scholarly journals Immunohistochemical Studies on Thyroid Peroxidase and Thyroglobulin in 13 Human Thyroid Tumors and 7 Graves' Goiters.

1993 ◽  
Vol 40 (6) ◽  
pp. 683-690 ◽  
Author(s):  
KAYO WATANABE ◽  
NARUMI KOIZUMI ◽  
OSAMU OZAKI ◽  
YUTAKA FUTAESAKU ◽  
TOICHIRO HOSOYA
Keyword(s):  
Human Thyroid ◽  
Thyroid Peroxidase ◽  
Thyroid Tumors ◽  
Immunohistochemical Studies

An Analysis of the Structure and Antigenicity of Different Forms of Human Thyroid Peroxidase

Thyroid ◽  
1994 ◽  
Vol 4 (2) ◽  
pp. 173-178 ◽  
Author(s):  
JAMES R. BAKER ◽  
PATRICIA ARSCOTT ◽  
JENNIFER JOHNSON
Keyword(s):  
Human Thyroid ◽  
Thyroid Peroxidase ◽  
Human Thyroid Peroxidase

scholarly journals Mutation screening of the thyroid peroxidase gene in a cohort of 55 Portuguese patients with congenital hypothyroidism

2005 ◽  
Vol 152 (2) ◽  
pp. 193-198 ◽  
Author(s):  
Carina Rodrigues ◽  
Paula Jorge ◽  
José Pires Soares ◽  
Isaura Santos ◽  
Regina Salomão ◽  
...  
Keyword(s):  
Congenital Hypothyroidism ◽  
Mutation Screening ◽  
Gene Mutations ◽  
Human Thyroid ◽  
Thyroid Peroxidase ◽  
Molecular Testing ◽  
Missense Mutations ◽  
Human Thyroid Peroxidase ◽  
Iodide Organification Defect ◽  
Organification Defect

Objective: Defects in the human thyroid peroxidase (TPO) gene are reported to be one of the causes of congenital hypothyroidism (CH) due to a total iodide organification defect. The aim of the present study was to determine the nature and frequency of TPO gene mutations in patients with CH, characterised by elevated TSH levels and orthotopic thyroid gland, identified in the Portuguese National Neonatal Screening Programme. Subjects and methods: The sample comprised 55 patients, from 53 unrelated families, with follow-up in the endocrinology clinics of the treatment centres of Porto and Lisbon. Mutation screening in the TPO gene (exons 1–17) was performed by single-strand conformational analysis followed by sequencing of fragments with abnormal migration patterns. Results: Eight different mutations were detected in 13 patients (seven homozygotes and six compound heterozygotes). Novel mutations included three missense mutations, namely 391T > C (S131P), 1274A > G (N425S) and 2512T > A (C838S), as well as the predictable splice mutation 2748G > A (Q916Q/spl?). The undocumented polymorphism 180-47A > C was also detected. Conclusion: The results are in accordance with previous observations confirming the genetic heterogeneity of TPO defects. The proportion of patients in which the aetiology was determined justifies the implementation of this molecular testing in our CH patients with dyshormonogenesis.

scholarly journals Notch Signaling Is Involved in Expression of Thyrocyte Differentiation Markers and Is Down-Regulated in Thyroid Tumors

2008 ◽  
Vol 93 (10) ◽  
pp. 4080-4087 ◽  
Author(s):  
E. Ferretti ◽  
E. Tosi ◽  
A. Po ◽  
A. Scipioni ◽  
R. Morisi ◽  
...  
Keyword(s):  
Gene Expression ◽  
Thyroid Cancer ◽  
Notch Signaling ◽  
Notch Pathway ◽  
Human Thyroid ◽  
Thyroid Tumors ◽  
Follicular Cells ◽  
Differentiation Markers ◽  
Thyroid Follicular Cells ◽  
Thyroid Cancer Cells

Context: Notch genes encode receptors for a signaling pathway that regulates cell growth and differentiation in various contexts, but the role of Notch signaling in thyroid follicular cells has never been fully published. Objective: The objective of the study was to characterize the expression of Notch pathway components in thyroid follicular cells and Notch signaling activities in normal and transformed thyrocytes. Design/Setting and Patients: Expression of Notch pathway components and key markers of thyrocyte differentiation was analyzed in murine and human thyroid tissues (normal and tumoral) by quantitative RT-PCR and immunohistochemistry. The effects of Notch overexpression in human thyroid cancer cells and FTRL-5 cells were explored with analysis of gene expression, proliferation assays, and experiments involving transfection of a luciferase reporter construct containing human NIS promoter regions. Results: Notch receptors are expressed during the development of murine thyrocytes, and their expression levels parallel those of thyroid differentiation markers. Notch signaling characterized also normal adult thyrocytes and is regulated by TSH. Notch pathway components are variably expressed in human normal thyroid tissue and thyroid tumors, but expression levels are clearly reduced in undifferentiated tumors. Overexpression of Notch-1 in thyroid cancer cells restores differentiation, reduces cell growth rates, and stimulates NIS expression via a direct action on the NIS promoter. Conclusion: Notch signaling is involved in the determination of thyroid cell fate and is a direct regulator of thyroid-specific gene expression. Its deregulation may contribute to the loss of differentiation associated with thyroid tumorigenesis.

Evaluation of human thyroid tumors by proton nuclear magnetic resonance

1984 ◽  
Vol 2 (1) ◽  
pp. 65-66
Author(s):  
J. deCertaines ◽  
J.Y. Herry ◽  
G. Lancien ◽  
L. Benoist ◽  
A.M. Bernard ◽  
...  
Keyword(s):  
Nuclear Magnetic Resonance ◽  
Magnetic Resonance ◽  
Proton Nuclear Magnetic Resonance ◽  
Human Thyroid ◽  
Thyroid Tumors ◽  
Nuclear Magnetic

Purification of recombinant human thyroid peroxidase (hTPO) from AD293 mammalian cells

2018 ◽  
Vol 106 ◽  
pp. 87-94
Author(s):  
Parvinder Kaur ◽  
Harshada Patil ◽  
Paresh B. Bhanushali ◽  
Shamkant B. Badgujar ◽  
Anuj Kumar Gupta
Keyword(s):  
Mammalian Cells ◽  
Human Thyroid ◽  
Thyroid Peroxidase ◽  
Human Thyroid Peroxidase
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