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Mutation analysis of IDH1 in paired gliomas revealed IDH1 mutation was not associated with malignant progression but predicted longer survival
Recurrence and progression to higher grade lesions are characteristic behaviors of gliomas. Though IDH1 mutation frequently occurs and is considered as an early event in gliomagenesis, little is known about its role in the recurrence and progression of gliomas. We therefore analysed IDH1 and IDH2 st...
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Published in: | PloS one 2013-06, Vol.8 (6), p.e67421-e67421 |
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description | Recurrence and progression to higher grade lesions are characteristic behaviors of gliomas. Though IDH1 mutation frequently occurs and is considered as an early event in gliomagenesis, little is known about its role in the recurrence and progression of gliomas. We therefore analysed IDH1 and IDH2 status at codon 132 of IDH1 and codon 172 of IDH2 by direct sequencing and anti-IDH1-R132H immunohistochemistry in 53 paired samples and their recurrences, including 29 low-grade gliomas, 16 anaplastic gliomas and 8 Glioblastomas. IDH1/IDH2 mutation was detected in 32 primary tumors, with 25 low-grade gliomas and 6 anaplastic gliomas harboring IDH1 mutation and 1 low-grade glioma harboring IDH2 mutation. All of the paired tumors showed consistent IDH1 and IDH2 status. Patients were analyzed according to IDH1 status and tumor-related factors. Malignant progression at recurrence was noted in 22 gliomas and was not associated with IDH1 mutation. Survival analysis revealed patients with IDH1 mutated gliomas had a significantly longer progression-free survival (PFS) and overall survival (OS). In conclusion, this study demonstrated a strong tendency of IDH1/IDH2 status being consistent during progression of glioma. IDH1 mutation was not a predictive marker for malignant progression and it was a potential prognostic marker for gliomas of Chinese patients. |
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Though IDH1 mutation frequently occurs and is considered as an early event in gliomagenesis, little is known about its role in the recurrence and progression of gliomas. We therefore analysed IDH1 and IDH2 status at codon 132 of IDH1 and codon 172 of IDH2 by direct sequencing and anti-IDH1-R132H immunohistochemistry in 53 paired samples and their recurrences, including 29 low-grade gliomas, 16 anaplastic gliomas and 8 Glioblastomas. IDH1/IDH2 mutation was detected in 32 primary tumors, with 25 low-grade gliomas and 6 anaplastic gliomas harboring IDH1 mutation and 1 low-grade glioma harboring IDH2 mutation. All of the paired tumors showed consistent IDH1 and IDH2 status. Patients were analyzed according to IDH1 status and tumor-related factors. Malignant progression at recurrence was noted in 22 gliomas and was not associated with IDH1 mutation. Survival analysis revealed patients with IDH1 mutated gliomas had a significantly longer progression-free survival (PFS) and overall survival (OS). In conclusion, this study demonstrated a strong tendency of IDH1/IDH2 status being consistent during progression of glioma. IDH1 mutation was not a predictive marker for malignant progression and it was a potential prognostic marker for gliomas of Chinese patients.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0067421</identifier><identifier>PMID: 23840696</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Adolescent ; Adult ; Aged ; Antigens ; Astrocytoma - genetics ; Astrocytoma - mortality ; Astrocytoma - pathology ; Biology ; Brain cancer ; Brain Neoplasms - genetics ; Brain Neoplasms - mortality ; Brain Neoplasms - pathology ; Brain tumors ; Child ; Child, Preschool ; Disease Progression ; Disease-Free Survival ; DNA Mutational Analysis ; Ethics ; Female ; Genetic Association Studies ; Genetic Predisposition to Disease ; Genomes ; Glioma ; Humans ; Immunohistochemistry ; Isocitrate Dehydrogenase - genetics ; Kaplan-Meier Estimate ; Lesions ; Male ; Medical prognosis ; Medicine ; Middle Aged ; Multivariate Analysis ; Mutation ; Mutation, Missense ; Neoplasm Recurrence, Local - genetics ; Nervous system ; Neurosurgery ; Pathology ; Patients ; Prognosis ; Proportional Hazards Models ; Statistical analysis ; Survival ; Tumors ; Young Adult</subject><ispartof>PloS one, 2013-06, Vol.8 (6), p.e67421-e67421</ispartof><rights>2013 Yao et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License: https://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2013 Yao et al 2013 Yao