Lancet Oncology, The, ISSN 1470-2045, 2015, Volume 16, Issue 5, pp. 569 - 582
Summary Background Rhabdoid brain tumours, also called atypical teratoid rhabdoid tumours, are lethal childhood cancers with characteristic genetic alterations...
Hematology, Oncology and Palliative Medicine | SURVIVAL | CELLS | FOREBRAIN | THERAPY | PROGNOSTIC-FACTORS | ONCOLOGY | GENE-EXPRESSION | MUTATIONS | HSNF5/INI1 | TERATOID/RHABDOID TUMORS | Immunohistochemistry | Basic Helix-Loop-Helix Transcription Factors - genetics | Prognosis | Genomics | Humans | Risk Factors | Gene Expression Regulation, Neoplastic | Child, Preschool | Infant | Male | Receptors, Notch - genetics | Signal Transduction - genetics | Rhabdoid Tumor - pathology | Teratoma - pathology | Rhabdoid Tumor - genetics | Receptors, Notch - biosynthesis | Basic Helix-Loop-Helix Transcription Factors - biosynthesis | Teratoma - genetics | Female | Child | Genetic research | Analysis | Tumors | Clinical Medicine | Medical and Health Sciences | Cancer and Oncology | Klinisk medicin | Medicin och hälsovetenskap | Cancer och onkologi
Hematology, Oncology and Palliative Medicine | SURVIVAL | CELLS | FOREBRAIN | THERAPY | PROGNOSTIC-FACTORS | ONCOLOGY | GENE-EXPRESSION | MUTATIONS | HSNF5/INI1 | TERATOID/RHABDOID TUMORS | Immunohistochemistry | Basic Helix-Loop-Helix Transcription Factors - genetics | Prognosis | Genomics | Humans | Risk Factors | Gene Expression Regulation, Neoplastic | Child, Preschool | Infant | Male | Receptors, Notch - genetics | Signal Transduction - genetics | Rhabdoid Tumor - pathology | Teratoma - pathology | Rhabdoid Tumor - genetics | Receptors, Notch - biosynthesis | Basic Helix-Loop-Helix Transcription Factors - biosynthesis | Teratoma - genetics | Female | Child | Genetic research | Analysis | Tumors | Clinical Medicine | Medical and Health Sciences | Cancer and Oncology | Klinisk medicin | Medicin och hälsovetenskap | Cancer och onkologi
Journal Article
Clinical Pediatric Emergency Medicine, ISSN 1522-8401, 2011, Volume 12, Issue 3, pp. 213 - 223
Central nervous system (CNS) tumors are the most common solid tumors in childhood and adolescence. Evaluation and management of patients with CNS tumors by...
Emergency | hydrocephalus | spinal cord compression | chemotherapy | central nervous system (CNS) tumors | radiation therapy | Chemotherapy | Radiation therapy | Hydrocephalus | Spinal cord compression | Central nervous system (CNS) tumors | Radiotherapy | Central nervous system | Cancer | Tumors | Pediatrics | Stroke | Medical treatment | Brain cancer | Emergencies | Headaches | Neurosurgery | Blood clots
Emergency | hydrocephalus | spinal cord compression | chemotherapy | central nervous system (CNS) tumors | radiation therapy | Chemotherapy | Radiation therapy | Hydrocephalus | Spinal cord compression | Central nervous system (CNS) tumors | Radiotherapy | Central nervous system | Cancer | Tumors | Pediatrics | Stroke | Medical treatment | Brain cancer | Emergencies | Headaches | Neurosurgery | Blood clots
Journal Article
PLoS ONE, ISSN 1932-6203, 2011, Volume 6, Issue 10, p. e25114
Introduction: We have examined expression of microRNAs (miRNAs) in ependymomas to identify molecular markers of value for clinical management. miRNAs are...
