Histopathology, classification, and grading of gliomas
Neoplastic transformation occurs in all glial cell types of the human nervous system, producing a wide variety of clinico‐pathological entities and morphological variants. Astrocytomas are most common and span an unusually wide spectrum, ranging from the slowly growing juvenile pilocytic astrocytoma...
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Veröffentlicht in: | Glia 1995-11, Vol.15 (3), p.211-221 |
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description | Neoplastic transformation occurs in all glial cell types of the human nervous system, producing a wide variety of clinico‐pathological entities and morphological variants. Astrocytomas are most common and span an unusually wide spectrum, ranging from the slowly growing juvenile pilocytic astrocytoma to the highly malignant glioblastoma multiforme. Diffusely infiltrating astrocytomas of the cerebral hemispheres show an inherent tendency for progression towards a more malignant phenotype. This change is morphologically categorized in histologic grading schemes (e.g., WHO Grade II to IV) and is associated with the sequential acquisition of genetic alteration, including mutation in the p53 and homozygous deletion of the p16 tumor suppressor genes. Loss of heterozygosity on chromosomes 10 and 19q as well as amplification of the EGF receptor are largely restricted to malignant gliomas and thus considered late events in astrocytoma progression. Gliomas often show phenotypic expresson of different glial cell lineages (e.g., oligoastrocytoma). Recent studies sugeest that the occurrence of mixed glomas is not indicative of a polyclonal orgin but rather reflects altered gene exprssion leading to a charge in the balance of growth factors influencing glioma defferentiation. © 1995 Wiley‐Liss, Inc. |
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Astrocytomas are most common and span an unusually wide spectrum, ranging from the slowly growing juvenile pilocytic astrocytoma to the highly malignant glioblastoma multiforme. Diffusely infiltrating astrocytomas of the cerebral hemispheres show an inherent tendency for progression towards a more malignant phenotype. This change is morphologically categorized in histologic grading schemes (e.g., WHO Grade II to IV) and is associated with the sequential acquisition of genetic alteration, including mutation in the p53 and homozygous deletion of the p16 tumor suppressor genes. Loss of heterozygosity on chromosomes 10 and 19q as well as amplification of the EGF receptor are largely restricted to malignant gliomas and thus considered late events in astrocytoma progression. Gliomas often show phenotypic expresson of different glial cell lineages (e.g., oligoastrocytoma). Recent studies sugeest that the occurrence of mixed glomas is not indicative of a polyclonal orgin but rather reflects altered gene exprssion leading to a charge in the balance of growth factors influencing glioma defferentiation. © 1995 Wiley‐Liss, Inc.</description><identifier>ISSN: 0894-1491</identifier><identifier>EISSN: 1098-1136</identifier><identifier>DOI: 10.1002/glia.440150303</identifier><identifier>PMID: 8586458</identifier><identifier>CODEN: GLIAEJ</identifier><language>eng</language><publisher>Hoboken: Wiley Subscription Services, Inc., A Wiley Company</publisher><subject>Astrocytoma ; Astrocytoma - classification ; Astrocytoma - pathology ; Biological and medical sciences ; Brain - pathology ; Brain Neoplasms - classification ; Brain Neoplasms - pathology ; Ependymoma ; Ependymoma - classification ; Ependymoma - pathology ; Glioblastoma - classification ; Glioblastoma - pathology ; Glioma ; Glioma - classification ; Glioma - pathology ; Grading ; Humans ; Medical sciences ; Neoplasm Invasiveness ; Neurology ; Oligodendroglioma ; Oligodendroglioma - classification ; Oligodendroglioma - pathology ; Pathology ; Tumor progression ; Tumors of the nervous system. Phacomatoses</subject><ispartof>Glia, 1995-11, Vol.15 (3), p.211-221</ispartof><rights>Copyright © 1995 Wiley‐Liss, Inc.