot per h) was markedly higher (P<0.005) than that in patients with CT-GD (194.8±131.6 fmol/mg prot per h). There was a significant correlation between the thyroidal D1 activity in patients with T3-P-GD and CT-GD and the serum FT3-to-FT4 ratio (r=0.370, P<0.05). Moreover, there was a strong correlation between the thyroidal D2 activity in those patients and the serum FT3-to-FT4 ratio (r=0.676, P<0.001).ConclusionsOur results suggest that the increment of thyroidal deiodinase activity, namely D1 and especially D2 activities, may be responsible for the higher serum FT3-to-FT4 ratio in T3-P-GD.

Macro creatine kinase type 2: results of a prospective study in hospitalized patients.

1985 ◽  
Vol 31 (12) ◽  
pp. 1959-1964 ◽  
Author(s):  
W Stein ◽  
J Bohner ◽  
W Renn ◽  
R Maulbetsch
Keyword(s):  
Malignant Tumors ◽  
Residual Activity ◽  
Hospitalized Patients ◽  
University Hospital ◽  
Serious Illness ◽  
Impending Death ◽  
A Prospective Study ◽  
Second Peak

Abstract We determined total CK activity with the N-acetylcysteine-activated method and residual activity after immunoinhibition of the CK-M subunits in the sera of 2018 patients consecutively admitted to our university hospital for internal diseases, and of 936 outpatients, regardless of the patients' diagnoses. We could detect not more than two types of macro CK: macro CK type 2, which we observed in the sera of 85 patients (prevalence, 3.7% for hospitalized patients), and macro CK type 1. Most patients showing macro CK type 2 were older than 50 years, but we additionally observed a second peak at 20-30 years of age. We saw no preponderance by sex. We detected macro CK type 2 predominantly in severely ill patients of all ages, mainly those with malignant tumors or cirrhosis of the liver. Our findings support the assumption that macro CK type 2 is the manifestation of mitochondrial CK in serum. Occasionally, macro CK type 2 disappeared from the circulation after amelioration of the associated disease. Its occurrence in serum nevertheless is a sign of a serious illness with high mortality but not inevitably a sign of impending death.

Type 1 and type 2 iodothyronine deiodinases in the thyroid gland of patients with huge goitrous Hashimoto’s thyroiditis

Endocrine ◽  
2019 ◽  
Vol 64 (3) ◽  
pp. 584-590 ◽  
Author(s):  
Azusa Harada ◽  
Emiko Nomura ◽  
Kumiko Nishimura ◽  
Mitsuru Ito ◽  
Hiroshi Yoshida ◽  
...  
Keyword(s):  
Thyroid Gland ◽  
Hashimoto’S Thyroiditis ◽  
Hashimoto's Thyroiditis ◽  
Iodothyronine Deiodinases

scholarly journals MEK inhibitors - novel targeted therapies of neurofibromatosis associated benign and malignant lesions

2021 ◽  
Vol 9 (1) ◽  
Author(s):  
Anja Harder
Keyword(s):  
Malignant Tumors ◽  
Neurofibromatosis Type ◽  
High Morbidity ◽  
Low Grade ◽  
Pathogenic Variants ◽  
Current State ◽  
Associated Lesions ◽  
Malignant Lesions

AbstractMAP/ERK kinase 1 and 2 (MEK 1/2) inhibitors (MEKi) are investigated in several trials to treat lesions that arise from pathogenic variants of the Neurofibromatosis type 1 and type 2 genes (NF1, NF2). These trials showed that MEKi are capable to shrink volume of low grade gliomas and plexiform neurofibromas in NF1. Targeting other lesions being associated with a high morbidity in NF1 seems to be promising. Due to involvement of multiple pathways in NF2 associated lesions as well as in malignant tumors, MEKi are also used in combination therapies. This review outlines the current state of MEKi application in neurofibromatosis and associated benign and malignant lesions.

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