World Health Organization grade II–III astrocytomas consist of genetically distinct tumor lineages
Recent investigations revealed genetic analysis provides important information in management of gliomas, and we previously reported grade II–III gliomas could be classified into clinically relevant subgroups based on the DNA copy number aberrations (CNAs). To develop more precise genetic subgrouping...
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| Veröffentlicht in: | Cancer science 2016-08, Vol.107 (8), p.1159-1164 |
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| creator | Hattori, Natsuki Hirose, Yuichi Sasaki, Hikaru Nakae, Shunsuke Hayashi, Saeko Ohba, Shigeo Adachi, Kazuhide Hayashi, Takuro Nishiyama, Yuya Hasegawa, Mitsuhiro Abe, Masato |
| description | Recent investigations revealed genetic analysis provides important information in management of gliomas, and we previously reported grade II–III gliomas could be classified into clinically relevant subgroups based on the DNA copy number aberrations (CNAs). To develop more precise genetic subgrouping, we investigated the correlation between CNAs and mutational status of the gene encoding isocitrate dehydrogenase (IDH) of those tumors. We analyzed the IDH status and CNAs of 174 adult supratentorial gliomas of astrocytic or oligodendroglial origin by PCR‐based direct sequencing and comparative genomic hybridization, respectively. We analyzed the relationship between genetic subclassification and clinical features. We found the most frequent aberrations in IDH mutant tumors were the combined whole arm‐loss of 1p and 19q (1p/19q codeletion) followed by gain on chromosome arm 7q (+7q). The gain of whole chromosome 7 (+7) and loss of 10q (−10q) were detected in IDH wild‐type tumors. Kaplan–Meier estimates for progression‐free survival showed that the tumors with mutant IDH, −1p/19q, or +7q (in the absence of +7p) survived longer than tumors with wild‐type IDH, +7, or −10q. As tumors with +7 (IDH wild‐type) showed a more aggressive clinical nature, they are probably not a subtype that developed from the slowly progressive tumors with +7q (IDH mutant). Thus, tumors with a gain on chromosome 7 (mostly astrocytic) comprise multiple lineages, and such differences in their biological nature should be taken into consideration during their clinical management.
Genetic subgrouping based on DNA copy number aberrations and IDH1 gene mutations revealed grade II–III astrocytomas consist of multiple lineages. The differences in their biological nature should be taken into consideration during their clinical management. |
| doi_str_mv | 10.1111/cas.12969 |
| format | Article |
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Genetic subgrouping based on DNA copy number aberrations and IDH1 gene mutations revealed grade II–III astrocytomas consist of multiple lineages. The differences in their biological nature should be taken into consideration during their clinical management.</description><identifier>ISSN: 1347-9032</identifier><identifier>EISSN: 1349-7006</identifier><identifier>DOI: 10.1111/cas.12969</identifier><identifier>PMID: 27196377</identifier><language>eng</language><publisher>England: John Wiley & Sons, Inc</publisher><subject>Astrocytoma ; Astrocytoma - genetics ; Astrocytoma - pathology ; Astrocytomas ; Brain cancer ; Cell Lineage - genetics ; Chromosome 7 ; Chromosomes ; Comparative Genomic Hybridization ; Copy number ; Disease Progression ; DNA copy number ; Genes, Neoplasm ; Genetic analysis ; genetic subgrouping ; Glioma - genetics ; Glioma - pathology ; Humans ; Hybridization ; IDH ; Isocitrate dehydrogenase ; Isocitrate Dehydrogenase - genetics ; Isocitrate Dehydrogenase - metabolism ; Kaplan-Meier Estimate ; Male ; Mutation ; Mutation - genetics ; Neoplasm Grading ; Original ; Studies ; Tumors ; World Health Organization</subject><ispartof>Cancer science, 2016-08, Vol.107 (8), p.1159-1164</ispartof><rights>2016 The Authors. Cancer Science published by John Wiley & Sons Australia, Ltd on behalf of Japanese Cancer Association.