Molecular mechanisms involved in gliomagenesis
The application of molecular parameters in the World Health Organization classification of central nervous system tumors has advanced remarkably in this field. Large-scale genomic DNA analyses, including gene expression profiling, genome-wide association studies, and single-nucleotide polymorphism a...
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| Veröffentlicht in: | Brain tumor pathology 2017, Vol.34 (1), p.1-7 |
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| container_title | Brain tumor pathology |
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| creator | Kondo, Toru |
| description | The application of molecular parameters in the World Health Organization classification of central nervous system tumors has advanced remarkably in this field. Large-scale genomic DNA analyses, including gene expression profiling, genome-wide association studies, and single-nucleotide polymorphism analysis, have revealed differences between tumors with the same pathological features. Because mutated genes and their signaling pathways can be targets for therapy, categorizing tumors by molecular parameters facilitates the selection of optimal therapeutic methods. Many genes are either oncogenes or tumor suppressor genes, and many of them are also involved in normal development, such as neural stem cell maintenance and neural differentiation. Moreover, genetic engineering has enabled the generation of tumors that phenocopy human tumors in mice. Here, I will discuss key molecular parameters, mechanisms of neural differentiation, isocitrate dehydrogenases, 1p36/19q13, and p53 in gliomagenesis. Because future therapeutic methods will be determined by the molecular mechanisms of tumors, identification of new parameters is still needed for further classification of glioma. |
| doi_str_mv | 10.1007/s10014-017-0278-8 |
| format | Article |
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Large-scale genomic DNA analyses, including gene expression profiling, genome-wide association studies, and single-nucleotide polymorphism analysis, have revealed differences between tumors with the same pathological features. Because mutated genes and their signaling pathways can be targets for therapy, categorizing tumors by molecular parameters facilitates the selection of optimal therapeutic methods. Many genes are either oncogenes or tumor suppressor genes, and many of them are also involved in normal development, such as neural stem cell maintenance and neural differentiation. Moreover, genetic engineering has enabled the generation of tumors that phenocopy human tumors in mice. Here, I will discuss key molecular parameters, mechanisms of neural differentiation, isocitrate dehydrogenases, 1p36/19q13, and p53 in gliomagenesis. 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Large-scale genomic DNA analyses, including gene expression profiling, genome-wide association studies, and single-nucleotide polymorphism analysis, have revealed differences between tumors with the same pathological features. Because mutated genes and their signaling pathways can be targets for therapy, categorizing tumors by molecular parameters facilitates the selection of optimal therapeutic methods. Many genes are either oncogenes or tumor suppressor genes, and many of them are also involved in normal development, such as neural stem cell maintenance and neural differentiation. Moreover, genetic engineering has enabled the generation of tumors that phenocopy human tumors in mice. Here, I will discuss key molecular parameters, mechanisms of neural differentiation, isocitrate dehydrogenases, 1p36/19q13, and p53 in gliomagenesis. Because future therapeutic methods will be determined by the molecular mechanisms of tumors, identification of new parameters is still needed for further classification of glioma.</description><subject>Animals</subject><subject>Apoptosis</subject><subject>Brain cancer</subject><subject>Brain Neoplasms - diagnosis</subject><subject>Brain Neoplasms - genetics</subject><subject>Brain Neoplasms - pathology</subject><subject>Cancer Research</subject><subject>Cell cycle</subject><subject>Chromosomes</subject><subject>Collagen</subject><subject>Cyclin-dependent kinases</subject><subject>DNA damage</subject><subject>DNA methylation</subject><subject>Gene expression</subject><subject>Gene Expression Profiling</subject><subject>Genome-Wide Association Study</subject><subject>Genomes</subject><subject>Glioma</subject><subject>Glioma - diagnosis</subject><subject>Glioma - genetics</subject><subject>Glioma - pathology</subject><subject>Growth factors</subject><subject>Humans</subject><subject>Hypoxia</subject><subject>Kinases</subject><subject>Leukemia</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Mutation</subject><subject>Mutation - genetics</subject><subject>Neurology</subject><subject>Neurosurgery</subject><subject>Oncology</subject><subject>Pathology</subject><subject>Phosphorylation</subject><subject>Review Article</subject><subject>Senescence</subject><subject>Signal Transduction - genetics</subject><subject>Stem cells</subject><subject>Transcription factors</subject><subject>Tumorigenesis</subject><subject>Tumors</subject><issn>1433-7398</issn><issn>1861-387X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNp1kMtKAzEUhoMotlYfwI0U3LhJzZlkcllK8QYVNwruQibJ1ClzqUmn4NuboVVBcJMcON_5k_MhdA5kBoSI65hOYJiAwCQTEssDNAbJAVMp3g5TzSjFgio5QicxrghhjAg4RqNMAvCcyjGaPXW1t31twrTx9t20VWzitGq3Xb31LhXTZV11jVn61scqnqKj0tTRn-3vCXq9u32ZP-DF8_3j_GaBLVV8g21eMOdyaUpmvAUJzlBVKHBFyaUVpXE8N5zJsgBJy4G2jADJnOVWGebpBF3tcteh--h93OimitbXtWl910c9bMlJLkEl9PIPuur60Kbf6UyBJCrjgiYKdpQNXYzBl3odqsaETw1EDzL1TqZOMvUgU8s0c7FP7ovGu5-Jb3sJyHZATK126cPv0_-nfgHjGH7g</recordid><startdate>2017</startdate><enddate>2017</enddate><creator>Kondo, Toru</creator><general>Springer Japan</general><general>Springer Nature B.V</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>M0S</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PSYQQ</scope><scope>7X8</scope></search><sort><creationdate>2017</creationdate><title>Molecular mechanisms involved in gliomagenesis</title><author>Kondo, Toru</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c396t-c5b4dd58af4aec181da39b91dbf68c7fad65a648fb183fc5b4c40102dc6c9a4e3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>Animals</topic><topic>Apoptosis</topic><topic>Brain cancer</topic><topic>Brain Neoplasms - diagnosis</topic><topic>Brain Neoplasms - genetics</topic><topic>Brain Neoplasms - pathology</topic><topic>Cancer Research</topic><topic>Cell cycle</topic><topic>Chromosomes</topic><topic>Collagen</topic><topic>Cyclin-dependent kinases</topic><topic>DNA damage</topic><topic>DNA methylation</topic><topic>Gene expression</topic><topic>Gene Expression Profiling</topic><topic>Genome-Wide Association Study</topic><topic>Genomes</topic><topic>Glioma</topic><topic>Glioma - diagnosis</topic><topic>Glioma - genetics</topic><topic>Glioma - pathology</topic><topic>Growth factors</topic><topic>Humans</topic><topic>Hypoxia</topic><topic>Kinases</topic><topic>Leukemia</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Mutation</topic><topic>Mutation - genetics</topic><topic>Neurology</topic><topic>Neurosurgery</topic><topic>Oncology</topic><topic>Pathology</topic><topic>Phosphorylation</topic><topic>Review Article</topic><topic>Senescence</topic><topic>Signal Transduction - 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Large-scale genomic DNA analyses, including gene expression profiling, genome-wide association studies, and single-nucleotide polymorphism analysis, have revealed differences between tumors with the same pathological features. Because mutated genes and their signaling pathways can be targets for therapy, categorizing tumors by molecular parameters facilitates the selection of optimal therapeutic methods. Many genes are either oncogenes or tumor suppressor genes, and many of them are also involved in normal development, such as neural stem cell maintenance and neural differentiation. Moreover, genetic engineering has enabled the generation of tumors that phenocopy human tumors in mice. Here, I will discuss key molecular parameters, mechanisms of neural differentiation, isocitrate dehydrogenases, 1p36/19q13, and p53 in gliomagenesis. 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| subjects | Animals Apoptosis Brain cancer Brain Neoplasms - diagnosis Brain Neoplasms - genetics Brain Neoplasms - pathology Cancer Research Cell cycle Chromosomes Collagen Cyclin-dependent kinases DNA damage DNA methylation Gene expression Gene Expression Profiling Genome-Wide Association Study Genomes Glioma Glioma - diagnosis Glioma - genetics Glioma - pathology Growth factors Humans Hypoxia Kinases Leukemia Medicine Medicine & Public Health Mutation Mutation - genetics Neurology Neurosurgery Oncology Pathology Phosphorylation Review Article Senescence Signal Transduction - genetics Stem cells Transcription factors Tumorigenesis Tumors |
| title | Molecular mechanisms involved in gliomagenesis |
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