ETV4 plays a role on the primary events during the adenoma-adenocarcinoma progression in colorectal cancer

Autor: Aline Simoneti Fonseca, Anelisa Ramão, Matheus Carvalho Bürger, Jorge Estefano Santana de Souza, Dalila Lucíola Zanette, Greice Andreotti de Molfetta, Luiza Ferreira de Araújo, Rafaela de Barros e Lima Bueno, Graziela Moura Aguiar, Jessica Rodrigues Plaça, Cleidson de Pádua Alves, Anemari Ramos Dinarte dos Santos, Daniel Onofre Vidal, Gyl Eanes Barros Silva, Rodrigo Alexandre Panepucci, Fernanda Maris Peria, Omar Feres, José Joaquim Ribeiro da Rocha, Marco Antonio Zago, Wilson Araújo Silva
Jazyk: angličtina
Rok vydání: 2021
Předmět:
Zdroj: BMC Cancer, Vol 21, Iss 1, Pp 1-14 (2021)
Druh dokumentu: article
ISSN: 1471-2407
DOI: 10.1186/s12885-021-07857-x
Popis: Abstract Background Colorectal cancer (CRC) is one of the most common cancers worldwide; it is the fourth leading cause of death in the world and the third in Brazil. Mutations in the APC, DCC, KRAS and TP53 genes have been associated with the progression of sporadic CRC, occurring at defined pathological stages of the tumor progression and consequently modulating several genes in the corresponding signaling pathways. Therefore, the identification of gene signatures that occur at each stage during the CRC progression is critical and can present an impact on the diagnosis and prognosis of the patient. In this study, our main goal was to determine these signatures, by evaluating the gene expression of paired colorectal adenoma and adenocarcinoma samples to identify novel genetic markers in association to the adenoma-adenocarcinoma stage transition. Methods Ten paired adenoma and adenocarcinoma colorectal samples were subjected to microarray gene expression analysis. In addition, mutations in APC, KRAS and TP53 genes were investigated by DNA sequencing in paired samples of adenoma, adenocarcinoma, normal tissue, and peripheral blood from ten patients. Results Gene expression analysis revealed a signature of 689 differentially expressed genes (DEG) (fold-change> 2, p
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