</rights><rights>2016. This work is published under http://creativecommons.org/licenses/by-nc-nd/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c6369-bd96d4b14759bd275d193231e55085c950e4848cb6832712ac1aba445121e2183</citedby><cites>FETCH-LOGICAL-c6369-bd96d4b14759bd275d193231e55085c950e4848cb6832712ac1aba445121e2183</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4982592/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4982592/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,315,728,781,785,865,886,1418,11567,27929,27930,45579,45580,46057,46481,53796,53798</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/27196377$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Hattori, Natsuki</creatorcontrib><creatorcontrib>Hirose, Yuichi</creatorcontrib><creatorcontrib>Sasaki, Hikaru</creatorcontrib><creatorcontrib>Nakae, Shunsuke</creatorcontrib><creatorcontrib>Hayashi, Saeko</creatorcontrib><creatorcontrib>Ohba, Shigeo</creatorcontrib><creatorcontrib>Adachi, Kazuhide</creatorcontrib><creatorcontrib>Hayashi, Takuro</creatorcontrib><creatorcontrib>Nishiyama, Yuya</creatorcontrib><creatorcontrib>Hasegawa, Mitsuhiro</creatorcontrib><creatorcontrib>Abe, Masato</creatorcontrib><title>World Health Organization grade II–III astrocytomas consist of genetically distinct tumor lineages</title><title>Cancer science</title><addtitle>Cancer Sci</addtitle><description>Recent investigations revealed genetic analysis provides important information in management of gliomas, and we previously reported grade II–III gliomas could be classified into clinically relevant subgroups based on the DNA copy number aberrations (CNAs). To develop more precise genetic subgrouping, we investigated the correlation between CNAs and mutational status of the gene encoding isocitrate dehydrogenase (IDH) of those tumors. We analyzed the IDH status and CNAs of 174 adult supratentorial gliomas of astrocytic or oligodendroglial origin by PCR‐based direct sequencing and comparative genomic hybridization, respectively. We analyzed the relationship between genetic subclassification and clinical features. We found the most frequent aberrations in IDH mutant tumors were the combined whole arm‐loss of 1p and 19q (1p/19q codeletion) followed by gain on chromosome arm 7q (+7q). The gain of whole chromosome 7 (+7) and loss of 10q (−10q) were detected in IDH wild‐type tumors. Kaplan–Meier estimates for progression‐free survival showed that the tumors with mutant IDH, −1p/19q, or +7q (in the absence of +7p) survived longer than tumors with wild‐type IDH, +7, or −10q. As tumors with +7 (IDH wild‐type) showed a more aggressive clinical nature, they are probably not a subtype that developed from the slowly progressive tumors with +7q (IDH mutant). Thus, tumors with a gain on chromosome 7 (mostly astrocytic) comprise multiple lineages, and such differences in their biological nature should be taken into consideration during their clinical management.
Genetic subgrouping based on DNA copy number aberrations and IDH1 gene mutations revealed grade II–III astrocytomas consist of multiple lineages. The differences in their biological nature should be taken into consideration during their clinical management.</description><subject>Astrocytoma</subject><subject>Astrocytoma - genetics</subject><subject>Astrocytoma - pathology</subject><subject>Astrocytomas</subject><subject>Brain cancer</subject><subject>Cell Lineage - genetics</subject><subject>Chromosome 7</subject><subject>Chromosomes</subject><subject>Comparative Genomic Hybridization</subject><subject>Copy number</subject><subject>Disease Progression</subject><subject>DNA copy number</subject><subject>Genes, Neoplasm</subject><subject>Genetic analysis</subject><subject>genetic subgrouping</subject><subject>Glioma - genetics</subject><subject>Glioma - pathology</subject><subject>Humans</subject><subject>Hybridization</subject><subject>IDH</subject><subject>Isocitrate dehydrogenase</subject><subject>Isocitrate Dehydrogenase - genetics</subject><subject>Isocitrate Dehydrogenase - metabolism</subject><subject>Kaplan-Meier Estimate</subject><subject>Male</subject><subject>Mutation</subject><subject>Mutation - genetics</subject><subject>Neoplasm Grading</subject><subject>Original</subject><subject>Studies</subject><subject>Tumors</subject><subject>World Health Organization</subject><issn>1347-9032</issn><issn>1349-7006</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>24P</sourceid><sourceid>WIN</sourceid><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNqNkc1qFTEUxwdRbK0ufAEJuNHFtPn-2Ajlonag0EUVlyGTyZ2mZJKaZJTrynfwDfskndtbixYEs0k4-fHjnPNvmpcIHqLlHFlTDhFWXD1q9hGhqhUQ8se3b9EqSPBe86yUSwgJp4o-bfawQIoTIfab4UvKYQAnzoR6Ac7yaKL_YapPEYzZDA503fXPX13XAVNqTnZT02QKsCkWXypIazC66Kq3JoQNGJaaj7aCOk8pg-CjM6Mrz5snaxOKe3F3HzSfP7z_tDppT88-dqvj09ZywlXbD4oPtEdUMNUPWLABKYIJcoxByaxi0FFJpe25JMsE2FhkekMpQxg5jCQ5aN7tvFdzP7nBulizCfoq-8nkjU7G679_or_QY_qmqZKYKbwI3twJcvo6u1L15It1IZjo0lw0kogJyKD4L3QbiSBkQV8_QC_TnOOyCY0xQ5JLRLbCtzvK5lRKduv7vhHU25j1ErO-jXlhX_056D35O9cFONoB331wm3-b9Or4fKe8Acdlsi0</recordid><startdate>201608</startdate><enddate>201608</enddate><creator>Hattori, Natsuki</creator><creator>Hirose, Yuichi</creator><creator>Sasaki, Hikaru</creator><creator>Nakae, Shunsuke</creator><creator>Hayashi, Saeko</creator><creator>Ohba, Shigeo</creator><creator>Adachi, Kazuhide</creator><creator>Hayashi, Takuro</creator><creator>Nishiyama, Yuya</creator><creator>Hasegawa, Mitsuhiro</creator><creator>Abe, Masato</creator><general>John Wiley & Sons, Inc</general><general>John Wiley and Sons Inc</general><scope>24P</scope><scope>WIN</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>8FE</scope><scope>8FH</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>LK8</scope><scope>M7P</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>7TO</scope><scope>H94</scope><scope>5PM</scope></search><sort><creationdate>201608</creationdate><title>World Health Organization grade II–III astrocytomas consist of genetically distinct tumor lineages</title><author>Hattori, Natsuki ; Hirose, Yuichi ; Sasaki, Hikaru ; Nakae, Shunsuke ; Hayashi, Saeko ; Ohba, Shigeo ; Adachi, Kazuhide ; Hayashi, Takuro ; Nishiyama, Yuya ; Hasegawa, Mitsuhiro ; Abe, Masato</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c6369-bd96d4b14759bd275d193231e55085c950e4848cb6832712ac1aba445121e2183</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>Astrocytoma</topic><topic>Astrocytoma - genetics</topic><topic>Astrocytoma - pathology</topic><topic>Astrocytomas</topic><topic>Brain cancer</topic><topic>Cell Lineage - genetics</topic><topic>Chromosome 7</topic><topic>Chromosomes</topic><topic>Comparative Genomic Hybridization</topic><topic>Copy number</topic><topic>Disease Progression</topic><topic>DNA copy number</topic><topic>Genes, Neoplasm</topic><topic>Genetic analysis</topic><topic>genetic subgrouping</topic><topic>Glioma - genetics</topic><topic>Glioma - pathology</topic><topic>Humans</topic><topic>Hybridization</topic><topic>IDH</topic><topic>Isocitrate dehydrogenase</topic><topic>Isocitrate Dehydrogenase - genetics</topic><topic>Isocitrate Dehydrogenase - metabolism</topic><topic>Kaplan-Meier Estimate</topic><topic>Male</topic><topic>Mutation</topic><topic>Mutation - genetics</topic><topic>Neoplasm Grading</topic><topic>Original</topic><topic>Studies</topic><topic>Tumors</topic><topic>World Health Organization</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Hattori, Natsuki</creatorcontrib><creatorcontrib>Hirose, Yuichi</creatorcontrib><creatorcontrib>Sasaki, Hikaru</creatorcontrib><creatorcontrib>Nakae, Shunsuke</creatorcontrib><creatorcontrib>Hayashi, Saeko</creatorcontrib><creatorcontrib>Ohba, Shigeo</creatorcontrib><creatorcontrib>Adachi, Kazuhide</creatorcontrib><creatorcontrib>Hayashi, Takuro</creatorcontrib><creatorcontrib>Nishiyama, Yuya</creatorcontrib><creatorcontrib>Hasegawa, Mitsuhiro</creatorcontrib><creatorcontrib>Abe, Masato</creatorcontrib><collection>Wiley