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Expression of pluripotency-related genes in human glioblastoma

BACKGROUND: Cancer is a group of heterogeneous diseases characterized by several disruptions of the genetic and epigenetic components of cell biology. Some types of cancer have been shown to be constituted by a mosaic of cells with variable differentiation states, with more aggressive tumors being m...

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Detalles Bibliográficos
Autores principales: Rios, Álvaro Fabrício Lopes, Tirapelli, Daniela Pretti da Cunha, Cirino, Mucio Luiz de Assis, Rodrigues, Andressa Romualdo, Ramos, Ester S, Carlotti, Carlos Gilberto
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Oxford University Press 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8903226/
https://www.ncbi.nlm.nih.gov/pubmed/35274101
http://dx.doi.org/10.1093/noajnl/vdab163
Descripción
Sumario:BACKGROUND: Cancer is a group of heterogeneous diseases characterized by several disruptions of the genetic and epigenetic components of cell biology. Some types of cancer have been shown to be constituted by a mosaic of cells with variable differentiation states, with more aggressive tumors being more undifferentiated. In most cases, undifferentiated tumor cells express associated embryonic markers such as the OCT4, NANOG, SOX2, and CARM1 genes. The ectopic or reminiscent expression of some master regulator genes of pluripotency has been indicated as the cause of the poorly differentiated state of tumors, and based on the evidence of some reports, can be used as a possible therapeutic target. Considering this information, a more detailed investigation of the expression of pluripotency-associated genes is necessary to evaluate the roles of these genes in the etiology of some tumors and their use targets of therapy. METHODS: The expression of four pluripotency-related genes was investigated (OCT4, NANOG, SOX2, and CARM1) in the most malignant primary human brain tumor, glioblastoma (GBM). RESULTS AND CONCLUSION: The results demonstrated a signature of OCT4/SOX2/CARM1 genes and a significant increase of CARM1 expression in GBM cases.