CELLS | GLIOMA | MULTIDISCIPLINARY SCIENCES | LET-7 | INTRACRANIAL EPENDYMOMA | EXPRESSION | PCR | Multivariate Analysis | Prognosis | Humans | Computational Biology | Gene Expression Regulation, Neoplastic | Proportional Hazards Models | Child, Preschool | Infant | Male | MicroRNAs - metabolism | Gene Expression Profiling | Ependymoma - genetics | Case-Control Studies | Regression Analysis | Adolescent | Survival Analysis | Biomarkers, Tumor - metabolism | Ependymoma - pathology | Female | Biomarkers, Tumor - genetics | MicroRNAs - genetics | Child | Development and progression | MicroRNA | Genetic translation | Brain tumors | Brain | Pediatrics | Correlation | Brain cancer | Identification | Biology | Metastasis | Paraffin | Parameter identification | Cancer therapies | Coding | Cell cycle | Chromosome 14 | Research centers | Chromosomes | Markers | MiRNA | Histology | Regression analysis | Gene expression | Children & youth | Medicine | Ependymal cells | Brain research | Hospitals | MicroRNAs | Medical prognosis | Stem cells | Epigenetics | Mutation | mRNA stability | Tumors
CELLS | GLIOMA | MULTIDISCIPLINARY SCIENCES | LET-7 | INTRACRANIAL EPENDYMOMA | EXPRESSION | PCR | Multivariate Analysis | Prognosis | Humans | Computational Biology | Gene Expression Regulation, Neoplastic | Proportional Hazards Models | Child, Preschool | Infant | Male | MicroRNAs - metabolism | Gene Expression Profiling | Ependymoma - genetics | Case-Control Studies | Regression Analysis | Adolescent | Survival Analysis | Biomarkers, Tumor - metabolism | Ependymoma - pathology | Female | Biomarkers, Tumor - genetics | MicroRNAs - genetics | Child | Development and progression | MicroRNA | Genetic translation | Brain tumors | Brain | Pediatrics | Correlation | Brain cancer | Identification | Biology | Metastasis | Paraffin | Parameter identification | Cancer therapies | Coding | Cell cycle | Chromosome 14 | Research centers | Chromosomes | Markers | MiRNA | Histology | Regression analysis | Gene expression | Children & youth | Medicine | Ependymal cells | Brain research | Hospitals | MicroRNAs | Medical prognosis | Stem cells | Epigenetics | Mutation | mRNA stability | Tumors
Journal Article
Cancer Cell, ISSN 1535-6108, 12/2016, Volume 30, Issue 6, pp. 891 - 908
We recently reported that atypical teratoid rhabdoid tumors (ATRTs) comprise at least two transcriptional subtypes with different clinical outcomes; however,...
genomics | epigenomics | subgroup-specific therapeutics | enhancer | ATRT | rhabdoid tumors | GENE | CHROMATIN | ONCOLOGY | CENTRAL-NERVOUS-SYSTEM | MUTATIONS | DIFFERENTIATION | ATYPICAL TERATOID/RHABDOID TUMORS | EXPRESSION | CANCER | GENOME | CHILDREN | CELL BIOLOGY | Cell Survival - drug effects | Rhabdoid Tumor - drug therapy | Central Nervous System Neoplasms - genetics | Humans | Dasatinib - therapeutic use | SMARCB1 Protein - genetics | Pyrimidines - pharmacology | Receptor, Platelet-Derived Growth Factor beta - genetics | Dasatinib - pharmacology | DNA Methylation | Receptor, Platelet-Derived Growth Factor beta - antagonists & inhibitors | Rhabdoid Tumor - genetics | Epigenomics - methods | Protein Kinase Inhibitors - therapeutic use | Pyrimidines - therapeutic use | Teratoma - drug therapy | Cell Line, Tumor | Teratoma - genetics | Cell Proliferation - drug effects | Epigenesis, Genetic - drug effects | Protein Kinase Inhibitors - pharmacology | Mutation | Central Nervous System Neoplasms - drug therapy | Chromatin - genetics | Genetic research | Health aspects | Analysis | Tumors | Index Medicus
genomics | epigenomics | subgroup-specific therapeutics | enhancer | ATRT | rhabdoid tumors | GENE | CHROMATIN | ONCOLOGY | CENTRAL-NERVOUS-SYSTEM | MUTATIONS | DIFFERENTIATION | ATYPICAL TERATOID/RHABDOID TUMORS | EXPRESSION | CANCER | GENOME | CHILDREN | CELL BIOLOGY | Cell Survival - drug effects | Rhabdoid Tumor - drug therapy | Central Nervous System Neoplasms - genetics | Humans | Dasatinib - therapeutic use | SMARCB1 Protein - genetics | Pyrimidines - pharmacology | Receptor, Platelet-Derived Growth Factor beta - genetics | Dasatinib - pharmacology | DNA Methylation | Receptor, Platelet-Derived Growth Factor beta - antagonists & inhibitors | Rhabdoid Tumor - genetics | Epigenomics - methods | Protein Kinase Inhibitors - therapeutic use | Pyrimidines - therapeutic use | Teratoma - drug therapy | Cell Line, Tumor | Teratoma - genetics | Cell Proliferation - drug effects | Epigenesis, Genetic - drug effects | Protein Kinase Inhibitors - pharmacology | Mutation | Central Nervous System Neoplasms - drug therapy | Chromatin - genetics | Genetic research | Health aspects | Analysis | Tumors | Index Medicus
Journal Article
Neuro-Oncology, ISSN 1522-8517, 11/2016, Volume 18, Issue 11, pp. 1519 - 1528
Background. Radiation therapy is the most commonly used postsurgical treatment for primary malignant brain tumors. Consequently, investigating the efficacy of...
