Childhood Medulloblastoma: An Overview

Author(s):  
Yujin Suk ◽  
William D. Gwynne ◽  
Ian Burns ◽  
Chitra Venugopal ◽  
Sheila K. Singh
2013 ◽  
Vol 8 (4) ◽  
pp. 1111-1117 ◽  
Author(s):  
JIPENG SHI ◽  
LIUZHONG YANG ◽  
TUANJIE WANG ◽  
JIAN ZHANG ◽  
XIXIA GUO ◽  
...  

2010 ◽  
Vol 9 (1) ◽  
pp. 167-179 ◽  
Author(s):  
Tarek Shalaby ◽  
André O. von Bueren ◽  
Marie-Louise Hürlimann ◽  
Giulio Fiaschetti ◽  
Deborah Castelletti ◽  
...  

2018 ◽  
Vol 27 (6) ◽  
pp. 479-502 ◽  
Author(s):  
Guilherme de Souza e Cassia ◽  
César Augusto Pinheiro Ferreira Alves ◽  
Ajay Taranath ◽  
Nicolás Sgarbi López ◽  
Ozgur Oztekin ◽  
...  

2021 ◽  
Vol 26 (3) ◽  
pp. 52-54
Author(s):  
Dragoş Horşia

Abstract Defined as a tumour with increased malignancy potential in childhood, medulloblastoma was first reported in the literature by Percival Bailey and Harvey Cushing in 1925. Scientific studies over the years have shown that this type of tumour represents about 20% of all intracranial tumours encountered in childhood, their percentage decreasing with advancing age. The genetic factor plays an important part in the appearance of medulloblastoma; there are certain diseases, in the patient’s history, that can be associated with this type of tumour. Here, we can specify Turcot syndrome (an autosomal recessive disease, rarely encountered) or basal cell carcinoma syndrome. This article presents the case of a young patient (41-year-old) suffering from a cerebellar tumour formation that turned out to be, after histopathological examination, a medulloblastoma. In practice we can find several types of medulloblastoma (desmoplastic or nodular, anaplastic, classical or undifferentiated). In what follows I will try to highlight a few aspects of a classic medulloblastoma.


Cancers ◽  
2021 ◽  
Vol 13 (23) ◽  
pp. 6042
Author(s):  
Jelena Milosevic ◽  
Diana Treis ◽  
Susanne Fransson ◽  
Gabriel Gallo-Oller ◽  
Baldur Sveinbjörnsson ◽  
...  

Childhood medulloblastoma and high-risk neuroblastoma frequently present with segmental gain of chromosome 17q corresponding to aggressive tumors and poor patient prognosis. Located within the 17q-gained chromosomal segments is PPM1D at chromosome 17q23.2. PPM1D encodes a serine/threonine phosphatase, WIP1, that is a negative regulator of p53 activity as well as key proteins involved in cell cycle control, DNA repair and apoptosis. Here, we show that the level of PPM1D expression correlates with chromosome 17q gain in medulloblastoma and neuroblastoma cells, and both medulloblastoma and neuroblastoma cells are highly dependent on PPM1D expression for survival. Comparison of different inhibitors of WIP1 showed that SL-176 was the most potent compound inhibiting medulloblastoma and neuroblastoma growth and had similar or more potent effects on cell survival than the MDM2 inhibitor Nutlin-3 or the p53 activator RITA. SL-176 monotherapy significantly suppressed the growth of established medulloblastoma and neuroblastoma xenografts in nude mice. These results suggest that the development of clinically applicable compounds inhibiting the activity of WIP1 is of importance since PPM1D activating mutations, genetic gain or amplifications and/or overexpression of WIP1 are frequently detected in several different cancers.


2011 ◽  
Vol 123 (4) ◽  
pp. 501-513 ◽  
Author(s):  
Sarra L. Ryan ◽  
Ed C. Schwalbe ◽  
Michael Cole ◽  
Yuan Lu ◽  
Meryl E. Lusher ◽  
...  

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