Aspectos moleculares del carcinoma papilar de tiroides
Autor(a) principal: | |
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Data de Publicação: | 2023 |
Outros Autores: | , , |
Tipo de documento: | Artigo |
Idioma: | por |
Título da fonte: | Research, Society and Development |
Texto Completo: | https://rsdjournal.org/index.php/rsd/article/view/39986 |
Resumo: | Introduction: Thyroid cancer is the most common endocrine neoplasm. The pathogenesis of thyroid cancer considers mutations leading to progression through a process of dedifferentiation generating well-differentiated carcinomas, such as papillary and follicular, and progressing to poorly differentiated, undifferentiated or anaplastic thyroid carcinomas. Objective: To describe the main molecular alterations for the development of PTC. Methodology: This is a narrative review. The databases PUBMED, SCIELO, Science Direct, Google Scholar and the National Cancer Institute were used. As inclusion/exclusion criteria, articles comprised between 2004 and 2022, in Portuguese and English. Results and discussion: PTC molecular alterations arise from the initial mutation in some gene involved in the regulation of proliferation and/or cell differentiation, leading to clonal expansion of the genetically modified cell due to its ability to proliferate and escape cell cycle control through changes in genes such as BRAF, KRAS, NTRK1 and RET. Conclusion: The onset and progression of thyroid cancer comprises multiple genetic changes, including mutations that lead to activation of MAPK and PI3K-AKT signaling pathways. Altered genes that affect this pathway include mutations in genes encoding RAS and BRAF intracellular signal transducers and rearrangements in RET/PTC receptor tyrosine kinase. These data are extremely important for understanding the pathophysiological mechanism of this condition, as well as providing the basis for a more assertive diagnosis and more specific treatment, providing a more favorable prognosis with fewer side effects. |
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Aspectos moleculares del carcinoma papilar de tiroidesMolecular aspects of papillary thyroid carcinoma Aspectos moleculares do carcinoma papilífero de tireoideThyroid cancerPapillary thyroid carcinomaGene mutations.Cáncer de tiroidesCarcinoma papilar de tiroidesMutaciones genéticas.Câncer de tireoideCarcinoma papilífero da tireoideMutações gênicas.Introduction: Thyroid cancer is the most common endocrine neoplasm. The pathogenesis of thyroid cancer considers mutations leading to progression through a process of dedifferentiation generating well-differentiated carcinomas, such as papillary and follicular, and progressing to poorly differentiated, undifferentiated or anaplastic thyroid carcinomas. Objective: To describe the main molecular alterations for the development of PTC. Methodology: This is a narrative review. The databases PUBMED, SCIELO, Science Direct, Google Scholar and the National Cancer Institute were used. As inclusion/exclusion criteria, articles comprised between 2004 and 2022, in Portuguese and English. Results and discussion: PTC molecular alterations arise from the initial mutation in some gene involved in the regulation of proliferation and/or cell differentiation, leading to clonal expansion of the genetically modified cell due to its ability to proliferate and escape cell cycle control through changes in genes such as BRAF, KRAS, NTRK1 and RET. Conclusion: The onset and progression of thyroid cancer comprises multiple genetic changes, including mutations that lead to activation of MAPK and PI3K-AKT signaling pathways. Altered genes that affect this pathway include mutations in genes encoding RAS and BRAF intracellular signal transducers and rearrangements in RET/PTC receptor tyrosine kinase. These data are extremely important for understanding the pathophysiological mechanism of this condition, as well as providing the basis for a more assertive diagnosis and more specific treatment, providing a more favorable prognosis with fewer side effects.Introducción: El cáncer de tiroides es la neoplasia endocrina más común. La patogenia del cáncer de tiroides considera mutaciones que conducen a la progresión a través de un proceso de desdiferenciación que genera carcinomas bien diferenciados, como papilar y folicular, y progresa a carcinomas de tiroides pobremente diferenciados, indiferenciados o anaplásicos. Objetivo: Describir las principales alteraciones moleculares para el desarrollo de CPT. Metodología: Esta es una revisión narrativa. Se utilizaron las bases de datos PUBMED, SCIELO, Science Direct, Google Scholar y el Instituto