Search for Articles:
Title / Keyword
Author / Affiliation / Email
Journal
Article Type
 
 
Advanced Search
 
Section
Special Issue
Volume
Issue
Number
Page
 
5.1
3.5
Journals
Genes
Special Issues
Genetic Perspectives in Thyroid Cancer
share announcement

Genetic Perspectives in Thyroid Cancer

A special issue of Genes (ISSN 2073-4425). This special issue belongs to the section "Human Genomics and Genetic Diseases".

Deadline for manuscript submissions: closed (31 July 2020) | Viewed by 20333

Printed Edition Available!
A printed edition of this Special Issue is available here.

Special Issue Editor

Dr. Susana Nunes Silva

E-Mail Website
Guest Editor
Centre for Toxicogenomics and Human Health, Genetics, Oncology and Human Toxicology, NOVA Medical School| Faculdade de Ciências Médicas, Universidade Nova de Lisboa, 1070 Lisboa, Portugal
Interests: breast cancer; thyroid cancer; genetic susceptibiliy; genetic variants; DNA repair

Special Issue Information

Dear Colleagues,

“Genetic Perspectives in Thyroid Cancer” is an issue that intends to cover several topics on thyroid cancer, including genetic analysis, genome sequence analysis, genome-wide analysis, gene expression regulation and also metabolomics and proteomics.

Thyroid cancer is an uncommon type of cancer, but it is one of the most common endocrine malignancies, with rising incidence over the last few decades. The aetiology of thyroid cancer is multifactorial, and radiation is the best documented risk factor related to the disease. Further risk factors have been hypothesized; however, we have yet to gather a wide range of information that will help us better understand the genetic mechanisms of thyroid cancer. The influence of genetics in the clinic and in therapeutics has been improved based on retrospective and prospective studies published worldwide in the last few decades, but the development of high through-put approaches has also been crucial.

The new advances in high through-put methodologies as Next Generation Sequencing will open the door to new genetic variants that will help to clarify genotype-phenotype correlations, new gene associations, new genetic targets useful as potential biomarkers, and so on. The new decade that now begins might provide new evidences for the disease—for which we count on you.

This Special Issue aims to reach new findings based on genetic evidences in thyroid cancer as expressed in case-studies, molecular approaches, and hereditary evidences, clinical and therapeutic developments. We would like to invite manuscripts that will help us broadly deepen our understanding of thyroid genetics.

Dr. Susana Nunes Silva
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. Genes is an international peer-reviewed open access monthly 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 2600 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
  • Genetic variants
  • Thyroid Omics
  • Biomarkers
  • Susceptibility
  • Risk Factors

Published Papers (7 papers)

Download All Papers
Order results
Result details
Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:

Editorial

Jump to: Research, Review

2 pages, 167 KiB  
Editorial
Special Issue: Genetic Perspectives in Thyroid Cancer
by Susana Nunes Silva
Genes 2021, 12(2), 126; https://0-doi-org.brum.beds.ac.uk/10.3390/genes12020126 - 20 Jan 2021
Cited by 5 | Viewed by 1662
Abstract
Thyroid cancer is not just a common type of cancer, it is the most frequently diagnosed endocrine malignancy worldwide [...] Full article
(This article belongs to the Special Issue Genetic Perspectives in Thyroid Cancer)

