Abstract
Medulloblastoma (MB) is one of the most frequent and malignant brain tumors in children. The prognosis depends on the advancement of the disease and the patient’s age. Current therapies, which include surgery, chemotherapy, and irradiation, despite being quite effective, cause significant side effects that influence the central nervous system’s function and cause neurocognitive deficits. Therefore, they substantially lower the quality of life, which is especially severe in a developing organism. Thus, there is a need for new therapies that are less toxic and even more effective. Recently, knowledge about the epigenetic mechanisms that are responsible for medulloblastoma development has increased. Epigenetics is a phenomenon that influences gene expression but can be easily modified by external factors. The best known epigenetic mechanisms are histone modifications, DNA methylation, or noncoding RNAs actions. Epigenetic mechanisms comprehensively explain the complex phenomena of carcinogenesis. At the same time, they seem to be a potential key to treating medulloblastoma with fewer complications than past therapies. This review presents the currently known epigenetic mechanisms that are involved in medulloblastoma pathogenesis and the potential therapies that use epigenetic traits to cure medulloblastoma while maintaining a good quality of life and ensuring a higher median overall survival rate.
Highlights
Trichostatin A is a class I and II Histone Deacetylase Inhibitors (HDACis) that is designed to decrease the viability of MB cells and induce their apoptosis by restoring Dickkopf WNT Signaling Pathway Inhibitor 1 (DKK1) expression
Polycomb Repressive Complex 2 (PRC2) is required for long-term epigenetic silencing of chromatin and is responsible for regulating genes that are connected with embryonic development [152]
It emphasizes that knowledge of the epigenetic basis of carcinogenesis is crucial for developing and choosing an adequate tumor treatment
Summary
Publisher’s Note: MDPI stays neutral with regard to jurisdictional claims in published maps and institutional affiliations. The currently achieved rates are 82 ± 5.2% and 76 ± 5.8% for median overall survival and 2-year progression-free survival, respectively [8]. These aggressive treatments carry a high risk of complications and neurological deficits [9,10]. Medulloblastoma with extensive nodularity in infants has a good prognosis, as does the DNMB type at young ages [12]. 2016 WHO revision introduced a new medulloblastoma classification based on defined molecular characteristics. It distinguishes four subtypes: WNT (wingless), SHH (sonic hedgehog), group 3, and group 4.
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