Exploring the Molecular Complexity of Medulloblastoma: Implications for Diagnosis and Treatment

被引:6
|
作者
Rechberger, Julian S. [1 ,2 ]
Toll, Stephanie A. [3 ]
Vanbilloen, Wouter J. F. [1 ,4 ]
Daniels, David J. [1 ,2 ]
Khatua, Soumen [5 ]
机构
[1] Mayo Clin, Dept Neurol Surg, Rochester, MN 55905 USA
[2] Mayo Clin, Dept Mol Pharmacol & Expt Therapeut, Rochester, MN 55905 USA
[3] Childrens Hosp Michigan, Dept Pediat, Div Hematol Oncol, Detroit, MI 48201 USA
[4] Elisabeth Tweesteden Hosp, Dept Neurol, NL-5022 Tilburg, Netherlands
[5] Mayo Clin, Dept Pediat Hematol Oncol, Sect NeuroOncol, Rochester, MN 55905 USA
关键词
medulloblastoma; molecular subtypes; diagnosis; epigenetic machinery; therapeutic resistance; chemotherapy; radiation therapy; targeted therapy; immunotherapy; adoptive cell therapy; TUMOR-ASSOCIATED MACROPHAGES; HISTONE LYSINE METHYLATION; CENTRAL-NERVOUS-SYSTEM; GROWTH-FACTOR RECEPTOR; CHILDHOOD MEDULLOBLASTOMA; SONIC HEDGEHOG; T-CELLS; OUTCOME PREDICTION; ONCOLYTIC VIRUSES; DENDRITIC CELLS;
D O I
10.3390/diagnostics13142398
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Medulloblastoma is the most common malignant brain tumor in children. Over the last few decades, significant progress has been made in revealing the key molecular underpinnings of this disease, leading to the identification of distinct molecular subgroups with different clinical outcomes. In this review, we provide an update on the molecular landscape of medulloblastoma and treatment strategies. We discuss the four main molecular subgroups (WNT-activated, SHH-activated, and non-WNT/non-SHH groups 3 and 4), highlighting the key genetic alterations and signaling pathways associated with each entity. Furthermore, we explore the emerging role of epigenetic regulation in medulloblastoma and the mechanism of resistance to therapy. We also delve into the latest developments in targeted therapies and immunotherapies. Continuing collaborative efforts are needed to further unravel the complex molecular mechanisms and profile optimal treatment for this devastating disease.
引用
收藏
页数:25
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