Research

Jump to: Editorial, Review

24 pages, 1265 KiB  
Article
Micronuclei Formation upon Radioiodine Therapy for Well-Differentiated Thyroid Cancer: The Influence of DNA Repair Genes Variants
by Luís S. Santos, Octávia M. Gil, Susana N. Silva, Bruno C. Gomes, Teresa C. Ferreira, Edward Limbert and José Rueff
Genes 2020, 11(9), 1083; https://0-doi-org.brum.beds.ac.uk/10.3390/genes11091083 - 17 Sep 2020
Cited by 7 | Viewed by 2906
Abstract
Radioiodine therapy with 131I remains the mainstay of standard treatment for well-differentiated thyroid cancer (DTC). Prognosis is good but concern exists that 131I-emitted ionizing radiation may induce double-strand breaks in extra-thyroidal tissues, increasing the risk of secondary malignancies. We, therefore, sought [...] Read more.
Radioiodine therapy with 131I remains the mainstay of standard treatment for well-differentiated thyroid cancer (DTC). Prognosis is good but concern exists that 131I-emitted ionizing radiation may induce double-strand breaks in extra-thyroidal tissues, increasing the risk of secondary malignancies. We, therefore, sought to evaluate the induction and 2-year persistence of micronuclei (MN) in lymphocytes from 26 131I-treated DTC patients and the potential impact of nine homologous recombination (HR), non-homologous end-joining (NHEJ), and mismatch repair (MMR) polymorphisms on MN levels. MN frequency was determined by the cytokinesis-blocked micronucleus assay while genotyping was performed through pre-designed TaqMan® Assays or conventional PCR-restriction fragment length polymorphism (RFLP). MN levels increased significantly one month after therapy and remained persistently higher than baseline for 2 years. A marked reduction in lymphocyte proliferation capacity was also apparent 2 years after therapy. MLH1 rs1799977 was associated with MN frequency (absolute or net variation) one month after therapy, in two independent groups. Significant associations were also observed for MSH3 rs26279, MSH4 rs5745325, NBN rs1805794, and tumor histotype. Overall, our results suggest that 131I therapy may pose a long-term challenge to cells other than thyrocytes and that the individual genetic profile may influence 131I sensitivity, hence its risk-benefit ratio. Further studies are warranted to confirm the potential utility of these single nucleotide polymorphisms (SNPs) as radiogenomic biomarkers in the personalization of radioiodine therapy. Full article
(This article belongs to the Special Issue Genetic Perspectives in Thyroid Cancer)
►▼ Show Figures

Figure 1

13 pages, 513 KiB  
Article
Association between Family Histories of Thyroid Cancer and Thyroid Cancer Incidence: A Cross-Sectional Study Using the Korean Genome and Epidemiology Study Data
by Soo-Hwan Byun, Chanyang Min, Hyo-Geun Choi and Seok-Jin Hong
Genes 2020, 11(9), 1039; https://0-doi-org.brum.beds.ac.uk/10.3390/genes11091039 - 03 Sep 2020
Cited by 8 | Viewed by 2392
Abstract
This study assessed the association between thyroid cancer and family history. This cross-sectional study used epidemiological data from the Korean Genome and Epidemiology Study from 2001 to 2013. Among 211,708 participants, 988 were in the thyroid cancer group and 199,588 were in the [...] Read more.
This study assessed the association between thyroid cancer and family history. This cross-sectional study used epidemiological data from the Korean Genome and Epidemiology Study from 2001 to 2013. Among 211,708 participants, 988 were in the thyroid cancer group and 199,588 were in the control group. Trained interviewers questioned the participants to obtain their thyroid cancer history and age at onset. The participants were examined according to their age, sex, monthly household income, obesity, smoking, alcohol consumption, and past medical history. The adjusted odds ratios (95% confidence intervals) for the family histories of fathers, mothers, and siblings were 6.59 (2.05–21.21), 4.76 (2.59–8.74), and 9.53 (6.92–13.11), respectively, and were significant. The results for the subgroup analyses according to sex were consistent. The rate of family histories of thyroid cancer for fathers and siblings were not different according to the thyroid cancer onset, while that of mothers were higher in participants with a younger age at onset (<50 years old group, 11/523 [2.1%], p = 0.007). This study demonstrated that thyroid cancer incidence was associated with thyroid cancer family history. This supports regular examination of individuals with a family history of thyroid cancer to prevent disease progression and ensure early management. Full article
(This article belongs to the Special Issue Genetic Perspectives in Thyroid Cancer)
►▼ Show Figures

