Genomic Instability as Mechanism in Thyroid Cancer Development

preprint OA: closed CC-BY-4.0
AI-generated deep summary by claude@2026-06, 2026-06-24 · read from full text

This preprint review investigates how genomic instability contributes to thyroid cancer development by synthesizing cytogenetic and molecular evidence on genetic mutations and chromosomal aberrations in both benign and malignant thyroid lesions. The authors report that accumulated genomic alterations disrupt key signaling pathways, shaping tumor phenotype and behavior across stages of progression, and they note that improved diagnostics are identifying novel gene variants and molecular profiles linked to distinct tumor phenotypes. A stated limitation is that the work is an analysis of existing cytogenetic and molecular studies (i.e., a synthesized, non-experimental review) without presenting new primary datasets. This paper does not explicitly discuss endometriosis or adenomyosis; it was included in the corpus via a keyword match in the upstream search index.

Read from the paper's body, not the abstract. Not a substitute for reading the paper. No clinical advice. How this works

Abstract

Introduction: Thyroid cancer arises in the context of numerous risk factors that reflect the intrinsically high proliferative potential of thyroid follicular cells. Among these factors, genomic instability has emerged as a fundamental mechanism driving thyroid tumorigenesis. Objective: This review aims to elucidate the role of genomic instability in the pathogenesis of thyroid cancer, examining the molecular alterations and key oncogenes implicated in tumor initiation and progression. Methods: An analysis of current cytogenetic and molecular studies was conducted to synthesize the knowledge surrounding genetic mutations and chromosomal aberrations associated with both benign and malignant thyroid lesions. Results: Genomic instability contributes significantly to thyroid tumor development through the accumulation of genetic alterations affecting crucial signaling pathways. These alterations influence tumor phenotype and behavior across different stages of progression. Moreover, advances in diagnostic technologies have improved the identification of novel gene variants and the characterization of molecular profiles linked to specific thyroid tumor phenotypes. Conclusion: Understanding the molecular underpinnings of genomic instability offers critical insights into thyroid carcinogenesis and highlights potential targets for diagnostic and therapeutic refinement. The principal oncogenes driving this process represent promising focal points for future research.
Full text 7,838 characters · extracted from preprint-html · click to expand
Genomic Instability as Mechanism in Thyroid Cancer Development | SciELO Preprints window.dataLayer = window.dataLayer || []; function gtag(){dataLayer.push(arguments);} gtag('js', new Date()); gtag('config', 'G-3TT8HYRH0Y'); Open Menu Registrar-se Acesso English Español Ir para o conteúdo principal Ir para o menu de navegação principal Ir para o rodapé Preprints Submissão Áreas do Conhecimento Ciências Agrárias Ciências Biológicas Ciências da Saúde Ciências Exatas e da Terra Ciências Humanas Ciências Sociais Aplicadas Engenharias Linguística, letras e artes Educação em Revista Memórias do Instituto Oswaldo Cruz 47º Encontro Anual da ANPOCS 48º Encontro Anual da ANPOCS 49º Encontro Anual da ANPOCS Sobre Sobre o Servidor Declaração de Privacidade Atualizações do Sistema Contato FAQ Ética no SciELO Preprints Avaliação de preprints Anotações em preprints (via Hypothesis) Avalie um preprint Notícias Início / Ciências da Saúde Preprint / Versão 1 Genomic Instability as Mechanism in Thyroid Cancer Development article.authors6a108c639f231 Luis Jesuino de Oliveira Andrade Universidade Estadual de Santa