Thyroid transcription factors in development, differentiation and disease

Fernández, Lilia; López-Márquez, Arístides; Santisteban, Pilar

doi:10.1038/nrendo.2014.186

Cited by 214 publications

(182 citation statements)

References 182 publications

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“…To determine if thyroid pathology in CD28 −/− mice is similar to TEC H/P in CD28-positive IFN-γ −/− NOD.H-2h4 mice, thyroids from IFN-γ −/− CD28 −/− mice given NaI water were examined by immunohistochemistry. Thyroid transcription factor (TTF-1) is a transcription factor expressed in the thyroid (24). If proliferating TEC are derived from epithelial cells, they will be TTF-1--positive.…”

Section: Resultsmentioning

confidence: 99%

“…If proliferating TEC are derived from epithelial cells, they will be TTF-1--positive. However, since they express p63 (5) and resemble thyroid solid cell nests histologically, they could be derived from ultimobrachial bodies, and would be TTF-1 negative (24). To distinguish between these possibilities, thyroids were stained with anti-TTF-1 (Supplemental Fig.…”

Section: Resultsmentioning

confidence: 99%

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New Murine Model of Early Onset Autoimmune Thyroid Disease/Hypothyroidism and Autoimmune Exocrinopathy of the Salivary Gland

Kayes

Weisman

Camden

et al. 2016

The Journal of Immunology

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60–70 % of IFN-γ−/− NOD.H-2h4 mice given NaI-supplemented water develop a slow onset autoimmune thyroid disease, characterized by thyrocyte epithelial cell hyperplasia/ proliferation (TEC H/P). TEC H/P develops much earlier in CD28−/− mice and nearly 100 % (both sexes) have severe TEC H/P at 4 months of age. Without NaI supplementation, 50% of 5–6 month old CD28−/−IfFN-γ−/− mice develop severe TEC H/P, and 2–3 weeks of NaI is sufficient for optimal development of severe TEC H/P. Mice with severe TEC H/P are hypothyroid and normalization of serum thyroxine (T4) levels does not reduce TEC H/P. Activated CD4+ T cells are sufficient to transfer TEC H/P to SCID recipients. Thyroids of mice with TEC H/P have infiltrating T cells and expanded numbers of proliferating thyrocytes that highly express CD40. CD40 facilitates, but is not required for development of severe TEC H/P, as CD40−/−IFN-γ−/−CD28−/− mice develop severe TEC H/P. Accelerated development of TEC H/P in IFN-γ−/− CD28−/− mice is a result of reduced Treg numbers as CD28−/− mice have significantly fewer Tregs, and transfer of CD28-positive Tregs inhibits TEC H/P. Essentially all female IFN-γ−/− CD28−/−NOD.H-2h4 mice have substantial lymphocytic infiltration of salivary glands and reduced salivary flow by 6 months of age, thereby providing an excellent new model of autoimmune exocrinopathy of the salivary gland. This is one of very few models where autoimmune thyroid disease and hypothyroidism develop in most mice by 4 months of age. This model will be useful for studying the effects of hypothyroidism on multiple organ systems.

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Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

New Murine Model of Early Onset Autoimmune Thyroid Disease/Hypothyroidism and Autoimmune Exocrinopathy of the Salivary Gland

Kayes

Weisman

Camden

et al. 2016

The Journal of Immunology

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“…Based on one of the largest series of thyroid cancer cases so far, the authors revealed a significant interaction between variants in PAX8 and STK17B (63), yet the mechanism through which these two gene variants interact remains unclear. Overall, it is worth to point out that FOXE1 and PAX8 are at the center of a regulatory network of transcription factors and cofactors that is essential for thyroid gland formation and the maintenance of the thyroid differentiated state in adults (66).…”

Section: New Steps In Thyroid Cancer Genetic Predispositionmentioning

confidence: 99%

ENDOCRINE TUMOURS: Advances in the molecular pathogenesis of thyroid cancer: lessons from the cancer genome

Riesco‐Eizaguirre

Santisteban

2016

European Journal of Endocrinology

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Thyroid cancer is the most common endocrine malignancy giving rise to one of the most indolent solid cancers, but also one of the most lethal. In recent years, systematic studies of the cancer genome, most importantly those derived from The Cancer Genome Altas (TCGA), have catalogued aberrations in the DNA, chromatin, and RNA of the genomes of thousands of tumors relative to matched normal cellular genomes and have analyzed their epigenetic and protein consequences. Cancer genomics is therefore providing new information on cancer development and behavior, as well as new insights into genetic alterations and molecular pathways. From this genomic perspective, we will review the main advances concerning some essential aspects of the molecular pathogenesis of thyroid cancer such as mutational mechanisms, new cancer genes implicated in tumor initiation and progression, the role of non-coding RNA, and the advent of new susceptibility genes in thyroid cancer predisposition. This look across these genomic and cellular alterations results in the reshaping of the multistep development of thyroid tumors and offers new tools and opportunities for further research and clinical development of novel treatment strategies.

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“…Together with the other thyroid TFs NKX2-1 and FOXE1, PAX8 is involved in thyroid follicular cell development and expression of thyroid-specific genes such as the sodium/iodide symporter (SLC5A5, also named as NIS), thyroglobulin (Tg), and thyroperoxidase (TPO; refs. 4,5). These genes are essential for thyroid differentiation as they mediate the metabolism of iodide, leading to the synthesis of active thyroid hormone.…”

Section: Introductionmentioning

confidence: 99%

The miR-146b-3p/PAX8/NIS Regulatory Circuit Modulates the Differentiation Phenotype and Function of Thyroid Cells during Carcinogenesis

et al. 2015

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Thyroid transcription factors in development, differentiation and disease

Cited by 214 publications

References 182 publications

New Murine Model of Early Onset Autoimmune Thyroid Disease/Hypothyroidism and Autoimmune Exocrinopathy of the Salivary Gland

New Murine Model of Early Onset Autoimmune Thyroid Disease/Hypothyroidism and Autoimmune Exocrinopathy of the Salivary Gland

ENDOCRINE TUMOURS: Advances in the molecular pathogenesis of thyroid cancer: lessons from the cancer genome

The miR-146b-3p/PAX8/NIS Regulatory Circuit Modulates the Differentiation Phenotype and Function of Thyroid Cells during Carcinogenesis

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