Graphical abstract

22 pages, 6746 KiB  
Article
Biomarkers, Master Regulators and Genomic Fabric Remodeling in a Case of Papillary Thyroid Carcinoma
by Dumitru A. Iacobas
Genes 2020, 11(9), 1030; https://0-doi-org.brum.beds.ac.uk/10.3390/genes11091030 - 02 Sep 2020
Cited by 11 | Viewed by 3121
Abstract
Publicly available (own) transcriptomic data have been analyzed to quantify the alteration in functional pathways in thyroid cancer, establish the gene hierarchy, identify potential gene targets and predict the effects of their manipulation. The expression data have been generated by profiling one case [...] Read more.
Publicly available (own) transcriptomic data have been analyzed to quantify the alteration in functional pathways in thyroid cancer, establish the gene hierarchy, identify potential gene targets and predict the effects of their manipulation. The expression data have been generated by profiling one case of papillary thyroid carcinoma (PTC) and genetically manipulated BCPAP (papillary) and 8505C (anaplastic) human thyroid cancer cell lines. The study used the genomic fabric paradigm that considers the transcriptome as a multi-dimensional mathematical object based on the three independent characteristics that can be derived for each gene from the expression data. We found remarkable remodeling of the thyroid hormone synthesis, cell cycle, oxidative phosphorylation and apoptosis pathways. Serine peptidase inhibitor, Kunitz type, 2 (SPINT2) was identified as the Gene Master Regulator of the investigated PTC. The substantial increase in the expression synergism of SPINT2 with apoptosis genes in the cancer nodule with respect to the surrounding normal tissue (NOR) suggests that SPINT2 experimental overexpression may force the PTC cells into apoptosis with a negligible effect on the NOR cells. The predictive value of the expression coordination for the expression regulation was validated with data from 8505C and BCPAP cell lines before and after lentiviral transfection with DDX19B. Full article
(This article belongs to the Special Issue Genetic Perspectives in Thyroid Cancer)
►▼ Show Figures

Figure 1

13 pages, 2383 KiB  
Article
VEGFA and NFE2L2 Gene Expression and Regulation by MicroRNAs in Thyroid Papillary Cancer and Colloid Goiter
by Leonardo P. Stuchi, Márcia Maria U. Castanhole-Nunes, Nathália Maniezzo-Stuchi, Patrícia M. Biselli-Chicote, Tiago Henrique, João Armando Padovani Neto, Dalisio de-Santi Neto, Ana Paula Girol, Erika C. Pavarino and Eny Maria Goloni-Bertollo
Genes 2020, 11(9), 954; https://0-doi-org.brum.beds.ac.uk/10.3390/genes11090954 - 19 Aug 2020
Cited by 18 | Viewed by 2804
Abstract
Deregulation of VEGFA (Vascular Endothelial Growth Factor A) and NFE2L2 (Nuclear Factor (Erythroid-derived 2)-Like 2), involved in angiogenesis and oxidative stress, can lead to thyroid cancer progression. MiR-17-5p and miR-612 are possible regulators of these genes and may promote thyroid disorders. In order [...] Read more.
Deregulation of VEGFA (Vascular Endothelial Growth Factor A) and NFE2L2 (Nuclear Factor (Erythroid-derived 2)-Like 2), involved in angiogenesis and oxidative stress, can lead to thyroid cancer progression. MiR-17-5p and miR-612 are possible regulators of these genes and may promote thyroid disorders. In order to evaluate the involvement of VEGFA, NFE2L2, hsa-miR-17-5p, and hsa-miR-612 in thyroid pathology, we examined tissue samples from colloid goiter, papillary thyroid cancer (PTC), and a normal thyroid. We found higher levels of VEGFA and NFE2L2 transcripts and the VEGFA protein in goiter and PTC samples than in normal tissue. In the goiter, miR-612 and miR-17-5p levels were lower than those in PTC. Tumors, despite showing lower VEGFA mRNA expression, presented higher VEGFA protein levels compared to goiter tissue. In addition, NRF2 (Nuclear Related Transcription Factor 2) protein levels in tumors were higher than those in goiter and normal tissues. Inhibition of miR-17-5p resulted in reduced NFE2L2 expression. Overall, both transcript and protein levels of NFE2L2 and VEGFA were elevated in PTC and colloid goiter. Hsa-miR-612 showed differential expression in PTC and colloid goiter, while hsa-miR-17-5p showed differential expression only in colloid goiter, suggesting that hsa-miR-17-5p may be a positive regulator of NFE2L2 expression in PTC. Full article
(This article belongs to the Special Issue Genetic Perspectives in Thyroid Cancer)
►▼ Show Figures

