Search Results
You are looking at 1 - 1 of 1 items for
- Author: Helton Estrela Ramos x
- Refine by access: All content x
Endocrinology Service of Institute Orizonti, Belo Horizonte, Minas Gerais, Brazil
Search for other papers by Gustavo Penna in
Google Scholar
PubMed
Biotechnology Post-graduation Program, Federal University of São Paulo, São Paulo, Brazil
Estructural and Functional Biology Program, Federal University of São Paulo, São Paulo, Brazil
Search for other papers by Ileana G S Rubio in
Google Scholar
PubMed
Biotechnology Post-graduation Program, Federal University of São Paulo, São Paulo, Brazil
Search for other papers by Ester Saraiva Brust in
Google Scholar
PubMed
Search for other papers by Juliana Cazarin in
Google Scholar
PubMed
Search for other papers by Fabio Hecht in
Google Scholar
PubMed
Post-Graduation Program Molecular Medicine, Faculty of Medicine, Federal University of Minas Gerais, Belo Horizonte, Brazil
Search for other papers by Nina Ramalho Alkmim in
Google Scholar
PubMed
Endocrinology Service of Hospital das Clínicas, Federal University of Minas Gerais, Belo Horizonte, Brazil
Search for other papers by Kamilla M A Brandão Rajão in
Google Scholar
PubMed
Post-Graduation Program Medicine and Health, Faculty of Medical Sciences, Federal University of Bahia, Salvador, Bahia, Brazil
Post-Graduate Program in Interactive Processes of Organs and Systems, Health & Science Institute, Federal University of Bahia, Salvador, Bahia, Brazil
Search for other papers by Helton Estrela Ramos in
Google Scholar
PubMed
Differentiated thyroid carcinoma (DTC) combined with congenital hypothyroidism (CH) is a rare situation, and there is no well-established causal relationship. CH is a common congenital endocrine, while DTC occurring in childhood represents 0.4–3% of all malignancies at this stage of life. The association of CH with DTC could be related to dyshormonogenetic goiter (DHG) or developmental abnormalities. This review will explore the clinical features and the molecular mechanisms potentially associated with the appearance of DTC in CH: sporadic somatic driver mutations, chronic increase of thyroid-stimulating hormone (TSH) levels, higher concentrations of hydrogen peroxide (H2O2), cell division cycle associated 8 (Borelain/CDC8) gene mutations, and in others genes associated with CH – either alone or associated with the mechanisms involved in dyshormonogenesis. There are some pitfalls in the diagnosis of thyroid cancer in patients with CH with nodular goiter, as the proper cytological diagnosis of nodules of patients with dyshormonogenesis might be demanding due to the specific architectural and cytological appearance, which may lead to an erroneous interpretation of malignancy. The purpose of this article is to suggest an analytical framework that embraces the fundamental relationships between the various aspects of CH and CDT. In face of this scenario, the entire genetic and epigenetic context, the complex functioning, and cross talk of cell signaling may determine cellular mechanisms promoting both the maintenance of the differentiated state of the thyroid follicular cell and the disruption of its homeostasis leading to cancer. Whereas, the exact mechanisms for thyroid cancer development in CH remain to be elucidated.