Cruz image/svg+xml .st0{fill:#A6CE39;} .st1{fill:#FFFFFF;} https://orcid.org/0000-0002-7714-0330 Conceptualization Data Curation Formal Analysis Investigation Methodology Supervision Writing – Original Draft Preparation Validation Visualization Writing – Review & Editing Gabriela Correia Matos de Oliveira José Silveira Foundation, Salvador, Bahia, Brazil .st0{fill:#A6CE39;} .st1{fill:#FFFFFF;} https://orcid.org/0000-0002-3447-3143 Data Curation Formal Analysis Investigation Methodology Supervision Validation Visualization Writing – Original Draft Preparation Paulo Roberto Santana de Melo Universidade Estadual de Santa Cruz image/svg+xml .st0{fill:#A6CE39;} .st1{fill:#FFFFFF;} https://orcid.org/0000-0002-4486-0200 Formal Analysis Methodology Visualization Writing – Original Draft Preparation Alcina Maria Vinhaes Bittencourt Universidade Federal da Bahia image/svg+xml .st0{fill:#A6CE39;} .st1{fill:#FFFFFF;} https://orcid.org/0000-0003-0506-9210 Formal Analysis Methodology Validation Visualization Osmário Jorge de Mattos Salles Escola Bahiana de Medicina e Saúde Pública image/svg+xml .st0{fill:#A6CE39;} .st1{fill:#FFFFFF;} https://orcid.org/0009-0002-1859-0478 Formal Analysis Methodology Validation Writing – Original Draft Preparation Visualization Luis Matos de Oliveira Universidade Estadual de Santa Cruz image/svg+xml .st0{fill:#A6CE39;} .st1{fill:#FFFFFF;} https://orcid.org/0000-0003-4854-6910 Conceptualization Data Curation Formal Analysis Investigation Methodology Supervision Validation Visualization Writing – Original Draft Preparation Writing – Review & Editing DOI: https://doi.org/10.1590/SciELOPreprints.13276 Palavras-chave: Thyroid cancer, Tumorigenesis, Genomic. Resumo Introduction : Thyroid cancer arises in the context of numerous risk factors that reflect the intrinsically high proliferative potential of thyroid follicular cells. Among these factors, genomic instability has emerged as a fundamental mechanism driving thyroid tumorigenesis. Objective : This review aims to elucidate the role of genomic instability in the pathogenesis of thyroid cancer, examining the molecular alterations and key oncogenes implicated in tumor initiation and progression. Methods: An analysis of current cytogenetic and molecular studies was conducted to synthesize the knowledge surrounding genetic mutations and chromosomal aberrations associated with both benign and malignant thyroid lesions. Results : Genomic instability contributes significantly to thyroid tumor development through the accumulation of genetic alterations affecting crucial signaling pathways. These alterations influence tumor phenotype and behavior across different stages of progression. Moreover, advances in diagnostic technologies have improved the identification of novel gene variants and the characterization of molecular profiles linked to specific thyroid tumor phenotypes. Conclusion: Understanding the molecular underpinnings of genomic instability offers critical insights into thyroid carcinogenesis and highlights potential targets for diagnostic and therapeutic refinement. The principal oncogenes driving this process represent promising focal points for future research. Downloads Os dados de download ainda não estão disponíveis. PDF Postado 10/11/2025 Como Citar Genomic Instability as Mechanism in Thyroid Cancer Development. (2025). Em SciELO Preprints . https://doi.org/10.1590/SciELOPreprints.13276 Formatos de Citação ACM ACS APA ABNT Chicago Harvard IEEE MLA Turabian Vancouver Baixar Citação Endnote/Zotero/Mendeley (RIS) BibTeX Série Ciências da Saúde Copyright (c) 2025 Luis Jesuino de Oliveira Andrade, Gabriela Correia Matos de Oliveira , Paulo Roberto Santana de Melo, Alcina Maria Vinhaes Bittencourt, Osmário Jorge de Mattos Salles , Luis Matos de Oliveira Este trabalho está licenciado sob uma licença Creative