We are analyzing https://link.springer.com/article/10.1007/s00401-015-1478-0.

Title:
Histone H3F3A and HIST1H3B K27M mutations define two subgroups of diffuse intrinsic pontine gliomas with different prognosis and phenotypes | Acta Neuropathologica
Description:
Diffuse intrinsic pontine glioma (DIPG) is the most severe paediatric solid tumour, with no significant therapeutic progress made in the past 50 years. Recent studies suggest that diffuse midline glioma, H3-K27M mutant, may comprise more than one biological entity. The aim of the study was to determine the clinical and biological variables that most impact their prognosis. Ninety-one patients with classically defined DIPG underwent a systematic stereotactic biopsy and were included in this observational retrospective study. Histone H3 genes mutations were assessed by immunochemistry and direct sequencing, whilst global gene expression profiling and chromosomal imbalances were determined by microarrays. A full description of the MRI findings at diagnosis and at relapse was integrated with the molecular profiling data and clinical outcome. All DIPG but one were found to harbour either a somatic H3-K27M mutation and/or loss of H3K27 trimethylation. We also discovered a novel K27M mutation in HIST2H3C, and a lysine-to-isoleucine substitution (K27I) in H3F3A, also creating a loss of trimethylation. Patients with tumours harbouring a K27M mutation in H3.3 (H3F3A) did not respond clinically to radiotherapy as well, relapsed significantly earlier and exhibited more metastatic recurrences than those in H3.1 (HIST1H3B/C). H3.3-K27M-mutated DIPG have a proneural/oligodendroglial phenotype and a pro-metastatic gene expression signature with PDGFRA activation, while H3.1-K27M-mutated tumours exhibit a mesenchymal/astrocytic phenotype and a pro-angiogenic/hypoxic signature supported by expression profiling and radiological findings. H3K27 alterations appear as the founding event in DIPG and the mutations in the two main histone H3 variants drive two distinct oncogenic programmes with potential specific therapeutic targets.
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Keywords {🔍}

dipg, tumours, pubmed, article, google, scholar, hkm, fig, histone, genes, cas, gene, mutations, tumour, mutation, analysis, expression, samples, survival, patients, cells, data, test, cancer, hmutated, subgroups, suppl, pontine, loss, observed, diffuse, found, intrinsic, glioma, mri, mutated, enhancement, panel, pvalue, clinical, diagnosis, distinct, identified, contrast, central, gliomas, alterations, genomic, cell, hkme,

Topics {✒️}

pro-angiogenic/hypoxic signature supported edema/cellular invasion mri-phenotypes article download pdf pediatric high-grade gliomas marie-anne debily paediatric high-grade gliomas brainstem high-grade glioma apparent diffusion coefficient translational research programme diffusion-weighted mr imaging hôpital necker-enfants malades �tumour compartment oligo/astro” 2-oxoglutarate-dependent dioxygenase inhibition high-grade glioma necker-enfants malades hospital sainte-anne hospital classification cell–matrix adhesion—confirming distributed diffusion coefficient chi-squared proportion test high-grade gliomas programme “brainomics” de diffuse midline glioma �cell–matrix adhesion pathways mutated histone-driven subgroups hôpital sainte-anne full size image apparent diffusion coefficients loco-regional leptomeningeal spread cell-cycle regulatory genes diffusion maps acquired histone h3-27 m-mutated identify gene sets distinct oncogenic programmes pdgfra/cen4 fish showing �ion channel activity �défi de fortunée” de pathologie médicale k-means subgroups identified post-hybridization wash central component common baseline array clinical trials analysis privacy choices/manage cookies diffusion-weighted imaging t1-weighted sequences patrick saulnier ludovic lacroix comparative genomic hybridization h3-k27m-mutated allele article castel

Questions {❓}

Puget S, Blauwblomme T, Grill J (2012) Is biopsy safe in children with newly diagnosed diffuse intrinsic pontine glioma?