bioluminescence imaging | Atypical teratoid rhabdoid tumor | glioblastoma | xenograft | palbociclib | PATHWAYS | CELLS | RADIATION SENSITIVITY | MODEL | P16(INK4A) | DISCOVERY | EGFR | CLINICAL NEUROLOGY | G ARREST | GENE | ONCOLOGY | GROWTH | atypical teratoid rhabdoid tumor | Cyclin-Dependent Kinase 6 - antagonists & inhibitors | Glioblastoma - enzymology | Humans | Antineoplastic Agents - therapeutic use | Glioblastoma - radiotherapy | Heterografts | Teratoma - radiotherapy | Female | Brain Neoplasms - radiotherapy | Cyclin-Dependent Kinase 4 - antagonists & inhibitors | Pyridines - therapeutic use | DNA Damage - drug effects | Rhabdoid Tumor - drug therapy | Brain Neoplasms - enzymology | Chemoradiotherapy - methods | DNA Repair - drug effects | Teratoma - enzymology | Retinoblastoma Protein - metabolism | Rhabdoid Tumor - radiotherapy | Combined Modality Therapy | Cyclin-Dependent Kinase 6 - metabolism | Piperazines - therapeutic use | Brain Neoplasms - drug therapy | Cyclin-Dependent Kinase 4 - metabolism | Rhabdoid Tumor - enzymology | Xenograft Model Antitumor Assays | Animals | Teratoma - drug therapy | Survival Analysis | Cell Line, Tumor | Cell Proliferation - drug effects | Mice, Inbred BALB C | Glioblastoma - drug therapy | Basic and Translational Investigation
bioluminescence imaging | Atypical teratoid rhabdoid tumor | glioblastoma | xenograft | palbociclib | PATHWAYS | CELLS | RADIATION SENSITIVITY | MODEL | P16(INK4A) | DISCOVERY | EGFR | CLINICAL NEUROLOGY | G ARREST | GENE | ONCOLOGY | GROWTH | atypical teratoid rhabdoid tumor | Cyclin-Dependent Kinase 6 - antagonists & inhibitors | Glioblastoma - enzymology | Humans | Antineoplastic Agents - therapeutic use | Glioblastoma - radiotherapy | Heterografts | Teratoma - radiotherapy | Female | Brain Neoplasms - radiotherapy | Cyclin-Dependent Kinase 4 - antagonists & inhibitors | Pyridines - therapeutic use | DNA Damage - drug effects | Rhabdoid Tumor - drug therapy | Brain Neoplasms - enzymology | Chemoradiotherapy - methods | DNA Repair - drug effects | Teratoma - enzymology | Retinoblastoma Protein - metabolism | Rhabdoid Tumor - radiotherapy | Combined Modality Therapy | Cyclin-Dependent Kinase 6 - metabolism | Piperazines - therapeutic use | Brain Neoplasms - drug therapy | Cyclin-Dependent Kinase 4 - metabolism | Rhabdoid Tumor - enzymology | Xenograft Model Antitumor Assays | Animals | Teratoma - drug therapy | Survival Analysis | Cell Line, Tumor | Cell Proliferation - drug effects | Mice, Inbred BALB C | Glioblastoma - drug therapy | Basic and Translational Investigation
Journal Article
Clinical Cancer Research, ISSN 1078-0432, 01/2015, Volume 21, Issue 1, pp. 184 - 192
Purpose: To investigate molecular alterations in choroid plexus tumors (CPT) using a genome-wide high-throughput approach to identify diagnostic and prognostic...