et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c526t-15e57fb6beacbb80cc7a91381982f495bca968c3a650ffaf5eac01174937631a3</citedby><cites>FETCH-LOGICAL-c526t-15e57fb6beacbb80cc7a91381982f495bca968c3a650ffaf5eac01174937631a3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.proquest.com/docview/1372350684/fulltextPDF?pq-origsite=primo$$EPDF$$P50$$Gproquest$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.proquest.com/docview/1372350684?pq-origsite=primo$$EHTML$$P50$$Gproquest$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,25753,27924,27925,37012,37013,44590,53791,53793,75126</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23840696$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Kotliarova, Svetlana</contributor><creatorcontrib>Yao, Yu</creatorcontrib><creatorcontrib>Chan, Aden Ka-Yin</creatorcontrib><creatorcontrib>Qin, Zhi Yong</creatorcontrib><creatorcontrib>Chen, Ling Chao</creatorcontrib><creatorcontrib>Zhang, Xin</creatorcontrib><creatorcontrib>Pang, Jesse Chung-Sean</creatorcontrib><creatorcontrib>Li, Hiu Ming</creatorcontrib><creatorcontrib>Wang, Yin</creatorcontrib><creatorcontrib>Mao, Ying</creatorcontrib><creatorcontrib>Ng, Ho-Keung</creatorcontrib><creatorcontrib>Zhou, Liang Fu</creatorcontrib><title>Mutation analysis of IDH1 in paired gliomas revealed IDH1 mutation was not associated with malignant progression but predicted longer survival</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>Recurrence and progression to higher grade lesions are characteristic behaviors of gliomas. Though IDH1 mutation frequently occurs and is considered as an early event in gliomagenesis, little is known about its role in the recurrence and progression of gliomas. We therefore analysed IDH1 and IDH2 status at codon 132 of IDH1 and codon 172 of IDH2 by direct sequencing and anti-IDH1-R132H immunohistochemistry in 53 paired samples and their recurrences, including 29 low-grade gliomas, 16 anaplastic gliomas and 8 Glioblastomas. IDH1/IDH2 mutation was detected in 32 primary tumors, with 25 low-grade gliomas and 6 anaplastic gliomas harboring IDH1 mutation and 1 low-grade glioma harboring IDH2 mutation. All of the paired tumors showed consistent IDH1 and IDH2 status. Patients were analyzed according to IDH1 status and tumor-related factors. Malignant progression at recurrence was noted in 22 gliomas and was not associated with IDH1 mutation. Survival analysis revealed patients with IDH1 mutated gliomas had a significantly longer progression-free survival (PFS) and overall survival (OS). In conclusion, this study demonstrated a strong tendency of IDH1/IDH2 status being consistent during progression of glioma. IDH1 mutation was not a predictive marker for malignant progression and it was a potential prognostic marker for gliomas of Chinese patients.</description><subject>Adolescent</subject><subject>Adult</subject><subject>Aged</subject><subject>Antigens</subject><subject>Astrocytoma - genetics</subject><subject>Astrocytoma - mortality</subject><subject>Astrocytoma - pathology</subject><subject>Biology</subject><subject>Brain cancer</subject><subject>Brain Neoplasms - genetics</subject><subject>Brain Neoplasms - mortality</subject><subject>Brain Neoplasms - pathology</subject><subject>Brain tumors</subject><subject>Child</subject><subject>Child, Preschool</subject><subject>Disease Progression</subject><subject>Disease-Free Survival</subject><subject>DNA Mutational Analysis</subject><subject>Ethics</subject><subject>Female</subject><subject>Genetic Association Studies</subject><subject>Genetic Predisposition to Disease</subject><subject>Genomes</subject><subject>Glioma</subject><subject>Humans</subject><subject>Immunohistochemistry</subject><subject>Isocitrate Dehydrogenase - genetics</subject><subject>Kaplan-Meier Estimate</subject><subject>Lesions</subject><subject>Male</subject><subject>Medical prognosis</subject><subject>Medicine</subject><subject>Middle Aged</subject><subject>Multivariate Analysis</subject><subject>Mutation</subject><subject>Mutation, Missense</subject><subject>Neoplasm Recurrence, Local - genetics</subject><subject>Nervous system</subject><subject>Neurosurgery</subject><subject>Pathology</subject><subject>Patients</subject><subject>Prognosis</subject><subject>Proportional Hazards Models</subject><subject>Statistical analysis</subject><subject>Survival</subject><subject>Tumors</subject><subject>Young Adult</subject><issn>1932-6203</issn><issn>1932-6203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><sourceid>PIMPY</sourceid><sourceid>DOA</sourceid><recordid>eNptkt9uFCEUxidGY2v1DYySeOPNrjAMDNyYmPqnm9R4o9fkwDBTGgZWmNmmL-Ezy3R3m9Z4BZzz-z7OgVNVrwleE9qSD9dxTgH8ehuDXWPM26YmT6pTImm94jWmTx_sT6oXOV9jzKjg_Hl1UlPRYC75afXn-zzB5GJAUMxus8so9mjz-YIgF9AWXLIdGryLI2SU7M6CL4G7_HhU3pRUiBOCnKNxMBXgxk1XaATvhgBhQtsUh2RzXmg9L2fbObOAPobBJpTntHM78C-rZz34bF8d1rPq19cvP88vVpc_vm3OP12uDKv5tCLMsrbXXFswWgtsTAuSUEGkqPtGMm1AcmEocIb7HnpWOExI20jackqAnlVv975bH7M6PGVW5WFryjAXTSE2e6KLcK22yY2QblUEp-4CMQ0K0uSMt0p2EqAXkmrZNVbXUtc1a2jTg8BCgyleHw-3zXq0nbFhSuAfmT7OBHelhrhTtPwRlqIYvD8YpPh7tnlSo8vGeg_BxnmpW0qGGyFYQd_9g_6_u2ZPmRRzTra_L4bghSNHlVrGSx3Gq8jePGzkXnScJ_oX1WTRWw</recordid><startdate>20130628</startdate><enddate>20130628</enddate><creator>Yao, Yu</creator><creator>Chan, Aden