</rights><rights>1996 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5043-d9072d7dc18e0b453099b8dfd7f24aee63654b122467502b667d955bdd9eafc83</citedby><cites>FETCH-LOGICAL-c5043-d9072d7dc18e0b453099b8dfd7f24aee63654b122467502b667d955bdd9eafc83</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2Fglia.440150303$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fglia.440150303$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,776,780,1411,27901,27902,45550,45551</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=2920800$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/8586458$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Kleihues, Paul</creatorcontrib><creatorcontrib>Soylemezoglu, Figen</creatorcontrib><creatorcontrib>Schäuble, Barbara</creatorcontrib><creatorcontrib>Scheithauer, Bernd W.</creatorcontrib><creatorcontrib>Burger, Peter C.</creatorcontrib><title>Histopathology, classification, and grading of gliomas</title><title>Glia</title><addtitle>Glia</addtitle><description>Neoplastic transformation occurs in all glial cell types of the human nervous system, producing a wide variety of clinico‐pathological entities and morphological variants. Astrocytomas are most common and span an unusually wide spectrum, ranging from the slowly growing juvenile pilocytic astrocytoma to the highly malignant glioblastoma multiforme. Diffusely infiltrating astrocytomas of the cerebral hemispheres show an inherent tendency for progression towards a more malignant phenotype. This change is morphologically categorized in histologic grading schemes (e.g., WHO Grade II to IV) and is associated with the sequential acquisition of genetic alteration, including mutation in the p53 and homozygous deletion of the p16 tumor suppressor genes. Loss of heterozygosity on chromosomes 10 and 19q as well as amplification of the EGF receptor are largely restricted to malignant gliomas and thus considered late events in astrocytoma progression. Gliomas often show phenotypic expresson of different glial cell lineages (e.g., oligoastrocytoma). Recent studies sugeest that the occurrence of mixed glomas is not indicative of a polyclonal orgin but rather reflects altered gene exprssion leading to a charge in the balance of growth factors influencing glioma defferentiation. © 1995 Wiley‐Liss, Inc.</description><subject>Astrocytoma</subject><subject>Astrocytoma - classification</subject><subject>Astrocytoma - pathology</subject><subject>Biological and medical sciences</subject><subject>Brain - pathology</subject><subject>Brain Neoplasms - classification</subject><subject>Brain Neoplasms - pathology</subject><subject>Ependymoma</subject><subject>Ependymoma - classification</subject><subject>Ependymoma - pathology</subject><subject>Glioblastoma - classification</subject><subject>Glioblastoma - pathology</subject><subject>Glioma</subject><subject>Glioma - classification</subject><subject>Glioma - pathology</subject><subject>Grading</subject><subject>Humans</subject><subject>Medical sciences</subject><subject>Neoplasm Invasiveness</subject><subject>Neurology</subject><subject>Oligodendroglioma</subject><subject>Oligodendroglioma - classification</subject><subject>Oligodendroglioma - pathology</subject><subject>Pathology</subject><subject>Tumor progression</subject><subject>Tumors of the nervous system. Phacomatoses</subject><issn>0894-1491</issn><issn>1098-1136</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1995</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkU1rGzEQhkVpSJ2k194Keyg5ZZ3Rt3RMTGqbmOSSj6PQSlpX7XrlrNa0_vdZY2N6CwwMwzzvzPAOQt8wjDEAuV420Y4ZA8yBAv2ERhi0KjGm4jMagdKsxEzjL-gs598AeCjkKTpVXAnG1QiJWcx9Wtv-V2rScntVuMbmHOvobB9Te1XY1hfLzvrYLotUF8O6tLL5Ap3Utsnh6yGfo-efd0-TWbl4nM4nN4vScWC09Bok8dI7rAJUjFPQulK-9rImzIYgqOCswoQwITmQSgjpNeeV9zrY2il6ji73c9ddetuE3JtVzC40jW1D2mQjpSJDwIcgFloTCnwAx3vQdSnnLtRm3cWV7bYGg9k5anaOmqOjg-D7YfKmWgV_xA8WDv0fh77NzjZ1Z1sX8xEjmoCC3YF6j_2NTdh-sNRMF_Ob_08o99rhV-HfUWu7P0ZIKrl5fZiae1Dq9nbyYhh9B7innLk</recordid><startdate>199511</startdate><enddate>199511</enddate><creator>Kleihues, Paul</creator><creator>Soylemezoglu, Figen</creator><creator>Schäuble, Barbara</creator><creator>Scheithauer, Bernd W.</creator><creator>Burger, Peter C.</creator><general>Wiley Subscription Services, Inc., A Wiley Company</general><general>Wiley-Liss</general><scope>BSCLL</scope><scope>IQODW</scope><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>7TK</scope><scope>7X8</scope></search><sort><creationdate>199511</creationdate><title>Histopathology, classification, and grading of gliomas</title><author>Kleihues, Paul ; Soylemezoglu, Figen ; Schäuble, Barbara ; Scheithauer, Bernd W. ; Burger, Peter C.