scholarly journals Unclear standard of care for pediatric high grade glioma patients

2013 ◽  
Vol 113 (2) ◽  
pp. 341-342 ◽  
Author(s):  
Jason Fangusaro ◽  
Katherine E. Warren
Keyword(s):  
Standard Of Care ◽  
High Grade Glioma ◽  
High Grade ◽  
Pediatric High Grade Glioma

scholarly journals Cutting Edge Therapeutic Insights Derived from Molecular Biology of Pediatric High-Grade Glioma and Diffuse Intrinsic Pontine Glioma (DIPG)

2018 ◽  
Vol 5 (4) ◽  
pp. 88 ◽  
Author(s):  
Cavan Bailey ◽  
Mary Figueroa ◽  
Sana Mohiuddin ◽  
Wafik Zaky ◽  
Joya Chandra
Keyword(s):  
Clinical Trial Data ◽  
Standard Of Care ◽  
High Grade Glioma ◽  
Diffuse Intrinsic Pontine Glioma ◽  
High Grade ◽  
Pontine Glioma ◽  
Clinical Models ◽  
Malignant Glioma Cells ◽  
Epigenetic Disruption ◽  
Pediatric High Grade Glioma

Pediatric high-grade glioma (pHGG) and brainstem gliomas are some of the most challenging cancers to treat in children, with no effective therapies and 5-year survival at ~2% for diffuse intrinsic pontine glioma (DIPG) patients. The standard of care for pHGG as a whole remains surgery and radiation combined with chemotherapy, while radiation alone is standard treatment for DIPG. Unfortunately, these therapies lack specificity for malignant glioma cells and have few to no reliable biomarkers of efficacy. Recent discoveries have revealed that epigenetic disruption by highly conserved mutations in DNA-packaging histone proteins in pHGG, especially DIPG, contribute to the aggressive nature of these cancers. In this review we pose unanswered questions and address unexplored mechanisms in pre-clinical models and clinical trial data from pHGG patients. Particular focus will be paid towards therapeutics targeting chromatin modifiers and other epigenetic vulnerabilities that can be exploited for pHGG therapy. Further delineation of rational therapeutic combinations has strong potential to drive development of safe and efficacious treatments for pHGG patients.

scholarly journals HGG-41. STRUCTURAL VARIANT DRIVERS IN PEDIATRIC HIGH-GRADE GLIOMA

2020 ◽  
Vol 22 (Supplement_3) ◽  
pp. iii351-iii351
Author(s):  
Frank Dubois ◽  
Ofer Shapira ◽  
Noah Greenwald ◽  
Travis Zack ◽  
Jessica W Tsai ◽  
...  
Keyword(s):  
Copy Number ◽  
High Grade Glioma ◽  
High Grade ◽  
Structural Variants ◽  
Single Nucleotide Variants ◽  
Single Nucleotide ◽  
Effector Domains ◽  
Topologically Associating Domains ◽  
Genome Wide ◽  
Pediatric High Grade Glioma

Abstract BACKGROUND Driver single nucleotide variants (SNV) and somatic copy number aberrations (SCNA) of pediatric high-grade glioma (pHGGs), including Diffuse Midline Gliomas (DMGs) are characterized. However, structural variants (SVs) in pHGGs and the mechanisms through which they contribute to glioma formation have not been systematically analyzed genome-wide. METHODS Using SvABA for SVs as well as the latest pipelines for SCNAs and SNVs we analyzed whole-genome sequencing from 174 patients. This includes 60 previously unpublished samples, 43 of which are DMGs. Signature analysis allowed us to define pHGG groups with shared SV characteristics. Significantly recurring SV breakpoints and juxtapositions were identified with algorithms we recently developed and the findings were correlated with RNAseq and H3K27ac ChIPseq. RESULTS The SV characteristics in pHGG showed three groups defined by either complex, intermediate or simple signature activities. These associated with distinct combinations of known driver oncogenes. Our statistical analysis revealed recurring SVs in the topologically associating domains of MYCN, MYC, EGFR, PDGFRA & MET. These correlated with increased mRNA expression and amplification of H3K27ac peaks. Complex recurring amplifications showed characteristics of extrachromosomal amplicons and were enriched in coding SVs splitting protein regulatory from effector domains. Integrative analysis of all SCNAs, SNVs & SVs revealed patterns of characteristic combinations between potential drivers and signatures. This included two distinct groups of H3K27M DMGs with either complex or simple signatures and different combinations of associated variants. CONCLUSION Recurrent SVs associate with signatures shaped by an underlying process, which can lead to distinct mechanisms to activate the same oncogene.