Commons Attribution 4.0 International License . .citations-container { overflow-y: auto; overflow-x: hidden; max-height: 1000px; } Plaudit Declaração de dados Os dados de pesquisa estão contidos no próprio manuscrito Aviso de preprints Preprints são manuscritos não avaliados por um periódico científico ou já avaliados mas em processo de publicação. .block_announcements_article:not(:last-child) { padding-bottom: 1.5em; border-bottom: 1px solid; } .block_announcements_article { text-align: left; } .block_announcements #show-all{ font-style: italic; } Notícias SciELO Preprints adota obrigatoriedade de declaração de disponibilização de dados de pesquisa 19 agosto 2025 A partir de 1º de setembro de 2025 os manuscritos submetidos ao SciELO Preprints devem incluir uma declaração de disponibilidade de dados informando sobre onde e como os dados da pesquisa que deram origem ao artigo podem ser acessados. Atualização da Política Editorial e FAQ 21 maio 2025 Todos(as) os(as) autores(as) são solicitados(as) a consultarem a nossa Política Editorial e nossas FAQs antes de submeterem o seu manuscrito. Prêmio Ben Barres Spotlight: Inscrições abertas para 2024 20 maio 2024 Prêmios de até US$ 5.000 estão agora disponíveis para pesquisadores de origens sub-representadas ou países com financiamento limitado para apoiar sua pesquisa, carreira e comunidade. Preprints do SciELO Preprints nas ciências da vida ou biomédicas com pelo menos uma revisão disponível no Sciety são elegíveis! Show all announcements ... SciELO - Scientific Electronic Library Online Rua Dr. Diogo de Faria, 1087 – 9º andar – Vila Clementino 04037-003 São Paulo/SP - Brasil E-mail: [email protected] app = {"hypothesisHandlerUrl":"https:\/\/preprints.scielo.org\/index.php\/scielo\/$$$call$$$\/plugins\/generic\/hypothesis\/controllers\/hypothesis\/"}; var pkpUsageStats = pkpUsageStats || {};pkpUsageStats.data = pkpUsageStats.data || {};pkpUsageStats.data.Submission = pkpUsageStats.data.Submission || {};pkpUsageStats.data.Submission[13276] = {"data":{"2025":{"11":"50","12":"11"},"2026":{"1":"16","2":"4","3":"9","4":"15","5":"17"}},"label":"Todos os downloads","color":"79,181,217","total":122}; var pkpUsageStats = pkpUsageStats || {};pkpUsageStats.locale = pkpUsageStats.locale || {};pkpUsageStats.locale.months = ["Jan","Fev","Mar","Abr","Mai","Jun","Jul","Ago","Set","Out","Nov","Dez"];pkpUsageStats.config = pkpUsageStats.config || {};pkpUsageStats.config.chartType = "bar"; (function (w, d, s, l, i) { w[l] = w[l] || []; var f = d.getElementsByTagName(s)[0], j = d.createElement(s), dl = l != 'dataLayer' ? '&l=' + l : ''; j.async = true; j.src = 'https://www.googletagmanager.com/gtag/js?id=' + i + dl; f.parentNode.insertBefore(j, f); function gtag(){dataLayer.push(arguments)}; gtag('js', new Date()); gtag('config', i); }) (window, document, 'script', 'dataLayer', '3TT8HYRH0Y');

Text is read by the "Ask this paper" AI Q&A widget below. Extraction quality varies by source — PMC NXML preserves structure cleanly, OA-HTML may include some navigation residue, and OA-PDF can have broken hyphenation. The publisher copy (via DOI) is the canonical version.

My notes (saved in your browser only)

Ask this paper AI returns verbatim quotes from the full text · source: preprint-html

Answers must be backed by verbatim quotes from this paper's full text. Hallucinated quotes are dropped automatically; if no verbatim passage answers the question, we say so. How this works

Citation neighborhood (no data yet)

We don't have any in-corpus citations linked to this paper yet. This is a recent paper (2025) — citers typically take a year or two to land, and the OpenAlex reference graph may still be filling in.

Source provenance

europepmc
last seen: 2026-05-20T01:45:00.602351+00:00
unpaywall
last seen: 2026-05-22T02:00:06.705733+00:00
License: CC-BY-4.0