Nacional del Cáncer. Se utilizaron como criterios de inclusión/exclusión artículos comprendidos entre 2004 y 2022, en portugués e inglés. Resultados y discusión: Las alteraciones moleculares del PTC surgen de la mutación inicial en algún gen involucrado en la regulación de la proliferación y/o diferenciación celular, dando lugar a la expansión clonal de la célula modificada genéticamente debido a su capacidad de proliferar y escapar al control del ciclo celular a través de cambios en genes como BRAF, KRAS, NTRK1 y RET. Conclusión: La aparición y progresión del cáncer de tiroides comprende múltiples cambios genéticos, incluidas mutaciones que conducen a la activación de las vías de señalización MAPK y PI3K-AKT. Los genes alterados que afectan esta vía incluyen mutaciones en genes que codifican transductores de señales intracelulares RAS y BRAF y reordenamientos en el receptor de tirosina cinasa RET/PTC. Estos datos son de suma importancia para comprender el mecanismo fisiopatológico de esta condición, además de brindar la base para un diagnóstico más asertivo y un tratamiento más específico, proporcionando un pronóstico más favorable con menos efectos secundarios.Introdução: O câncer de tireoide apresenta-se como a neoplasia endócrina mais frequente. A patogênese do câncer de tireoide considera mutações conduzindo à progressão através de um processo de desdiferenciação gerando carcinomas bem diferenciados, como papilar e folicular, e progredindo para carcinomas de tireoide pouco diferenciados, indiferenciados ou anaplásicos. Objetivo: Descrever as principais alterações moleculares para o desenvolvimento do CPT. Metodologia: Trata-se de uma revisão narrativa. Foram utilizadas as bases de dados, PUBMED, SCIELO, Science Direct, Google Acadêmico e Instituto Nacional de Câncer. Como critério de inclusão/exclusão, foram utilizados artigos compreendidos entre 2004 e 2022, nas línguas portuguesa e inglesa. Resultados e discussão: As alterações moleculares do PTC, surgem pela mutação inicial em algum gene envolvido na regulação de proliferação e/ou na diferenciação celular, levando a expansão clonal da célula geneticamente modificada devido a sua capacidade de proliferação e escape ao controle do ciclo celular através de alterações em genes, tais como, BRAF, KRAS, NTRK1 e RET. Conclusão: O início e a progressão do câncer de tireoide compreendem múltiplas alterações genéticas, das quais as mutações que levam à ativação das vias de sinalização MAPK e PI3K-AKT. Os genes alterados que afetam esta via incluem mutações nos genes que codificam transdutores de sinal intracelulares RAS e BRAF e rearranjos nos receptores tirosina quinase RET/PTC. Esses dados são de suma importância para a compreensão do mecanismo fisiopatológico desta condição, bem como oferecem a base para um diagnóstico mais assertivo e tratamento mais específico, propiciando um prognóstico mais favorável e com menos efeitos colaterais.Research, Society and Development2023-02-01info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionapplication/pdfhttps://rsdjournal.org/index.php/rsd/article/view/3998610.33448/rsd-v12i2.39986Research, Society and Development; Vol. 12 No. 2; e11812239986Research, Society and Development; Vol. 12 Núm. 2; e11812239986Research, Society and Development; v. 12 n. 2; e118122399862525-3409reponame:Research, Society and Developmentinstname:Universidade Federal de Itajubá (UNIFEI)instacron:UNIFEIporhttps://rsdjournal.org/index.php/rsd/article/view/39986/32821Copyright (c) 2023 Ana Cristina Carneiro Mendes; Larissa Carvalho Viegas; Leila Rodrigues Danziger; Eriston Vieira Gomeshttps://creativecommons.org/licenses/by/4.0info:eu-repo/semantics/openAccessMendes, Ana Cristina Carneiro Viegas, Larissa Carvalho Danziger, Leila Rodrigues Gomes, Eriston Vieira 2023-02-14T20:07:52Zoai:ojs.pkp.sfu.ca:article/39986Revistahttps://rsdjournal.org/index.php/rsd/indexPUBhttps://rsdjournal.org/index.php/rsd/oairsd.articles@gmail.com2525-34092525-3409opendoar:2023-02-14T20:07:52Research, Society and Development - Universidade Federal de Itajubá (UNIFEI)false |
dc.title.none.fl_str_mv |
Aspectos moleculares del carcinoma papilar de tiroides Molecular aspects of papillary thyroid carcinoma Aspectos moleculares do carcinoma papilífero de tireoide |
title |
Aspectos moleculares del carcinoma papilar de tiroides |
spellingShingle |
Aspectos moleculares del carcinoma papilar de tiroides Mendes, Ana Cristina Carneiro Thyroid cancer Papillary thyroid carcinoma Gene mutations. Cáncer de tiroides Carcinoma papilar de tiroides Mutaciones genéticas. Câncer de tireoide Carcinoma papilífero da tireoide Mutações gênicas. |
title_short |
