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DOI: 10.1055/s-0042-1743555
The Role of Transforming Growth Factor Beta and Smad Receptors in Determining Prognosis in High-Grade Primary Brain Tumors: Glioblastoma Multiforme
O papel do fator de crescimento transformador beta e receptores smad na determinação do prognóstico em tumores cerebrais primários de alto grau: glioblastoma multiforme
Abstract
Introduction High-grade primary brain tumors cause serious morbidity and mortality. This study aimed to investigate the role of transforming growth factor beta (TGF-β) and suppressor of mothers against decapentaplegic (Smad) receptors in high-grade primary brain tumors.
Material and Method Thirteen patients with a pathological diagnosis of glioblastoma multiforme were included in the study. Pathological preparations of each patient were analyzed retrospectively in histochemistry and immunohistochemistry laboratories. Transforming growth factor beta 1, TGF-β2, TGF-β3, Smad 1/2/3, Smad 6, and Smad 7 stainings were evaluated, and the immunoreactivity densities were examined.
Result We found out an increase in the expression of TGF-β1 and TGF-β3 protein. Regarding the inhibitin receptors, Smad 6 showed much more expression than Smad 7. Thus, we found that Smad 6 has a protective effect and role in the tissue. Immunhistochemically, TGF-β family stains, which are activated by types I-and -II receptors, and the stainless staining of the Smad family might also be showing that the TGF-β family is taking action with a secondary pathway other than the Smad family.
Conclusion In addition to Smad family receptors, Shc-GBR2, SARA, and Ras-Erk1/2 receptors should be investigated in future research. After that, the prognosis, diagnosis, and patient-based chemotherapy strategies for the treatment of glioblastoma multiforme may take a more prominent role.
Resumo
Objetivo Tumores cerebrais primários de alto grau causam morbidade e mortalidade graves. Este estudo teve como objetivo investigar o papel dos receptores fato de crescimento transformante beta (TGF-β) e mães contra homólogo decapentaplégico (Smad, na sigla em inglês) em tumores cerebrais primários de alto grau.
Métodos Treze pacientes com diagnóstico patológico de glioblastoma multiforme foram incluídos no estudo. As preparações patológicas de cada paciente foram analisadas retrospectivamente em laboratórios de histoquímica e imunohistoquímica. As colorações de TGF-β1, TGF-β2, TGF-β3, Smad 1/2/3, Smad 6, e Smad 7 foram avaliadas, e as densidades de imunorreatividade foram examinadas.
Resultados Encontramos aumento na expressão das proteínas TGF-β1 e TGF-β3. Em relação aos receptores de inibitina, o Smad 6 mostrou muito mais expressão do que o Smad 7. Assim, concluímos que o Smad 6 tem efeito e função protetores no tecido. As colorações imunohistoquímicas da família TGF-β, que são ativadas pelos receptores do tipo I e do tipo II, e as colorações menos da família Smad também podem estar mostrando que a família TGF-β está agindo com outra via secundária que não a família Smad.
Conclusão Assim como os estudos na família Smad, receptores como Shc-GBR2, SARA, Ras-Erk1/2 devem ser investigados em pesquisas futuras. Posteriormente, o prognóstico, o diagnóstico, e as estratégias de quimioterapia baseadas no paciente podem assumir um lugar mais priminente no futuro, no glioblastoma multiforme.
Keywords
glioblastoma multiforme - transforming growth factor beta - smad proteins - endothelial-mesenchymal transitionPalavras-chave
glioblastoma multiforme - fato de crescimento transformante beta - proteínas smad - transição endotelial-mesenquimalPublication History
Received: 06 August 2021
Accepted: 13 October 2021
Article published online:
29 November 2022
© 2022. Sociedade Brasileira de Neurocirurgia. This is an open access article published by Thieme under the terms of the Creative Commons Attribution-NonDerivative-NonCommercial License, permitting copying and reproduction so long as the original work is given appropriate credit. Contents may not be used for commecial purposes, or adapted, remixed, transformed or built upon. (https://creativecommons.org/licenses/by-nc-nd/4.0/)
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