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5043-d9072d7dc18e0b453099b8dfd7f24aee63654b122467502b667d955bdd9eafc83</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1995</creationdate><topic>Astrocytoma</topic><topic>Astrocytoma - classification</topic><topic>Astrocytoma - pathology</topic><topic>Biological and medical sciences</topic><topic>Brain - pathology</topic><topic>Brain Neoplasms - classification</topic><topic>Brain Neoplasms - pathology</topic><topic>Ependymoma</topic><topic>Ependymoma - classification</topic><topic>Ependymoma - pathology</topic><topic>Glioblastoma - classification</topic><topic>Glioblastoma - pathology</topic><topic>Glioma</topic><topic>Glioma - classification</topic><topic>Glioma - pathology</topic><topic>Grading</topic><topic>Humans</topic><topic>Medical sciences</topic><topic>Neoplasm Invasiveness</topic><topic>Neurology</topic><topic>Oligodendroglioma</topic><topic>Oligodendroglioma - classification</topic><topic>Oligodendroglioma - pathology</topic><topic>Pathology</topic><topic>Tumor progression</topic><topic>Tumors of the nervous system. Phacomatoses</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Kleihues, Paul</creatorcontrib><creatorcontrib>Soylemezoglu, Figen</creatorcontrib><creatorcontrib>Schäuble, Barbara</creatorcontrib><creatorcontrib>Scheithauer, Bernd W.</creatorcontrib><creatorcontrib>Burger, Peter C.</creatorcontrib><collection>Istex</collection><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Neurosciences Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Glia</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Kleihues, Paul</au><au>Soylemezoglu, Figen</au><au>Schäuble, Barbara</au><au>Scheithauer, Bernd W.</au><au>Burger, Peter C.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Histopathology, classification, and grading of gliomas</atitle><jtitle>Glia</jtitle><addtitle>Glia</addtitle><date>1995-11</date><risdate>1995</risdate><volume>15</volume><issue>3</issue><spage>211</spage><epage>221</epage><pages>211-221</pages><issn>0894-1491</issn><eissn>1098-1136</eissn><coden>GLIAEJ</coden><abstract>Neoplastic transformation occurs in all glial cell types of the human nervous system, producing a wide variety of clinico‐pathological entities and morphological variants. Astrocytomas are most common and span an unusually wide spectrum, ranging from the slowly growing juvenile pilocytic astrocytoma to the highly malignant glioblastoma multiforme. Diffusely infiltrating astrocytomas of the cerebral hemispheres show an inherent tendency for progression towards a more malignant phenotype. This change is morphologically categorized in histologic grading schemes (e.g., WHO Grade II to IV) and is associated with the sequential acquisition of genetic alteration, including mutation in the p53 and homozygous deletion of the p16 tumor suppressor genes. Loss of heterozygosity on chromosomes 10 and 19q as well as amplification of the EGF receptor are largely restricted to malignant gliomas and thus considered late events in astrocytoma progression. Gliomas often show phenotypic expresson of different glial cell lineages (e.g., oligoastrocytoma). Recent studies sugeest that the occurrence of mixed glomas is not indicative of a polyclonal orgin but rather reflects altered gene exprssion leading to a charge in the balance of growth factors influencing glioma defferentiation. © 1995 Wiley‐Liss, Inc.</abstract><cop>Hoboken</cop><pub>Wiley Subscription Services, Inc., A Wiley Company</pub><pmid>8586458</pmid><doi>10.1002/glia.440150303</doi><tpages>11</tpages></addata></record> |
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subjects | Astrocytoma Astrocytoma - classification Astrocytoma - pathology Biological and medical sciences Brain - pathology Brain Neoplasms - classification Brain Neoplasms - pathology Ependymoma Ependymoma - classification Ependymoma - pathology Glioblastoma - classification Glioblastoma - pathology Glioma Glioma - classification Glioma - pathology Grading Humans Medical sciences Neoplasm Invasiveness Neurology Oligodendroglioma Oligodendroglioma - classification Oligodendroglioma - pathology Pathology Tumor progression Tumors of the nervous system. Phacomatoses |
title | Histopathology, classification, and grading of gliomas |
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