Epigenetic and Posttranscriptional Regulation in Retinoblastoma ()
ABSTRACT
The Retinoblastoma 1 (RB1) gene, located on chromosome 13q14 and
encodes the tumor-suppressor retinoblastoma protein, is the cause of Retinoblastoma.
The mutational inactivation of both gene alleles brings on this cancer.
Retinoblastoma (RB) high-risk histopathological characteristics indicate
metastasis or local recurrence with rapid progresses following RB1 inactivation. There is growing interest in regulatory activities unconnected to
the coding region of the genome, or exome, in addition to epigenetic control
mechanisms. The altered epigenome is significant, though by no means the only,
problem in the etiology of Retinoblastoma. After all, cancer development is a
multistep process in which numerous dissimilar genetic, epigenetic, and posttranscriptional modifications result in a shared
phenotype. This study emphasizes the most recent developments in
posttranscriptional change and epigenetics related to retinoblastoma
tumor biology. Here, we highlight the novel biomarkers the retinoblastoma tumor
has expressed to improve patient survival.
Share and Cite:
Karla, T. , Matilde, R. and Meraz-Ríos, M. (2023) Epigenetic and Posttranscriptional Regulation in Retinoblastoma.
Advances in Bioscience and Biotechnology,
14, 190-209. doi:
10.4236/abb.2023.144013.
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