Aspectos moleculares del carcinoma papilar de tiroides |
title_full |
Aspectos moleculares del carcinoma papilar de tiroides |
title_fullStr |
Aspectos moleculares del carcinoma papilar de tiroides |
title_full_unstemmed |
Aspectos moleculares del carcinoma papilar de tiroides |
title_sort |
Aspectos moleculares del carcinoma papilar de tiroides |
author |
Mendes, Ana Cristina Carneiro |
author_facet |
Mendes, Ana Cristina Carneiro Viegas, Larissa Carvalho Danziger, Leila Rodrigues Gomes, Eriston Vieira |
author_role |
author |
author2 |
Viegas, Larissa Carvalho Danziger, Leila Rodrigues Gomes, Eriston Vieira |
author2_role |
author author author |
dc.contributor.author.fl_str_mv |
Mendes, Ana Cristina Carneiro Viegas, Larissa Carvalho Danziger, Leila Rodrigues Gomes, Eriston Vieira |
dc.subject.por.fl_str_mv |
Thyroid cancer Papillary thyroid carcinoma Gene mutations. Cáncer de tiroides Carcinoma papilar de tiroides Mutaciones genéticas. Câncer de tireoide Carcinoma papilífero da tireoide Mutações gênicas. |
topic |
Thyroid cancer Papillary thyroid carcinoma Gene mutations. Cáncer de tiroides Carcinoma papilar de tiroides Mutaciones genéticas. Câncer de tireoide Carcinoma papilífero da tireoide Mutações gênicas. |
description |
Introduction: Thyroid cancer is the most common endocrine neoplasm. The pathogenesis of thyroid cancer considers mutations leading to progression through a process of dedifferentiation generating well-differentiated carcinomas, such as papillary and follicular, and progressing to poorly differentiated, undifferentiated or anaplastic thyroid carcinomas. Objective: To describe the main molecular alterations for the development of PTC. Methodology: This is a narrative review. The databases PUBMED, SCIELO, Science Direct, Google Scholar and the National Cancer Institute were used. As inclusion/exclusion criteria, articles comprised between 2004 and 2022, in Portuguese and English. Results and discussion: PTC molecular alterations arise from the initial mutation in some gene involved in the regulation of proliferation and/or cell differentiation, leading to clonal expansion of the genetically modified cell due to its ability to proliferate and escape cell cycle control through changes in genes such as BRAF, KRAS, NTRK1 and RET. Conclusion: The onset and progression of thyroid cancer comprises multiple genetic changes, including mutations that lead to activation of MAPK and PI3K-AKT signaling pathways. Altered genes that affect this pathway include mutations in genes encoding RAS and BRAF intracellular signal transducers and rearrangements in RET/PTC receptor tyrosine kinase. These data are extremely important for understanding the pathophysiological mechanism of this condition, as well as providing the basis for a more assertive diagnosis and more specific treatment, providing a more favorable prognosis with fewer side effects. |
publishDate |
2023 |
dc.date.none.fl_str_mv |
2023-02-01 |
dc.type.driver.fl_str_mv |
info:eu-repo/semantics/article info:eu-repo/semantics/publishedVersion |
format |
article |
status_str |
publishedVersion |
dc.identifier.uri.fl_str_mv |
https://rsdjournal.org/index.php/rsd/article/view/39986 10.33448/rsd-v12i2.39986 |
url |
https://rsdjournal.org/index.php/rsd/article/view/39986 |
identifier_str_mv |
10.33448/rsd-v12i2.39986 |
dc.language.iso.fl_str_mv |
por |
language |
por |
dc.relation.none.fl_str_mv |
https://rsdjournal.org/index.php/rsd/article/view/39986/32821 |
dc.rights.driver.fl_str_mv |
https://creativecommons.org/licenses/by/4.0 info:eu-repo/semantics/openAccess |
rights_invalid_str_mv |
https://creativecommons.org/licenses/by/4.0 |
eu_rights_str_mv |
openAccess |
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application/pdf |
dc.publisher.none.fl_str_mv |
Research, Society and Development |
publisher.none.fl_str_mv |
Research, Society and Development |
dc.source.none.fl_str_mv |
Research, Society and Development; Vol. 12 No. 2; e11812239986 Research, Society and Development; Vol. 12 Núm. 2; e11812239986 Research, Society and Development; v. 12 n. 2; e11812239986 2525-3409 reponame:Research, Society and Development instname:Universidade Federal de Itajubá (UNIFEI) instacron:UNIFEI |
instname_str |
Universidade Federal de Itajubá (UNIFEI) |
instacron_str |
UNIFEI |
institution |
UNIFEI |
reponame_str |
Research, Society and Development |
collection |
Research, Society and Development |
repository.name.fl_str_mv |
Research, Society and Development - Universidade Federal de Itajubá (UNIFEI) |
repository.mail.fl_str_mv |
rsd.articles@gmail.com |
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1797052617436692480 |