scholarly journals Anaplastic Medulloblastoma

2020 ◽  
Author(s):  
Keyword(s):  
Anaplastic Medulloblastoma

scholarly journals Large cell anaplastic medulloblastoma metastatic to the scalp: tumor and derived stem-like cells features

BMC Cancer ◽  
2014 ◽  
Vol 14 (1) ◽  
Author(s):  
Angela Mastronuzzi ◽  
Evelina Miele ◽  
Agnese Po ◽  
Manila Antonelli ◽  
Francesca Romana Buttarelli ◽  
...  
Keyword(s):  
Large Cell ◽  
Anaplastic Medulloblastoma

Anaplastic medulloblastoma in a child with Duchenne muscular dystrophy

2012 ◽  
Vol 10 (1) ◽  
pp. 21-24 ◽  
Author(s):  
Machiel van den Akker ◽  
Paul Northcott ◽  
Michael D. Taylor ◽  
William Halliday ◽  
Ute Bartels ◽  
...  
Keyword(s):  
Brain Tumor ◽  
Duchenne Muscular Dystrophy ◽  
Muscular Dystrophy ◽  
Subtotal Resection ◽  
Walking Ability ◽  
Malignant Cells ◽  
Ethical Considerations ◽  
Increased Intracranial Pressure ◽  
Craniospinal Radiation ◽  
Anaplastic Medulloblastoma

A 9-year-old boy with known Duchenne type muscular dystrophy (DMD) presented with signs of increased intracranial pressure. Radiological investigations revealed a lesion in the midline of the posterior fossa. Subtotal resection was performed. Pathology findings were consistent with the diagnosis of anaplastic medulloblastoma. The postoperative lumbar CSF was positive for malignant cells. Postoperatively, the patient showed severe neurological deterioration and lost his capacity to walk. He was treated with craniospinal radiation followed by nonintensive chemotherapy. At 30 months postsurgery, he was still in complete remission but had not recovered his walking ability. This is the second report of a malignant brain tumor in a boy with DMD. The possible link between the 2 conditions is discussed, as are ethical considerations regarding the management of medulloblastoma in children with DMD.

scholarly journals Proteomic Profile Modification of Anaplastic Medulloblastoma after in-Vivo Radiotherapy: A Case Study

2010 ◽  
Vol 01 (02) ◽  
pp. 97-103 ◽  
Author(s):  
C. Zanini ◽  
G. Mandili ◽  
D. Baci ◽  
M. Leone ◽  
I. Morra ◽  
...  
Keyword(s):  
Proteomic Profile ◽  
Profile Modification ◽  
Anaplastic Medulloblastoma

The TP53-ARF tumor suppressor pathway is frequently disrupted in large/cell anaplastic medulloblastoma

2004 ◽  
Vol 121 (1-2) ◽  
pp. 137-140 ◽  
Author(s):  
Adrian J. Frank ◽  
Roberto Hernan ◽  
Andrew Hollander ◽  
Janet C. Lindsey ◽  
Meryl E. Lusher ◽  
...  
Keyword(s):  
Tumor Suppressor ◽  
Large Cell ◽  
Anaplastic Medulloblastoma

scholarly journals PATH-09. SJMB12 CLINICAL TRIAL: DISCREPANCY BETWEEN LOCAL AND CENTRAL PATHOLOGY IN ASSESSING ANAPLASTIC MEDULLOBLASTOMA – REPORT FROM A SINGLE SITE EXPERIENCE

2020 ◽  
Vol 22 (Supplement_3) ◽  
pp. iii426-iii426
Author(s):  
Dong-Anh Khuong-Quang ◽  
Karli Williamson ◽  
Duncan MacGregor ◽  
Brent A Orr ◽  
Amar Gajjar ◽  
...  
Keyword(s):  
Clinical Trial ◽  
Independent Risk Factor ◽  
Large Cell ◽  
Diagnostic Tools ◽  
Phase 2 ◽  
Discordance Rate ◽  
Phase 2 Clinical Trial ◽  
Future Risk ◽  
Central Pathology ◽  
Anaplastic Medulloblastoma

Abstract INTRODUCTION SJMB12 is a phase 2 clinical trial led by the St. Jude Children’s Research Hospital (St. Jude) that enrolls patients with medulloblastoma based on their biological subgroup. The large cell/anaplastic (LCA) histologic variant has been identified as an important independent risk factor associated with poor outcome. However, the histologic criteria for LCA is subjective, making the distinction between anaplastic and non-anaplastic medulloblastoma difficult in some cases. METHODS Pathological central review was performed at St. Jude. For all patients enrolled in the study to date, concordance was assessed between the initial and central review diagnosis and histologic variant calls made at the Royal Children’s Hospital Melbourne (RCH) and at St. Jude, respectively. RESULTS Since the SJMB12 clinical trial opened locally in 2014, 34 patients were enrolled, and 31 were eligible for this retrospective study. A total of 12 (39%) cases with discordance were identified. The most frequent disagreement was between the designation of LCA (10 cases, 32%). In five cases the tumour was not designated as LCA variant locally. In five cases the initial designation of LCA was refuted centrally. Overall, this led to a change of treatment stratum for four patients (13%). CONCLUSION A high discordance rate exists between neuropathologists in the designation of LCA variant. Differences in interpretation of the subjective histologic criteria and inconsistencies in the material submitted for central review contributed to the discordance. Incorporation of more objective histologic criteria and implementation of unbiased diagnostic tools may improve the generalisability of future risk stratification.

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