Pediatric High-Grade Glioma Patterns of Failure by Molecular Subgroup

2020 ◽  
Vol 108 (3) ◽  
pp. e239-e240
Author(s):  
L.J. Sudmeier ◽  
T. Morgan ◽  
P. Mendoza ◽  
J. Switchenko ◽  
E. Schreibmann ◽  
...  
Keyword(s):  
High Grade Glioma ◽  
High Grade ◽  
Patterns Of Failure ◽  
Molecular Subgroup ◽  
Pediatric High Grade Glioma

scholarly journals HG-35MET-PET DELINEATES NON-CONTRAST ENHANCING TUMOR (nCET) REGIONS AT HIGH RISK FOR RECURRENCE IN PEDIATRIC HIGH GRADE GLIOMA

2016 ◽  
Vol 18 (suppl 3) ◽  
pp. iii55.2-iii55
Author(s):  
John T. Lucas ◽  
Nick Serrano ◽  
Hyun Kim ◽  
Yimei Li ◽  
Alberto Broniscer ◽  
...  
Keyword(s):  
High Risk ◽  
High Grade Glioma ◽  
High Grade ◽  
Pediatric High Grade Glioma

scholarly journals COT-21 EFFECT OF BEVACIZUMAB FOR PEDIATRIC HIGH GRADE GLIOMA

2019 ◽  
Vol 1 (Supplement_2) ◽  
pp. ii44-ii44
Author(s):  
Yoshihiro Tsukamoto ◽  
Manabu Natsumeda ◽  
Masayasu Okada ◽  
Takeyoshi Eda ◽  
Junichi Yoshimura ◽  
...  
Keyword(s):  
Tumor Progression ◽  
Therapeutic Agent ◽  
High Grade Glioma ◽  
Wound Complication ◽  
Symptomatic Improvement ◽  
Diffuse Intrinsic Pontine Glioma ◽  
Rapid Progression ◽  
High Grade ◽  
Diffuse Midline Glioma ◽  
Pediatric High Grade Glioma

Abstract INTRODUCTION Bevacizumab (BEV) therapy has been used for pediatric high grade glioma,however the evidence and effectiveness are not understood yet. METHODS We report 7 cases (age 2 to 10 years old) of pediatric high grade glioma treated with BEV. One case is thalamic diffuse midline glioma H3K27 mutant (DMGH3K27M),one case is brain stem DMGH3K27M,one case is cerebellar high grade glioma,and 4 cases are diffuse intrinsic pontine glioma (DIPG) diagnosed clinically without biopsy. 5 cases were treated with BEV when diagnosed as recurrence after chemo-radiotherapy. One case was treated for rapid tumor progression during radiotherapy. One case was started on BEV therapy with radiation and concomitant temozolomide therapy. RESULT The number of times of BEV was 2 to 13 times (median 7 times). The period of BEV was 1 to 9 months (median 4 months). One case which was treated with BEV at rapid progression during radiation showed good response on imaging and improvement of symptoms. 4 of 5 cases who were treated at recurrence clinically showed mild symptomatic improvement. One case treated with BEV and radiotherapy initially was not evaluated. The adverse effects of BEV included wound complication of tracheostomy and rash. CONCLUSION BEV showed good response for rapid progression during radiotherapy,and mild response for recurrence cases. BEV is thought to be an effective therapeutic agent for pediatric HGG at recurrence and rapid tumor progression during radiotherapy.

scholarly journals Therapeutic Targeting of Histone Modifications in Adult and Pediatric High-Grade Glioma

2017 ◽  
Vol 7 ◽  
Author(s):  
Maria J. Williams ◽  
Will G. B. Singleton ◽  
Stephen P. Lowis ◽  
Karim Malik ◽  
Kathreena M. Kurian
Keyword(s):  
Histone Modifications ◽  
High Grade Glioma ◽  
High Grade ◽  
Therapeutic Targeting ◽  
Pediatric High Grade Glioma

Pediatric High Grade Glioma

2017 ◽  
pp. 241-266
Author(s):  
Chitra Sarkar ◽  
Suvendu Purkait ◽  
Pankaj Pathak ◽  
Prerana Jha
Keyword(s):  
High Grade Glioma ◽  
High Grade ◽  
Pediatric High Grade Glioma
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