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Intracranial Orthotopic Allografting of Medulloblastoma Cells in Immunocompromised Mice

Intracranial Orthotopic Allografting of Medulloblastoma Cells in Immunocompromised Mice

Published on: October 3, 2010

Anaplastic large cell neuroblastoma.

Carlos R Abramowsky¹, Howard M Katzenstein, Carlos S Alvarado

¹Department of Pathology and Pediatrics, Children's Healthcare of Atlanta at Egleston and Emory University School of Medicine, Atlanta, GA, USA. cabramo@emory.edu

Pediatric and Developmental Pathology : the Official Journal of the Society for Pediatric Pathology and the Paediatric Pathology Society

|April 10, 2008

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Anaplastic large cell neuroblastomas (ALCNB) are challenging to diagnose but show promising treatment outcomes. These tumors, despite unique markers like Fli-1 positivity, are confirmed as neuroblastomas through N-MYC amplification and maturation post-therapy.

Area of Science:

Pediatric Oncology
Cancer Biology
Pathology

Background:

Anaplastic large cell neuroblastomas (ALCNB) present diagnostic challenges due to pleomorphic and anaplastic features.
ALCNB are a subset of undifferentiated neuroblastomas requiring careful characterization.

Purpose of the Study:

To review clinical, biologic, and pathologic characteristics of ALCNB patients.
To evaluate treatment outcomes for ALCNB.

Main Methods:

Retrospective review of 7 ALCNB patients diagnosed between 1998-2006.
Analysis of clinical presentation, N-MYC amplification, catecholamine levels, immunohistochemistry (NSE, synaptophysin, chromogranin, Fli-1, CD-99), and molecular testing (Ewing sarcoma transcripts).
Assessment of posttreatment biopsies and patient survival.

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Last Updated: Jul 6, 2026

Intracranial Orthotopic Allografting of Medulloblastoma Cells in Immunocompromised Mice

Intracranial Orthotopic Allografting of Medulloblastoma Cells in Immunocompromised Mice

Published on: October 3, 2010

Main Results:

All patients had high-risk, abdominal-pelvic or thoracic masses.
N-MYC amplification occurred in 3 cases; elevated catecholamines in 5/6.
Tumors showed pleomorphic morphology, positive NSE, synaptophysin, and Fli-1, but negative CD-99 and Ewing sarcoma transcripts.
Posttreatment biopsies revealed maturation in 5/7 cases.
Five of seven patients survived, with a median follow-up of 25 months.

Conclusions:

ALCNB are characterized by undifferentiated morphology, NSE/synaptophysin positivity, Fli-1 positivity, and negative CD-99/EWS transcripts.
N-MYC amplification, catecholamine production, and posttherapy maturation support their neuroblastic origin.
Observed survival rates appear better than previously reported, warranting further investigation into optimal therapy and distinct biologic classification.