ARTICLE | EXPERIENCE | ONCOLOGY | PROGRESSION | PAPILLOMA | Prognosis | Neoplasm Proteins - biosynthesis | Humans | Gene Expression Regulation, Neoplastic | Child, Preschool | Infant | Male | DNA Methylation - genetics | Choroid Plexus Neoplasms - pathology | Tumor Suppressor Protein p53 - genetics | Disease-Free Survival | Choroid Plexus Neoplasms - genetics | Adolescent | Female | Mutation | Neoplasm Staging | Child | Choroid Plexus Neoplasms - classification
ARTICLE | EXPERIENCE | ONCOLOGY | PROGRESSION | PAPILLOMA | Prognosis | Neoplasm Proteins - biosynthesis | Humans | Gene Expression Regulation, Neoplastic | Child, Preschool | Infant | Male | DNA Methylation - genetics | Choroid Plexus Neoplasms - pathology | Tumor Suppressor Protein p53 - genetics | Disease-Free Survival | Choroid Plexus Neoplasms - genetics | Adolescent | Female | Mutation | Neoplasm Staging | Child | Choroid Plexus Neoplasms - classification
Journal Article
Nature Medicine, ISSN 1078-8956, 04/2017, Volume 23, Issue 4, pp. 493 - 500
Diffuse intrinsic pontine glioma (DIPG) is a highly aggressive pediatric brainstem tumor characterized by rapid and uniform patient demise(1). A heterozygous...
MEDICINE, RESEARCH & EXPERIMENTAL | METHYLATION | INHIBITION | ALIGNMENT | HISTONE H3 | BIOCHEMISTRY & MOLECULAR BIOLOGY | TRANSCRIPTION | MUTATION | GENE-EXPRESSION | CELL | CELL BIOLOGY | Chromatin - metabolism | Humans | Nucleosomes - drug effects | Molecular Targeted Therapy | Glioma - genetics | Neurogenesis - genetics | Histone Code - drug effects | Neurogenesis - drug effects | Gene Expression Regulation, Neoplastic - drug effects | Chromatin - drug effects | Gene Expression Regulation, Neoplastic - genetics | RNA-Binding Proteins - antagonists & inhibitors | Cell Proliferation - genetics | Epigenomics | Nucleosomes - metabolism | Polycomb Repressive Complex 2 - drug effects | Histones - drug effects | Protein Transport | Azepines - pharmacology | Triazoles - pharmacology | Xenograft Model Antitumor Assays | Acetylation - drug effects | Animals | Brain Stem Neoplasms - genetics | Histones - genetics | Methylation - drug effects | Cell Line, Tumor | Cell Proliferation - drug effects | Mice | Mutation | Polycomb Repressive Complex 2 - metabolism | Histone Code - genetics | RNA-Binding Proteins - metabolism | Molecular targeted therapy | Care and treatment | Gliomas | Histones | Development and progression | Genetic aspects | Tumor proteins | Health aspects
MEDICINE, RESEARCH & EXPERIMENTAL | METHYLATION | INHIBITION | ALIGNMENT | HISTONE H3 | BIOCHEMISTRY & MOLECULAR BIOLOGY | TRANSCRIPTION | MUTATION | GENE-EXPRESSION | CELL | CELL BIOLOGY | Chromatin - metabolism | Humans | Nucleosomes - drug effects | Molecular Targeted Therapy | Glioma - genetics | Neurogenesis - genetics | Histone Code - drug effects | Neurogenesis - drug effects | Gene Expression Regulation, Neoplastic - drug effects | Chromatin - drug effects | Gene Expression Regulation, Neoplastic - genetics | RNA-Binding Proteins - antagonists & inhibitors | Cell Proliferation - genetics | Epigenomics | Nucleosomes - metabolism | Polycomb Repressive Complex 2 - drug effects | Histones - drug effects | Protein Transport | Azepines - pharmacology | Triazoles - pharmacology | Xenograft Model Antitumor Assays | Acetylation - drug effects | Animals | Brain Stem Neoplasms - genetics | Histones - genetics | Methylation - drug effects | Cell Line, Tumor | Cell Proliferation - drug effects | Mice | Mutation | Polycomb Repressive Complex 2 - metabolism | Histone Code - genetics | RNA-Binding Proteins - metabolism | Molecular targeted therapy | Care and treatment | Gliomas | Histones | Development and progression | Genetic aspects | Tumor proteins | Health aspects
Journal Article
Acta neuropathologica communications, ISSN 2051-5960, 04/2017, Volume 5, Issue 1, pp. 28 - 12
Diffuse midline gliomas (including diffuse intrinsic pontine glioma, DIPG) are highly morbid glial neoplasms of the thalamus or brainstem that typically arise...
