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Keywords {🔍}

pubmed, article, google, scholar, cas, central, cancer, idhmutant, gliomas, instability, tumor, glioblastoma, httpsdoiorgs, dna, idh, mutations, cell, methylation, molecular, heterogeneity, epigenetic, chromosomal, tumors, glioma, astrocytomas, cells, neuropathol, mutation, nat, cin, grade, repair, singlecell, astrocytoma, number, mmr, clinical, acta, analysis, mgmt, including, genetic, survival, cancers, cases, promoter, progression, mismatch, diffuse, features,

Topics {✒️}

idh-wild-type high-grade gliomas single-cell rna-seq reveals idh-mutant 1p/19q-codeleted oligodendrogliomas single-cell rna-seq supports alpha-ketoglutarate-dependent dioxygenases including idh-wild-type glioblastoma o6-methylguanine-dna methyltransferase low-grade idh-mutant astrocytomas copy-number profiling identify temozolomide-resistant mmr-deficient clones idh1-mutant low-grade glioma article download pdf idh2-mutant low-grade glioma de souza cf multifaceted mismatch-repair system central nervous system idh-mutant astrocytoma category distinguish idh-mutant astrocytoma surviving mmr-deficient subclone user-friendly bioinformatic toolsets mellinghoff ik single-cell rna sequencing single-cell rna-sequencing single-cell rna-seq therapy reveals cell-intrinsic idh-wild-type glioblastoma idh-wild-type glioblastoma [38 idh-wild-type glioblastomas idh-wild-type glioblastomas [87] open chromatin accessibility separates idh-mutant astrocytomas full size image adult-type diffuse gliomas perform single-cell sequencing enhancing demethylation-induced differentiation conics integrates scrna-seq idh-mutant astrocytic gliomas dna methylation-based mapping idh-wild-type gbm g-cimp-high astrocytomas idh-mutant astrocytomas frequently single-cell dna sequencing g-cimp-high clusters [38] g-cimp-high status idh-mutant glioblastoma determined primary idh-mutant astrocytomas isocitrate dehydrogenase-mutant astrocytoma atrx-deficient malignant glioma including idh-mutant astrocytomas targeting drug-resistant glioblastoma

Questions {❓}

• Della Puppa A, Persano L, Masi G, Rampazzo E, Sinigaglia A, Pistollato F et al (2012) MGMT expression and promoter methylation status may depend on the site of surgical sample collection within glioblastoma: a possible pitfall in stratification of patients?
• Jasencakova Z, Groth A (2010) Replication stress, a source of epigenetic aberrations in cancer?

