RESUMO
BACKGROUND/AIM: In female dogs, mammary cancer is the most frequent cancer type, accounting for 50% of all tumors affecting these animals. Amongst the commonly altered genes in cancer is the cell-cycle regulator cyclin-dependent kinase inhibitor 2B (Cdkn2b), whose expression is negatively regulated by protein products of BMI1 proto-oncogene (Bmi1), MYC proto-oncogene (Myc) and T-box gene transcription factor 2 (Tbx2) genes. Considering this, the aim of this study was to evaluate the expression pattern of the Cdkn2b gene and these regulators in canine mammary tumors of dogs from Northern Brazil (Belém, Pará). MATERIAL AND METHODS: Gene expression in samples from 33 animals was assessed by real-time polymerase chain reaction. To check the influence of methylation on gene expression, bisulfite sequencing polymerase chain reaction was also performed. RESULTS: All studied genes, except Cdkn2b, were found at increased expression levels in tumor tissue when compared with control samples. No correlation between expression and methylation data was observed. CONCLUSION: Our results suggest these markers may have a diagnostic value in the veterinary clinic.
Assuntos
Inibidor de Quinase Dependente de Ciclina p15/genética , Doenças do Cão/genética , Neoplasias Mamárias Animais/genética , Proteína Quinase 7 Ativada por Mitógeno/genética , Proteínas Proto-Oncogênicas c-myc/genética , Proteínas com Domínio T/genética , Animais , Metilação de DNA , Cães , Epigênese Genética , Feminino , Perfilação da Expressão Gênica/veterinária , Regulação Neoplásica da Expressão Gênica , Proto-Oncogene Mas , Análise de Sequência de DNA/veterináriaRESUMO
Glioblastomas, also known as glioblastoma multiforme (GBM), are the most aggressive and malignant type of primary brain tumor in adults, exhibiting notable variability at the histopathological, genetic and epigenetic levels. Recently, epigenetic alterations have emerged as a common hallmark of many tumors, including GBM. Considering that a deeper understanding of the epigenetic modifications that occur in GBM may increase the knowledge regarding the tumorigenesis, progression and recurrence of this disease, in this review we discuss the recent major advances in GBM epigenetics research involving histone modification, glioblastoma stem cells, DNA methylation, noncoding RNAs expression, including their main alterations and the use of epigenetic therapy as a valid option for GBM treatment.