Liquid biopsy | Cerebrospinal fluid | Diffuse midline glioma | H3K27M | Diffuse intrinsic pontine glioma (DIPG) | H3F3A | BIOPSY | SUBGROUPS | PEDIATRIC GLIOBLASTOMA | NEUROSCIENCES | LINEAR POLYACRYLAMIDE | PRECIPITATION | K27M MUTATION | INTRINSIC PONTINE GLIOMAS | CENTRAL-NERVOUS-SYSTEM | BRAIN | Immunohistochemistry | Humans | Brain Neoplasms - genetics | DNA Mutational Analysis - methods | Glioma - cerebrospinal fluid | Brain Neoplasms - metabolism | Brain Neoplasms - surgery | Feasibility Studies | Glioma - metabolism | Brain - metabolism | Glioma - genetics | Histones - genetics | Biomarkers, Tumor - cerebrospinal fluid | Brain - pathology | Cell Line, Tumor | Brain - surgery | Histones - cerebrospinal fluid | Biomarkers, Tumor - genetics | Mutation | Glioma - surgery | Brain Neoplasms - cerebrospinal fluid | DNA, Neoplasm - cerebrospinal fluid | Gene mutations | Gliomas | DNA | Genetic aspects | Research | Children | Health aspects | Pediatrics | Biopsy | Brain cancer | DNA methylation | Gene expression | Patients | Deoxyribonucleic acid--DNA | Tumors
Liquid biopsy | Cerebrospinal fluid | Diffuse midline glioma | H3K27M | Diffuse intrinsic pontine glioma (DIPG) | H3F3A | BIOPSY | SUBGROUPS | PEDIATRIC GLIOBLASTOMA | NEUROSCIENCES | LINEAR POLYACRYLAMIDE | PRECIPITATION | K27M MUTATION | INTRINSIC PONTINE GLIOMAS | CENTRAL-NERVOUS-SYSTEM | BRAIN | Immunohistochemistry | Humans | Brain Neoplasms - genetics | DNA Mutational Analysis - methods | Glioma - cerebrospinal fluid | Brain Neoplasms - metabolism | Brain Neoplasms - surgery | Feasibility Studies | Glioma - metabolism | Brain - metabolism | Glioma - genetics | Histones - genetics | Biomarkers, Tumor - cerebrospinal fluid | Brain - pathology | Cell Line, Tumor | Brain - surgery | Histones - cerebrospinal fluid | Biomarkers, Tumor - genetics | Mutation | Glioma - surgery | Brain Neoplasms - cerebrospinal fluid | DNA, Neoplasm - cerebrospinal fluid | Gene mutations | Gliomas | DNA | Genetic aspects | Research | Children | Health aspects | Pediatrics | Biopsy | Brain cancer | DNA methylation | Gene expression | Patients | Deoxyribonucleic acid--DNA | Tumors
Journal Article
PLoS ONE, ISSN 1932-6203, 03/2015, Volume 10, Issue 3, pp. e0121707 - e0121707
There is growing evidence and a consensus in the field that most pediatric brain tumors originate from stem cells, of which radial glial cells constitute a...