Ka-Yin</creator><creator>Qin, Zhi Yong</creator><creator>Chen, Ling Chao</creator><creator>Zhang, Xin</creator><creator>Pang, Jesse Chung-Sean</creator><creator>Li, Hiu Ming</creator><creator>Wang, Yin</creator><creator>Mao, Ying</creator><creator>Ng, Ho-Keung</creator><creator>Zhou, Liang Fu</creator><general>Public Library of Science</general><general>Public Library of Science (PLoS)</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>7QG</scope><scope>7QL</scope><scope>7QO</scope><scope>7RV</scope><scope>7SN</scope><scope>7SS</scope><scope>7T5</scope><scope>7TG</scope><scope>7TM</scope><scope>7U9</scope><scope>7X2</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABJCF</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>ARAPS</scope><scope>ATCPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>D1I</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB.</scope><scope>KB0</scope><scope>KL.</scope><scope>L6V</scope><scope>LK8</scope><scope>M0K</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>M7S</scope><scope>NAPCQ</scope><scope>P5Z</scope><scope>P62</scope><scope>P64</scope><scope>PATMY</scope><scope>PDBOC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PTHSS</scope><scope>PYCSY</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope></search><sort><creationdate>20130628</creationdate><title>Mutation analysis of IDH1 in paired gliomas revealed IDH1 mutation was not associated with malignant progression but predicted longer survival</title><author>Yao, Yu ; Chan, Aden Ka-Yin ; Qin, Zhi Yong ; Chen, Ling Chao ; Zhang, Xin ; Pang, Jesse Chung-Sean ; Li, Hiu Ming ; Wang, Yin ; Mao, Ying ; Ng, Ho-Keung ; Zhou, Liang Fu</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c526t-15e57fb6beacbb80cc7a91381982f495bca968c3a650ffaf5eac01174937631a3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><topic>Adolescent</topic><topic>Adult</topic><topic>Aged</topic><topic>Antigens</topic><topic>Astrocytoma - 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Though IDH1 mutation frequently occurs and is considered as an early event in gliomagenesis, little is known about its role in the recurrence and progression of gliomas. We therefore analysed IDH1 and IDH2 status at codon 132 of IDH1 and codon 172 of IDH2 by direct sequencing and anti-IDH1-R132H immunohistochemistry in 53 paired samples and their recurrences, including 29 low-grade gliomas, 16 anaplastic gliomas and 8 Glioblastomas. IDH1/IDH2 mutation was detected in 32 primary tumors, with 25 low-grade gliomas and 6 anaplastic gliomas harboring IDH1 mutation and 1 low-grade glioma harboring IDH2 mutation. All of the paired tumors showed consistent IDH1 and IDH2 status. Patients were analyzed according to IDH1 status and tumor-related factors. Malignant progression at recurrence was noted in 22 gliomas and was not associated with IDH1 mutation. Survival analysis revealed patients with IDH1 mutated gliomas had a significantly longer progression-free survival (PFS) and overall survival (OS). In conclusion, this study demonstrated a strong tendency of IDH1/IDH2 status being consistent during progression of glioma. IDH1 mutation was not a predictive marker for malignant progression and it was a potential prognostic marker for gliomas of Chinese patients.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>23840696</pmid><doi>10.1371/journal.pone.0067421</doi><oa>free_for_read</oa></addata></record> |
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subjects | Adolescent Adult Aged Antigens Astrocytoma - genetics Astrocytoma - mortality Astrocytoma - pathology Biology Brain cancer Brain Neoplasms - genetics Brain Neoplasms - mortality Brain Neoplasms - pathology Brain tumors Child Child, Preschool Disease Progression Disease-Free Survival DNA Mutational Analysis Ethics Female Genetic Association Studies Genetic Predisposition to Disease Genomes Glioma Humans Immunohistochemistry Isocitrate Dehydrogenase - genetics Kaplan-Meier Estimate Lesions Male Medical prognosis Medicine Middle Aged Multivariate Analysis Mutation Mutation, Missense Neoplasm Recurrence, Local - genetics Nervous system Neurosurgery Pathology Patients Prognosis Proportional Hazards Models Statistical analysis Survival Tumors Young Adult |
title | Mutation analysis of IDH1 in paired gliomas revealed IDH1 mutation was not associated with malignant progression but predicted longer survival |
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