Michael Blough
YOU?
Author Swipe
View article: Mitogen-induced defective mitosis transforms neural progenitor cells
Mitogen-induced defective mitosis transforms neural progenitor cells Open
Background Chromosome instability (CIN) with recurrent copy number alterations is a feature of many solid tumors, including glioblastoma (GBM), yet the genes that regulate cell division are rarely mutated in cancers. Here, we show that the…
View article: Supplementary Figure S1 from <i>IDH1</i> Mutation Induces Reprogramming of Pyruvate Metabolism
Supplementary Figure S1 from <i>IDH1</i> Mutation Induces Reprogramming of Pyruvate Metabolism Open
Effect of 2-HG on cell proliferation of IDH1 wild-type cells for the U87 (A) and NHA (B) models.
View article: Supplementary Figure S2 from <i>IDH1</i> Mutation Induces Reprogramming of Pyruvate Metabolism
Supplementary Figure S2 from <i>IDH1</i> Mutation Induces Reprogramming of Pyruvate Metabolism Open
Cytotoxicity of DCA against IDH1 wild-type and mutant cells for the U87 (A) and NHA (B) models (* indicates significant difference (p<0.05) relative to control).
View article: Supplementary Table S1 from <i>IDH1</i> Mutation Induces Reprogramming of Pyruvate Metabolism
Supplementary Table S1 from <i>IDH1</i> Mutation Induces Reprogramming of Pyruvate Metabolism Open
Comparison of PDH activity in the various models used in this study.
View article: Supplementary Table S1 from <i>IDH1</i> Mutation Induces Reprogramming of Pyruvate Metabolism
Supplementary Table S1 from <i>IDH1</i> Mutation Induces Reprogramming of Pyruvate Metabolism Open
Comparison of PDH activity in the various models used in this study.
View article: Supplementary Figure S2 from <i>IDH1</i> Mutation Induces Reprogramming of Pyruvate Metabolism
Supplementary Figure S2 from <i>IDH1</i> Mutation Induces Reprogramming of Pyruvate Metabolism Open
Cytotoxicity of DCA against IDH1 wild-type and mutant cells for the U87 (A) and NHA (B) models (* indicates significant difference (p<0.05) relative to control).
View article: Data from <i>IDH1</i> Mutation Induces Reprogramming of Pyruvate Metabolism
Data from <i>IDH1</i> Mutation Induces Reprogramming of Pyruvate Metabolism Open
Mutant isocitrate dehydrogenase 1 (IDH1) catalyzes the production of 2-hydroxyglutarate but also elicits additional metabolic changes. Levels of both glutamate and pyruvate dehydrogenase (PDH) activity have been shown to be affected in U87…
View article: Data from <i>IDH1</i> Mutation Induces Reprogramming of Pyruvate Metabolism
Data from <i>IDH1</i> Mutation Induces Reprogramming of Pyruvate Metabolism Open
Mutant isocitrate dehydrogenase 1 (IDH1) catalyzes the production of 2-hydroxyglutarate but also elicits additional metabolic changes. Levels of both glutamate and pyruvate dehydrogenase (PDH) activity have been shown to be affected in U87…
View article: Supplementary Figure S1 from <i>IDH1</i> Mutation Induces Reprogramming of Pyruvate Metabolism
Supplementary Figure S1 from <i>IDH1</i> Mutation Induces Reprogramming of Pyruvate Metabolism Open
Effect of 2-HG on cell proliferation of IDH1 wild-type cells for the U87 (A) and NHA (B) models.