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         headline:Genetic and epigenetic instability as an underlying driver of progression and aggressive behavior in IDH-mutant astrocytoma
         description:In recent years, the classification of adult-type diffuse gliomas has undergone a revolution, wherein specific molecular features now represent defining diagnostic criteria of IDH-wild-type glioblastomas, IDH-mutant astrocytomas, and IDH-mutant 1p/19q-codeleted oligodendrogliomas. With the introduction of the 2021 WHO CNS classification, additional molecular alterations are now integrated into the grading of these tumors, given equal weight to traditional histologic features. However, there remains a great deal of heterogeneity in patient outcome even within these established tumor subclassifications that is unexplained by currently codified molecular alterations, particularly in the IDH-mutant astrocytoma category. There is also significant intercellular genetic and epigenetic heterogeneity and plasticity with resulting phenotypic heterogeneity, making these tumors remarkably adaptable and robust, and presenting a significant barrier to the design of effective therapeutics. Herein, we review the mechanisms and consequences of genetic and epigenetic instability, including chromosomal instability (CIN), microsatellite instability (MSI)/mismatch repair (MMR) deficits, and epigenetic instability, in the underlying biology, tumorigenesis, and progression of IDH-mutant astrocytomas. We also discuss the contribution of recent high-resolution transcriptomics studies toward defining tumor heterogeneity with single-cell resolution. While intratumoral heterogeneity is a well-known feature of diffuse gliomas, the contribution of these various processes has only recently been considered as a potential driver of tumor aggressiveness. CIN has an independent, adverse effect on patient survival, similar to the effect of histologic grade and homozygous CDKN2A deletion, while MMR mutation is only associated with poor overall survival in univariate analysis but is highly correlated with higher histologic/molecular grade and other aggressive features. These forms of genomic instability, which may significantly affect the natural progression of these tumors, response to therapy, and ultimately clinical outcome for patients, are potentially measurable features which could aid in diagnosis, grading, prognosis, and development of personalized therapeutics.
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      headline:Genetic and epigenetic instability as an underlying driver of progression and aggressive behavior in IDH-mutant astrocytoma
      description:In recent years, the classification of adult-type diffuse gliomas has undergone a revolution, wherein specific molecular features now represent defining diagnostic criteria of IDH-wild-type glioblastomas, IDH-mutant astrocytomas, and IDH-mutant 1p/19q-codeleted oligodendrogliomas. With the introduction of the 2021 WHO CNS classification, additional molecular alterations are now integrated into the grading of these tumors, given equal weight to traditional histologic features. However, there remains a great deal of heterogeneity in patient outcome even within these established tumor subclassifications that is unexplained by currently codified molecular alterations, particularly in the IDH-mutant astrocytoma category. There is also significant intercellular genetic and epigenetic heterogeneity and plasticity with resulting phenotypic heterogeneity, making these tumors remarkably adaptable and robust, and presenting a significant barrier to the design of effective therapeutics. Herein, we review the mechanisms and consequences of genetic and epigenetic instability, including chromosomal instability (CIN), microsatellite instability (MSI)/mismatch repair (MMR) deficits, and epigenetic instability, in the underlying biology, tumorigenesis, and progression of IDH-mutant astrocytomas. We also discuss the contribution of recent high-resolution transcriptomics studies toward defining tumor heterogeneity with single-cell resolution. While intratumoral heterogeneity is a well-known feature of diffuse gliomas, the contribution of these various processes has only recently been considered as a potential driver of tumor aggressiveness. CIN has an independent, adverse effect on patient survival, similar to the effect of histologic grade and homozygous CDKN2A deletion, while MMR mutation is only associated with poor overall survival in univariate analysis but is highly correlated with higher histologic/molecular grade and other aggressive features. These forms of genomic instability, which may significantly affect the natural progression of these tumors, response to therapy, and ultimately clinical outcome for patients, are potentially measurable features which could aid in diagnosis, grading, prognosis, and development of personalized therapeutics.
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      dateModified:2024-07-16T00:00:00Z
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         Glioma
         Astrocytoma
         Glioblastoma
         Oligodendroglioma
         Heterogeneity
         Chromosomal instability
         Microsatellite instability
         Mismatch repair defects
         Methylation profiling
         Epigenetics
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         Neurosciences
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               name:Department of Pathology, Molecular and Cell-Based Medicine, Icahn School of Medicine at Mount Sinai, New York, USA
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            name:Icahn School of Medicine at Mount Sinai
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      name:Nash Family Department of Neuroscience, Icahn School of Medicine at Mount Sinai, New York, USA
      name:Department of Oncological Sciences, The Tisch Cancer Institute, Mount Sinai Icahn School of Medicine, New York, USA
      name:Department of Neurosurgery, Mount Sinai Icahn School of Medicine, New York, USA
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      name:Glioblastoma Translational Center of Excellence, Abramson Cancer Center, University of Pennsylvania, Philadelphia, USA
      name:Department of Pathology, University of Texas Southwestern Medical Center, Dallas, USA
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      name:Department of Pathology, Molecular and Cell-Based Medicine, Icahn School of Medicine at Mount Sinai, New York, USA
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      name:Nash Family Department of Neuroscience, Icahn School of Medicine at Mount Sinai, New York, USA

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