Online Library (Open Access Collection)</collection><collection>Wiley Online Library (Open Access Collection)</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Biological Science Collection</collection><collection>Biological Science Database</collection><collection>Access via ProQuest (Open Access)</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Cancer science</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Hattori, Natsuki</au><au>Hirose, Yuichi</au><au>Sasaki, Hikaru</au><au>Nakae, Shunsuke</au><au>Hayashi, Saeko</au><au>Ohba, Shigeo</au><au>Adachi, Kazuhide</au><au>Hayashi, Takuro</au><au>Nishiyama, Yuya</au><au>Hasegawa, Mitsuhiro</au><au>Abe, Masato</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>World Health Organization grade II–III astrocytomas consist of genetically distinct tumor lineages</atitle><jtitle>Cancer science</jtitle><addtitle>Cancer Sci</addtitle><date>2016-08</date><risdate>2016</risdate><volume>107</volume><issue>8</issue><spage>1159</spage><epage>1164</epage><pages>1159-1164</pages><issn>1347-9032</issn><eissn>1349-7006</eissn><abstract>Recent investigations revealed genetic analysis provides important information in management of gliomas, and we previously reported grade II–III gliomas could be classified into clinically relevant subgroups based on the DNA copy number aberrations (CNAs). To develop more precise genetic subgrouping, we investigated the correlation between CNAs and mutational status of the gene encoding isocitrate dehydrogenase (IDH) of those tumors. We analyzed the IDH status and CNAs of 174 adult supratentorial gliomas of astrocytic or oligodendroglial origin by PCR‐based direct sequencing and comparative genomic hybridization, respectively. We analyzed the relationship between genetic subclassification and clinical features. We found the most frequent aberrations in IDH mutant tumors were the combined whole arm‐loss of 1p and 19q (1p/19q codeletion) followed by gain on chromosome arm 7q (+7q). The gain of whole chromosome 7 (+7) and loss of 10q (−10q) were detected in IDH wild‐type tumors. Kaplan–Meier estimates for progression‐free survival showed that the tumors with mutant IDH, −1p/19q, or +7q (in the absence of +7p) survived longer than tumors with wild‐type IDH, +7, or −10q. As tumors with +7 (IDH wild‐type) showed a more aggressive clinical nature, they are probably not a subtype that developed from the slowly progressive tumors with +7q (IDH mutant). Thus, tumors with a gain on chromosome 7 (mostly astrocytic) comprise multiple lineages, and such differences in their biological nature should be taken into consideration during their clinical management.
Genetic subgrouping based on DNA copy number aberrations and IDH1 gene mutations revealed grade II–III astrocytomas consist of multiple lineages. The differences in their biological nature should be taken into consideration during their clinical management.</abstract><cop>England</cop><pub>John Wiley & Sons, Inc</pub><pmid>27196377</pmid><doi>10.1111/cas.12969</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Astrocytoma Astrocytoma - genetics Astrocytoma - pathology Astrocytomas Brain cancer Cell Lineage - genetics Chromosome 7 Chromosomes Comparative Genomic Hybridization Copy number Disease Progression DNA copy number Genes, Neoplasm Genetic analysis genetic subgrouping Glioma - genetics Glioma - pathology Humans Hybridization IDH Isocitrate dehydrogenase Isocitrate Dehydrogenase - genetics Isocitrate Dehydrogenase - metabolism Kaplan-Meier Estimate Male Mutation Mutation - genetics Neoplasm Grading Original Studies Tumors World Health Organization |
| title | World Health Organization grade II–III astrocytomas consist of genetically distinct tumor lineages |
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