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Updated: Sep 7, 2025
A Protocol for Rapid Post-mortem Cell Culture of Diffuse Intrinsic Pontine Glioma DIPG
Published on: March 7, 2017
[Case report: molecular analysis of congenital glioblastoma in a newborn]
Alexandra Maráczi1, Béla Kajtár2, Ádám Nagy1
1Molekuláris Patológia, Markusovszky Egyetemi Oktatókórház, Szombathely, Hungary. maraczi.alexandra@gmail.com.
Insights
Congenital glioblastoma (cGBM) is a rare newborn brain tumor. Molecular analysis revealed ALK gene alterations, suggesting targeted therapies for cGBM.
Area of Science:
- Pediatric Oncology
- Neuro-oncology
- Molecular Diagnostics
Background:
- Congenital glioblastoma (cGBM) is an exceptionally rare brain tumor in neonates.
- cGBM exhibits distinct characteristics compared to pediatric and adult glioblastoma (GBM).
Observation:
- A case of cGBM with 14 days of postnatal survival was analyzed.
- Tumor samples were examined using immunohistochemical and molecular genetic techniques (FISH, pyrosequencing).
Findings:
- ALK fluorescence in situ hybridization (FISH) detected polysomy of chromosome 2 and a 5' deletion of the ALK gene.
- These genetic alterations were identified within the glioma cells.
Implications:
- Molecular analyses are crucial for accurate cGBM diagnosis.
- Identified ALK gene alterations suggest potential for personalized, targeted therapies like crizotinib or alectinib.
Background:
Congenital glioblastoma (cGBM) is a brain tumor very rarely observed in newborns and young infants, and differs in several respects from glioblastoma (GBM) of childhood and adulthood. Our aim was the presentation of a cGBM case with 14 days of postnatal survival at the Pediatric Oncology Center of the Markusovszky University Teaching Hospital in 2004. We investigated formalin-fixed, paraffin-embedded autoptic tumor samples of the newborn by immunohistochemical and molecular genetic (FISH and pyrosequencing) methods. We found polysomy of chromosome 2 and 5' deletion of the ALK gene in the glioma cells by ALK FISH. This result indicates the importance of molecular analyses in the diagnostic evaluation of cGBM, and raises the possibility of a personalized, targeted therapy (crizotinib, alectinib).
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