EPITHELIAL-MESENCHYMAL TRANSITION | STEM-CELLS | ROLES | MULTIDISCIPLINARY SCIENCES | DIFFERENTIATION | MEDULLOBLASTOMA | EXPRESSION | CHROMOSOMAL INSTABILITY | Neuroglia - cytology | Animals | Humans | Cell Line, Tumor | Tumor Microenvironment | Cell Transplantation | Mice, Inbred NOD | Mice | Mice, SCID | Disease Models, Animal | Neuroectodermal Tumors, Primitive - pathology | Brain | Models | Brain tumors | Stem cells | Pediatrics | Transformation | Mesenchyme | Brain stem | Brain cancer | Central nervous system | Radial glial cells | Stem cell transplantation | Oncology | Ventricles (cerebral) | Transplantation | Biology | Glial cells | Drug screening | Subventricular zone | Angiogenesis | Toxicology | Alterations | Genetics | Pharmaceutical sciences | Medical research | Phenotypes | Nervous system diseases | Hematology | Invasiveness | Interdisciplinary aspects | Molecular chains | Endothelial cells | Medicine | Brain research | Cytogenetics | Hypoxia | Ventricle | Mutation | Laboratory animals | Tumors | Cancer | Index Medicus
EPITHELIAL-MESENCHYMAL TRANSITION | STEM-CELLS | ROLES | MULTIDISCIPLINARY SCIENCES | DIFFERENTIATION | MEDULLOBLASTOMA | EXPRESSION | CHROMOSOMAL INSTABILITY | Neuroglia - cytology | Animals | Humans | Cell Line, Tumor | Tumor Microenvironment | Cell Transplantation | Mice, Inbred NOD | Mice | Mice, SCID | Disease Models, Animal | Neuroectodermal Tumors, Primitive - pathology | Brain | Models | Brain tumors | Stem cells | Pediatrics | Transformation | Mesenchyme | Brain stem | Brain cancer | Central nervous system | Radial glial cells | Stem cell transplantation | Oncology | Ventricles (cerebral) | Transplantation | Biology | Glial cells | Drug screening | Subventricular zone | Angiogenesis | Toxicology | Alterations | Genetics | Pharmaceutical sciences | Medical research | Phenotypes | Nervous system diseases | Hematology | Invasiveness | Interdisciplinary aspects | Molecular chains | Endothelial cells | Medicine | Brain research | Cytogenetics | Hypoxia | Ventricle | Mutation | Laboratory animals | Tumors | Cancer | Index Medicus
Journal Article
Science signaling, ISSN 1945-0877, 01/2019, Volume 12, Issue 565
In medulloblastomas (MBs), the expression and activity of RE1-silencing transcription factor (REST) is increased in tumors driven by the sonic hedgehog (SHH)...
TARGET | REST/NRSF | REGULATOR | PROTEIN | SIGNALING PATHWAY | BIOCHEMISTRY & MOLECULAR BIOLOGY | MOLECULAR SUBGROUPS | PROLIFERATION | EXPRESSION | G9A | SONIC-HEDGEHOG | CELL BIOLOGY | Cell proliferation | Cerebellum | Brain | Brain tumors | AKT protein | Activation | Infants | Subgroups | Signal transduction | Rest | Rodents | Tumorigenesis | Children | Maturation | Therapeutic applications | Transgenic mice | Patients | Chromatin remodeling | Gene silencing | Signaling | Hedgehog protein | Medulloblastoma | Neural stem cells | Methylation | PTEN protein | Tumors | Apoptosis
TARGET | REST/NRSF | REGULATOR | PROTEIN | SIGNALING PATHWAY | BIOCHEMISTRY & MOLECULAR BIOLOGY | MOLECULAR SUBGROUPS | PROLIFERATION | EXPRESSION | G9A | SONIC-HEDGEHOG | CELL BIOLOGY | Cell proliferation | Cerebellum | Brain | Brain tumors | AKT protein | Activation | Infants | Subgroups | Signal transduction | Rest | Rodents | Tumorigenesis | Children | Maturation | Therapeutic applications | Transgenic mice | Patients | Chromatin remodeling | Gene silencing | Signaling | Hedgehog protein | Medulloblastoma | Neural stem cells | Methylation | PTEN protein | Tumors | Apoptosis
Journal Article
Oncotarget, ISSN 1949-2553, 2018, Volume 9, Issue 4, pp. 5233 - 5250
Diffuse intrinsic pontine glioma (DIPG) is a highly aggressive glial tumor that occurs in children. The extremely poor median and 5-year survival in children...