Figure 1

Review

Jump to: Editorial, Research

21 pages, 342 KiB  
Review
Genetic Mutations and Variants in the Susceptibility of Familial Non-Medullary Thyroid Cancer
by Fabíola Yukiko Miasaki, Cesar Seigi Fuziwara, Gisah Amaral de Carvalho and Edna Teruko Kimura
Genes 2020, 11(11), 1364; https://0-doi-org.brum.beds.ac.uk/10.3390/genes11111364 - 18 Nov 2020
Cited by 9 | Viewed by 3671
Abstract
Thyroid cancer is the most frequent endocrine malignancy with the majority of cases derived from thyroid follicular cells and caused by sporadic mutations. However, when at least two or more first degree relatives present thyroid cancer, it is classified as familial non-medullary thyroid [...] Read more.
Thyroid cancer is the most frequent endocrine malignancy with the majority of cases derived from thyroid follicular cells and caused by sporadic mutations. However, when at least two or more first degree relatives present thyroid cancer, it is classified as familial non-medullary thyroid cancer (FNMTC) that may comprise 3–9% of all thyroid cancer. In this context, 5% of FNMTC are related to hereditary syndromes such as Cowden and Werner Syndromes, displaying specific genetic predisposition factors. On the other hand, the other 95% of cases are classified as non-syndromic FNMTC. Over the last 20 years, several candidate genes emerged in different studies of families worldwide. Nevertheless, the identification of a prevalent polymorphism or germinative mutation has not progressed in FNMTC. In this work, an overview of genetic alteration related to syndromic and non-syndromic FNMTC is presented. Full article
(This article belongs to the Special Issue Genetic Perspectives in Thyroid Cancer)
►▼ Show Figures

Figure 1

9 pages, 1087 KiB  
Review
Actions of L-thyroxine (T4) and Tetraiodothyroacetic Acid (Tetrac) on Gene Expression in Thyroid Cancer Cells
by Paul J. Davis, Hung-Yun Lin, Aleck Hercbergs and Shaker A. Mousa
Genes 2020, 11(7), 755; https://0-doi-org.brum.beds.ac.uk/10.3390/genes11070755 - 07 Jul 2020
Cited by 7 | Viewed by 3169
Abstract
The clinical behavior of thyroid cancers is seen to reflect inherent transcriptional activities of mutated genes and trophic effects on tumors of circulating pituitary thyrotropin (TSH). The thyroid hormone, L-thyroxine (T4), has been shown to stimulate proliferation of a large number of different [...] Read more.
The clinical behavior of thyroid cancers is seen to reflect inherent transcriptional activities of mutated genes and trophic effects on tumors of circulating pituitary thyrotropin (TSH). The thyroid hormone, L-thyroxine (T4), has been shown to stimulate proliferation of a large number of different forms of cancer. This activity of T4 is mediated by a cell surface receptor on the extracellular domain of integrin αvβ3. In this brief review, we describe what is known about T4 as a circulating trophic factor for differentiated (papillary and follicular) thyroid cancers. Given T4′s cancer-stimulating activity in differentiated thyroid cancers, it was not surprising to find that genomic actions of T4 were anti-apoptotic. Transduction of the T4-generated signal at the integrin primarily involved mitogen-activated protein kinase (MAPK). In thyroid C cell-origin medullary carcinoma of the thyroid (MTC), effects of thyroid hormone analogues, such as tetraiodothyroacetic acid (tetrac), include pro-angiogenic and apoptosis-linked genes. Tetrac is an inhibitor of the actions of T4 at αvβ3, and it is assumed, but not yet proved, that the anti-angiogenic and pro-apoptotic actions of tetrac in MTC cells are matched by T4 effects that are pro-angiogenic and anti-apoptotic. We also note that papillary thyroid carcinoma cells may express the leptin receptor, and circulating leptin from adipocytes may stimulate tumor cell proliferation. Transcription was stimulated by leptin in anaplastic, papillary, and follicular carcinomas of genes involved in invasion, such as matrix metalloproteinases (MMPs). In summary, thyroid hormone analogues may act at their receptor on integrin αvβ3 in a variety of types of thyroid cancer to modulate transcription of genes relevant to tumor invasiveness, apoptosis, and angiogenesis. These effects are independent of TSH. Full article
(This article belongs to the Special Issue Genetic Perspectives in Thyroid Cancer)
►▼ Show Figures

Figure 1

Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:
 
Displaying articles 1-7
Back to TopTop