View article: PDGF gene expression and p53 alterations contribute to the biology of diffuse astrocytic gliomas
PDGF gene expression and p53 alterations contribute to the biology of diffuse astrocytic gliomas Open
Diffuse, histologically lower grade astrocytomas of adults (LGAs) are classified based on the mutational status of the isocitrate dehydrogenase ( IDH ) genes. While wild-type (WT) LGAs often evolve quickly to glioblastoma (GBM), mutant tum…
View article: Single-cell landscapes of primary glioblastomas and matched explants and cell lines show variable retention of inter- and intratumor heterogeneity
Single-cell landscapes of primary glioblastomas and matched explants and cell lines show variable retention of inter- and intratumor heterogeneity Open
Glioblastomas (GBMs) are aggressive brain tumors characterized by extensive inter- and intratumor heterogeneity. Patient-derived models, such as organoids and explants, have recently emerged as useful models to study such heterogeneity, al…
View article: PATH-11. PDGFA INITIATES ABERRANT MITOSIS AND MALIGNANT TRANSFORMATION OF NEURAL PROGENITOR CELLS
PATH-11. PDGFA INITIATES ABERRANT MITOSIS AND MALIGNANT TRANSFORMATION OF NEURAL PROGENITOR CELLS Open
BACKGROUND Imagining ways to prevent or treat glioblastoma (GBM) have been hindered by a lack of understanding of its pathogenesis. Although platelet derived growth factor-A (PDGFA) overexpression may be an early event, critical details of…
View article: EPCO-06. MOLECULAR DETERMINANTS OF EVOLUTION AND PROGNOSIS AMONG DIFFUSE LOWER GRADE ASTROCYTOMAS
EPCO-06. MOLECULAR DETERMINANTS OF EVOLUTION AND PROGNOSIS AMONG DIFFUSE LOWER GRADE ASTROCYTOMAS Open
Gliomas with wild type (WT) isocitrate dehydrogenase (IDH) are considerably more aggressive than those with mutant IDH. To identify putative drivers of the distinct progression trajectories of IDH WT and mutant disease, we analyzed transcr…
View article: Molecular Determinants of Prognosis and Evolution in Diffuse-Lower Grade Astrocytomas
Molecular Determinants of Prognosis and Evolution in Diffuse-Lower Grade Astrocytomas Open
Low grade astrocytomas (LGAs) are classified based on the mutational status of the isocitrate dehydrogenase (IDH) gene. While IDH wild-type (WT) LGAs evolve rapidly to glioblastoma, mutant tumors generally have a more indolent course. To i…
View article: In vitro modeling of glioblastoma initiation using PDGF-AA and p53-null neural progenitors
In vitro modeling of glioblastoma initiation using PDGF-AA and p53-null neural progenitors Open
Background Imagining ways to prevent or treat glioblastoma (GBM) has been hindered by a lack of understanding of its pathogenesis. Although overexpression of platelet derived growth factor with two A-chains (PDGF-AA) may be an early event,…
View article: Beyond Conventional Models: Recreating the Initiation, Evolution, and Genome of GBM
Beyond Conventional Models: Recreating the Initiation, Evolution, and Genome of GBM Open
Background Imagining ways to prevent or treat glioblastoma (GBM) have been hindered by a lack of understanding of its pathogenesis. Although PDGF-AA overexpression may be an early event, critical details of the core biology are lacking. Ex…
View article: TMOD-02. A MODEL OF THE INITIATION AND GENOMIC LANDSCAPE OF GLIOBLASTOMA (GBM)
TMOD-02. A MODEL OF THE INITIATION AND GENOMIC LANDSCAPE OF GLIOBLASTOMA (GBM) Open
IDH-wildtype GBM is the most common variant of this cancer and occurs in older adults. Unfortunately patients’ tumors are either inherently resistant to standard treatment, which includes radio- and chemo-therapy, or acquire resistance dur…
View article: Comprehensive genomic profiling of glioblastoma tumors, BTICs, and xenografts reveals stability and adaptation to growth environments
Comprehensive genomic profiling of glioblastoma tumors, BTICs, and xenografts reveals stability and adaptation to growth environments Open
