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Cells
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Changes in Thyrocytes during Thyroid Disease and Thyroid Cancer
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Changes in Thyrocytes during Thyroid Disease and Thyroid Cancer

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cellular Pathology".

Deadline for manuscript submissions: closed (30 June 2024) | Viewed by 3998

Special Issue Editor

Prof. Dr. Artur Bossowski

E-Mail Website
Guest Editor
Department of Pediatrics, Endocrinology, Diabetology with Cardiology Divisions, Faculty of Medicine, Medical University of Bialystok, Białystok, Poland
Interests: pediatric endocrinology; diabetology; thyroid diseases
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The main objective of this research topic is to provide an update on the most important topics of thyroid molecular pathology, with particular attention to innovations in the field of pathogenesis, diagnosis, and treatment strategies for hyper- and hypothyroidism, autoimmune thyroid diseases, thyroid nodules, and cancer. Moreover, the experiences with the peculiarity of thyroid molecular pathology in genetic syndromes and in chronic diseases will also be addressed. In addition, we are interested in the topic of comorbidities in autoimmune thyroid diseases and thyroid cancer.

We look forward to receiving your contributions.

Prof. Dr. Artur Bossowski
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Cells is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • thyroid cancer
  • thyroid nodules
  • hypothyroidism
  • hyperthyroidism
  • immunogenetic markers
  • molecular pathways for autoimmune thyroid diseases
  • therapeutic approaches

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Published Papers (2 papers)

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Research

12 pages, 2031 KiB  
Article
Expression of pY397-FAK and Its miR Regulators Drive Dedifferentiation in the Thyroid Neoplasia Spectrum
by Valentina Ignjatović Jocić, Jelena Janković Miljuš, Tijana Išić Denčić, Vladan Živaljević, Svetislav Tatić, Ilona Đorić and Sonja Šelemetjev
Cells 2023, 12(13), 1721; https://doi.org/10.3390/cells12131721 - 26 Jun 2023
Cited by 1 | Viewed by 1275
Abstract
Thyroid carcinomas are growing malignancies worldwide. They encompass several diagnostic categories with varying degrees of dedifferentiation. Focal adhesion kinase is involved in cellular communication and locomotion. It is regulated on a posttranscriptional level by miR-7, miR-135a, and miR-138 and on a posttranslational level [...] Read more.
Thyroid carcinomas are growing malignancies worldwide. They encompass several diagnostic categories with varying degrees of dedifferentiation. Focal adhesion kinase is involved in cellular communication and locomotion. It is regulated on a posttranscriptional level by miR-7, miR-135a, and miR-138 and on a posttranslational level by autophosphorylation at Y397 (pY397-FAK). We related regulators of FAK with histologic dedifferentiation, clinicopathological factors, and differential diagnosis in the thyroid neoplasia spectrum. We classified 82 cases into 5 groups with increasing aggressiveness: healthy tissue, follicular and classical variants of papillary thyroid carcinoma (PTC), dedifferentiated PTC, and anaplastic carcinoma. MiRs were analyzed by RT-qPCR. Protein expression of pY397-FAK was analyzed by immunohistochemistry (separately in the membrane, cytoplasm, and nuclear compartment) and Western blot. All three miRs were upregulated in healthy tissue compared to malignant, while pY397-FAK was downregulated. MiRs and pY397-FAK were not mutually correlated. MiR-135a-5p was decreasing while membranous and cytoplasmic pY397-FAK increased with dedifferentiation. Neither miR correlated with clinicopathological factors. MiR-135a-5p, miR-138-5p, and membranous and cytoplasmic pY397-FAK discriminated the follicular from the classical variant of PTC. Disturbances of FAK regulation on different levels contribute to neoplastic dedifferentiation. pY397-FAK exerts its oncogenic role in the membrane and cytoplasm. Diagnostically, miRs-135a-5p, miR-138-5p, and membranous and cytoplasmic pY397-FAK differentiated between classical and follicular PTC. Full article
(This article belongs to the Special Issue Changes in Thyrocytes during Thyroid Disease and Thyroid Cancer)
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16 pages, 4237 KiB  
Article
Identification of R-Spondin Gene Signature Predictive of Metastatic Progression in BRAFV600E-Positive Papillary Thyroid Cancer
by Sabrina Daniela da Silva, Grégoire B. Morand, Luciana Diesel, Jefferson Muniz de Lima, Krikor Bijian, Senthilkumar Kailasam, Francois Lefebvre, Guillaume Bourque, Michael Hier and Moulay A. Alaoui-Jamali
Cells 2023, 12(1), 139; https://doi.org/10.3390/cells12010139 - 29 Dec 2022
Cited by 2 | Viewed by 1877
Abstract
Papillary thyroid carcinoma (PTC) is the most common malignancy of the thyroid gland and early stages are curable. However, a subset of PTCs shows an unusually aggressive phenotype with extensive lymph node metastasis and higher incidence of locoregional recurrence. In this study, we [...] Read more.
Papillary thyroid carcinoma (PTC) is the most common malignancy of the thyroid gland and early stages are curable. However, a subset of PTCs shows an unusually aggressive phenotype with extensive lymph node metastasis and higher incidence of locoregional recurrence. In this study, we investigated a large cohort of PTC cases with an unusual aggressive phenotype using a high-throughput RNA sequencing (RNA-Seq) to identify differentially regulated genes associated with metastatic PTC. All metastatic PTC with mutated BRAF (V600E) but not BRAF wild-type expressed an up-regulation of R-Spondin Protein 4 (RSPO4) concomitant with an upregulation of genes involved in focal adhesion and cell-extracellular matrix signaling. Further immunohistochemistry validation confirmed the upregulation of these target genes in metastatic PTC cases. Preclinical studies using established PTC cell lines support that RSPO4 overexpression is associated with BRAF V600E mutation and is a critical upstream event that promote activation of kinases of focal adhesion signaling known to drive cancer cell locomotion and invasion. This finding opens up the potential of co-targeting B-Raf, RSPO and focal adhesion proteins as a pharmacological approach for aggressive BRAF V600E PTC. Full article
(This article belongs to the Special Issue Changes in Thyrocytes during Thyroid Disease and Thyroid Cancer)
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