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WebPage:
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         headline:Histone H3F3A and HIST1H3B K27M mutations define two subgroups of diffuse intrinsic pontine gliomas with different prognosis and phenotypes
         description:Diffuse intrinsic pontine glioma (DIPG) is the most severe paediatric solid tumour, with no significant therapeutic progress made in the past 50 years. Recent studies suggest that diffuse midline glioma, H3-K27M mutant, may comprise more than one biological entity. The aim of the study was to determine the clinical and biological variables that most impact their prognosis. Ninety-one patients with classically defined DIPG underwent a systematic stereotactic biopsy and were included in this observational retrospective study. Histone H3 genes mutations were assessed by immunochemistry and direct sequencing, whilst global gene expression profiling and chromosomal imbalances were determined by microarrays. A full description of the MRI findings at diagnosis and at relapse was integrated with the molecular profiling data and clinical outcome. All DIPG but one were found to harbour either a somatic H3-K27M mutation and/or loss of H3K27 trimethylation. We also discovered a novel K27M mutation in HIST2H3C, and a lysine-to-isoleucine substitution (K27I) in H3F3A, also creating a loss of trimethylation. Patients with tumours harbouring a K27M mutation in H3.3 (H3F3A) did not respond clinically to radiotherapy as well, relapsed significantly earlier and exhibited more metastatic recurrences than those in H3.1 (HIST1H3B/C). H3.3-K27M-mutated DIPG have a proneural/oligodendroglial phenotype and a pro-metastatic gene expression signature with PDGFRA activation, while H3.1-K27M-mutated tumours exhibit a mesenchymal/astrocytic phenotype and a pro-angiogenic/hypoxic signature supported by expression profiling and radiological findings. H3K27 alterations appear as the founding event in DIPG and the mutations in the two main histone H3 variants drive two distinct oncogenic programmes with potential specific therapeutic targets.
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            Diffuse Intrinsic Pontine Glioma
            MYCN Amplification
            K27M Mutation
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      headline:Histone H3F3A and HIST1H3B K27M mutations define two subgroups of diffuse intrinsic pontine gliomas with different prognosis and phenotypes
      description:Diffuse intrinsic pontine glioma (DIPG) is the most severe paediatric solid tumour, with no significant therapeutic progress made in the past 50 years. Recent studies suggest that diffuse midline glioma, H3-K27M mutant, may comprise more than one biological entity. The aim of the study was to determine the clinical and biological variables that most impact their prognosis. Ninety-one patients with classically defined DIPG underwent a systematic stereotactic biopsy and were included in this observational retrospective study. Histone H3 genes mutations were assessed by immunochemistry and direct sequencing, whilst global gene expression profiling and chromosomal imbalances were determined by microarrays. A full description of the MRI findings at diagnosis and at relapse was integrated with the molecular profiling data and clinical outcome. All DIPG but one were found to harbour either a somatic H3-K27M mutation and/or loss of H3K27 trimethylation. We also discovered a novel K27M mutation in HIST2H3C, and a lysine-to-isoleucine substitution (K27I) in H3F3A, also creating a loss of trimethylation. Patients with tumours harbouring a K27M mutation in H3.3 (H3F3A) did not respond clinically to radiotherapy as well, relapsed significantly earlier and exhibited more metastatic recurrences than those in H3.1 (HIST1H3B/C). H3.3-K27M-mutated DIPG have a proneural/oligodendroglial phenotype and a pro-metastatic gene expression signature with PDGFRA activation, while H3.1-K27M-mutated tumours exhibit a mesenchymal/astrocytic phenotype and a pro-angiogenic/hypoxic signature supported by expression profiling and radiological findings. H3K27 alterations appear as the founding event in DIPG and the mutations in the two main histone H3 variants drive two distinct oncogenic programmes with potential specific therapeutic targets.
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      dateModified:2015-09-23T00:00:00Z
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      sameAs:https://doi.org/10.1007/s00401-015-1478-0
      keywords:
         Apparent Diffusion Coefficient
         Diffuse Intrinsic Pontine Glioma
         MYCN Amplification
         K27M Mutation
         Distribute Diffusion Coefficient
         Pathology
         Neurosciences
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