Glioblastoma multiforme (GBM) is the most deadly brain tumor, and currently lacks effective treatment options. Brain tumor-initiating cells (BTICs) and orthotopic xenografts are widely used in investigating GBM biology and new therapies fo…
View article: Capicua regulates neural stem cell proliferation and lineage specification through control of Ets factors
Capicua regulates neural stem cell proliferation and lineage specification through control of Ets factors Open
Capicua (Cic) is a transcriptional repressor mutated in the brain cancer oligodendroglioma. Despite its cancer link, little is known of Cic’s function in the brain. We show that nuclear Cic expression is strongest in astrocytes and neurons…
View article: DRES-06. PREVENTING THE EMERGENCE OF TEMOZOLOMIDE RESISTANCE IN GLIOBLASTOMA BY PARP-1 INHIBITION
DRES-06. PREVENTING THE EMERGENCE OF TEMOZOLOMIDE RESISTANCE IN GLIOBLASTOMA BY PARP-1 INHIBITION Open
The DNA alkylating agent temozolomide (TMZ) is active against the subset of glioblastomas (GBMs) in which the O6-methylguanine DNA methyltransferase (MGMT) gene is silenced by promoter methylation. However, despite their initial sensitivit…
View article: DRES-04. CHARACTERIZATION OF A MODEL OF TEMOZOLOMIDE RESISTANCE IN GLIOBLASTOMA
DRES-04. CHARACTERIZATION OF A MODEL OF TEMOZOLOMIDE RESISTANCE IN GLIOBLASTOMA Open
Despite the discovery and widespread use of the chemotherapeutic drug temozolomide (TMZ), glioblastoma (GBM) remains a fatal cancer. TMZ, a DNA alkylating agent, provides a moderate survival benefit to patients whose tumours do not express…
ABT-888 restores sensitivity in temozolomide resistant glioma cells and xenografts Open
In laboratory models, the addition of ABT-888 to TMZ overcame resistance to TMZ.
View article: 21 Inhibiting PARP-1 to restore temozolomide sensitivity and prevent resistance in glioblastoma
21 Inhibiting PARP-1 to restore temozolomide sensitivity and prevent resistance in glioblastoma Open
Adult Glioblastomas (GBMs) remain one of the least curable brain cancers despite the discovery and use of DNA alkylating agent Temozolomide (TMZ). TMZ provides a moderate survival benefit to sensitive patients whose O6-methylguanine-methyl…
View article: Capicua regulates neural stem cell proliferation and lineage specification through control of Ets factors
Capicua regulates neural stem cell proliferation and lineage specification through control of Ets factors Open
Capicua (Cic) is a transcriptional repressor mutated in the brain cancer oligodendroglioma. Despite its cancer link, little is known of Cic’s function in the brain. Here, we investigated the relationship between Cic expression and cell typ…
View article: STMC-31. STIMULATION OF MICROGLIA AND MACROPHAGES AND GROWTH ATTENUATION OF BRAIN TUMOR-INITIATING CELLS WITH TUMOR NECROSIS FACTOR-ALPHA
STMC-31. STIMULATION OF MICROGLIA AND MACROPHAGES AND GROWTH ATTENUATION OF BRAIN TUMOR-INITIATING CELLS WITH TUMOR NECROSIS FACTOR-ALPHA Open
Microglia and macrophages (M/Ms) are functionally plastic entities that are compelled by glioblastoma (GBM) to adopt anti-inflammatory phenotypes and become major players in GBM progression. Understanding how to reverse this compulsion and…
View article: CSIG-19. RECEPTOR TYROSINE KINASE PHOSPHORYLATION IN A MODEL SYSTEM OF GBM
CSIG-19. RECEPTOR TYROSINE KINASE PHOSPHORYLATION IN A MODEL SYSTEM OF GBM Open
Glioblastoma Multiforme (GBM) is the most common brain tumour in adults, and despite our best treatments is fatal. Multiple receptor tyrosine kinases (RTKs) are amplified in GBM: 45% have elevated expression of Epidermal Growth Factor Rece…
View article: GENT-27. COMPREHENSIVE MOLECULAR CHARACTERIZATION OF N-ETHYL-N-NITROSOUREA INDUCED RAT GLIOMAS
GENT-27. COMPREHENSIVE MOLECULAR CHARACTERIZATION OF N-ETHYL-N-NITROSOUREA INDUCED RAT GLIOMAS Open
Gliomas affecting children and young adults are genetically distinct from those in older adults. Next-generation sequencing has revealed unique mutations, methylation patterns, and expression profiles, which now define age- and location-sp…