VEGFR2 | REST | Gremlin | DIPG | Vasculature | vasculature | PEDIATRIC GLIOMAS | BONE MORPHOGENETIC PROTEIN | ACTIVATING ACVR1 MUTATIONS | BRAIN-TUMORS | CELL BIOLOGY | GLIOBLASTOMA STEM-CELLS | gremlin | NEURONAL GENES | RESTRICTIVE SILENCER FACTOR | HIGH-GRADE GLIOMAS | ONCOGENIC PROPERTIES | ENDOTHELIAL GROWTH-FACTOR
VEGFR2 | REST | Gremlin | DIPG | Vasculature | vasculature | PEDIATRIC GLIOMAS | BONE MORPHOGENETIC PROTEIN | ACTIVATING ACVR1 MUTATIONS | BRAIN-TUMORS | CELL BIOLOGY | GLIOBLASTOMA STEM-CELLS | gremlin | NEURONAL GENES | RESTRICTIVE SILENCER FACTOR | HIGH-GRADE GLIOMAS | ONCOGENIC PROPERTIES | ENDOTHELIAL GROWTH-FACTOR
Journal Article
ONCOTARGET, ISSN 1949-2553, 05/2016, Volume 7, Issue 22, pp. 33192 - 33201
The PIM family of proteins encodes serine/threonine kinases with important roles in protein synthesis and cancer cell metabolism. In glioblastoma (GBM) cell...
ACTIVATION | PIM kinase | PHOSPHORYLATION | mTOR signaling | MULTIFORME | MTOR | CELL BIOLOGY | glioblastoma | CANCER GENOMICS | PIK3CA GENE | SIGNALING PATHWAY | GROWTH | p110 alpha | REGULATORS | MUTATIONS | Class I Phosphatidylinositol 3-Kinases - metabolism | Neoplastic Stem Cells - drug effects | Humans | Brain Neoplasms - pathology | Proto-Oncogene Proteins c-pim-1 - metabolism | Pyridazines - pharmacology | Molecular Targeted Therapy | Antineoplastic Combined Chemotherapy Protocols - pharmacology | Dose-Response Relationship, Drug | Biphenyl Compounds - pharmacology | Proto-Oncogene Proteins c-pim-1 - antagonists & inhibitors | Glioma - pathology | Neoplastic Stem Cells - pathology | Thiazolidines - pharmacology | Brain Neoplasms - enzymology | Glioma - enzymology | Imidazoles - pharmacology | Brain Neoplasms - drug therapy | Class I Phosphatidylinositol 3-Kinases - antagonists & inhibitors | Signal Transduction - drug effects | Cell Line, Tumor | Protein Kinase Inhibitors - pharmacology | Thiazoles - pharmacology | Neoplastic Stem Cells - enzymology | Glioma - drug therapy
ACTIVATION | PIM kinase | PHOSPHORYLATION | mTOR signaling | MULTIFORME | MTOR | CELL BIOLOGY | glioblastoma | CANCER GENOMICS | PIK3CA GENE | SIGNALING PATHWAY | GROWTH | p110 alpha | REGULATORS | MUTATIONS | Class I Phosphatidylinositol 3-Kinases - metabolism | Neoplastic Stem Cells - drug effects | Humans | Brain Neoplasms - pathology | Proto-Oncogene Proteins c-pim-1 - metabolism | Pyridazines - pharmacology | Molecular Targeted Therapy | Antineoplastic Combined Chemotherapy Protocols - pharmacology | Dose-Response Relationship, Drug | Biphenyl Compounds - pharmacology | Proto-Oncogene Proteins c-pim-1 - antagonists & inhibitors | Glioma - pathology | Neoplastic Stem Cells - pathology | Thiazolidines - pharmacology | Brain Neoplasms - enzymology | Glioma - enzymology | Imidazoles - pharmacology | Brain Neoplasms - drug therapy | Class I Phosphatidylinositol 3-Kinases - antagonists & inhibitors | Signal Transduction - drug effects | Cell Line, Tumor | Protein Kinase Inhibitors - pharmacology | Thiazoles - pharmacology | Neoplastic Stem Cells - enzymology | Glioma - drug therapy
Journal Article
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