7 research outputs found
Additional file 2: Table S2. of Characterizing temporal genomic heterogeneity in pediatric high-grade gliomas
Somatic and putative somatic mutation information for 16 pairs of pHGGs analyzed in this study. (XLSX 301Â kb
Additional file 6: Figure S3. of Characterizing temporal genomic heterogeneity in pediatric high-grade gliomas
Immunohistochemical staining for the MMR panel (MLH1, MSH2, MSH6 and PMS2) in the HGG11 primary tumor. (PDF 23521Â kb
Additional file 3: Figure S1. of Characterizing temporal genomic heterogeneity in pediatric high-grade gliomas
IGV views a subclonal low frequency PIK3CA mutation in HGG3 from a clinical sequencing panel, WES, and targeted sequencing. (PDF 2380Â kb
Additional file 4: Table S3. of Characterizing temporal genomic heterogeneity in pediatric high-grade gliomas
Number of Single Nucleotide Variants (SNVs) and regions of Allelic Imbalance (AI) present in tumors as shared, primary only, or recurrence only in the pHGG tumor pairs analyzed in this study. (XLSX 13Â kb
Additional file 7: Figure S4. of Characterizing temporal genomic heterogeneity in pediatric high-grade gliomas
Genome-wide view of copy number variations in HGG9 primary and recurrence tumors calculated from Whole Exome Sequencing data. (PDF 2757Â kb
Additional file 1: of Medulloblastoma therapy generates risk of a poorly-prognostic H3 wild-type subgroup of diffuse intrinsic pontine glioma: a report from the International DIPG Registry
Table S1. Treatment details for primary medulloblastoma. Table S2. Multivariate analysis of overall survival for primary and radiation-associated DIPGs. Table S3. Sequencing of radiation-associated DIPGs. Figure S1. Immunohistochemical staining for H3K27Â M of positive and negative control pediatric high-grade gliomas. Figure S2. Diagnosis and management of case 2, which included non-standard treatment for medulloblastoma. Figure S3. Diagnosis and management of case 3, which included standard therapy for medulloblastoma. (DOCX 5366 kb