The impact of MGMT methylation and IDH-1 mutation on long-term outcome for glioblastoma treated with chemoradiotherapy
Background Increasingly, biomarkers have been identified that correlate with improved overall and progression-free survival (OS and PFS) in glioblastoma, including MGMT methylation status and mutations in the IDH1 gene. In this study, we investigated the clinical and biological factors associated wi...
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| Veröffentlicht in: | Acta neurochirurgica 2016-10, Vol.158 (10), p.1943-1953 |
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| creator | Millward, Christopher P. Brodbelt, Andrew R. Haylock, Brian Zakaria, Rasheed Baborie, Atik Crooks, Daniel Husband, David Shenoy, Aditya Wong, Helen Jenkinson, Michael D. |
| description | Background
Increasingly, biomarkers have been identified that correlate with improved overall and progression-free survival (OS and PFS) in glioblastoma, including MGMT methylation status and mutations in the IDH1 gene. In this study, we investigated the clinical and biological factors associated with long-term survival in glioblastoma patients treated with chemoradiotherapy.
Method
Demographic and clinical data were collected for all patients with glioblastoma diagnosed between May 2004 and September 2007, treated with chemoradiotherapy and with associated tissue samples available for biomarker analysis. MGMT methylation was determined by pyrosequencing. IDH1 mutation was identified by R132H immunohistochemistry. Univariate Cox regression analysis of factors associated with survival and Kaplan-Meier survival analysis was performed using the SPSS statistics package.
Results
One hundred patients were included in the study. Median follow-up was 12.2 months (range 1.6–102.4). Median OS was 12.1 months (95 % CI: 10.8–13.3) and median PFS was 8.2 months (95 % CI: 6.8–9.5). The 2-, 3- and 5-year survival was 18, 9 and 6 % respectively. Three patients are still alive at 7.4, 8.3 and 8.5 years after diagnosis.
Cox proportional-hazards regression identified independent prognostic factors for OS, female (
p
= 0.019), MGMT methylation (
p
|
| doi_str_mv | 10.1007/s00701-016-2928-8 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_1827901603</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>1820594027</sourcerecordid><originalsourceid>FETCH-LOGICAL-c405t-3d291d22665ef1f0343a435d61f526f2665af5fe6b603ba44f2c443a5f6a7dd03</originalsourceid><addsrcrecordid>eNqNkc9rHSEQx6W05FfzB-QShF56sVVX3d1jSdIkkJDLy1l8q77dsK6v6ia8_z7z2DSUQqEgo46fmXHmi9AZo98YpfX3DIYyQpkivOUNaT6gI9oKTsDQj3Cm8Kq4ag7Rcc5PcOO1qA7QIa8lV6qlR-h51Ts8hK3pCo4e31_fr3Bwpd-Npgxxwmay-PbyhjAc5rK4YI1x2pDiUsBxLl0MDvuY8GYc4no0ucRgcEnOFGfxy1B63PUuxGTsEEvvktnuPqNP3ozZnb7tJ-jx59Xq4obcPVzfXvy4I52gspDK8pZZDn-VzjNPK1EZUUmrmIcG_N5vvPROrRWt1kYIzzsBjPTK1NbS6gR9XfJuU_w1u1x0GHLnxtFMLs5Zs4bXLcyPVv-DUglz5TWgX_5Cn-KcJmgEKNYqKQVnQLGF6lLMOTmvt2kIJu00o3qvn17001Bf7_XTDcScv2We18HZ94jfggHAFyDD07Rx6Y_S_8z6CrkopKc</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1819655421</pqid></control><display><type>article</type><title>The impact of MGMT methylation and IDH-1 mutation on long-term outcome for glioblastoma treated with chemoradiotherapy</title><source>MEDLINE</source><source>Springer Nature - Complete Springer Journals</source><creator>Millward, Christopher P. ; Brodbelt, Andrew R. ; Haylock, Brian ; Zakaria, Rasheed ; Baborie, Atik ; Crooks, Daniel ; Husband, David ; Shenoy, Aditya ; Wong, Helen ; Jenkinson, Michael D.</creator><creatorcontrib>Millward, Christopher P. ; Brodbelt, Andrew R. ; Haylock, Brian ; Zakaria, Rasheed ; Baborie, Atik ; Crooks, Daniel ; Husband, David ; Shenoy, Aditya ; Wong, Helen ; Jenkinson, Michael D.</creatorcontrib><description>Background
Increasingly, biomarkers have been identified that correlate with improved overall and progression-free survival (OS and PFS) in glioblastoma, including MGMT methylation status and mutations in the IDH1 gene. In this study, we investigated the clinical and biological factors associated with long-term survival in glioblastoma patients treated with chemoradiotherapy.
Method
Demographic and clinical data were collected for all patients with glioblastoma diagnosed between May 2004 and September 2007, treated with chemoradiotherapy and with associated tissue samples available for biomarker analysis. MGMT methylation was determined by pyrosequencing. IDH1 mutation was identified by R132H immunohistochemistry. Univariate Cox regression analysis of factors associated with survival and Kaplan-Meier survival analysis was performed using the SPSS statistics package.
Results
One hundred patients were included in the study. Median follow-up was 12.2 months (range 1.6–102.4). Median OS was 12.1 months (95 % CI: 10.8–13.3) and median PFS was 8.2 months (95 % CI: 6.8–9.5). The 2-, 3- and 5-year survival was 18, 9 and 6 % respectively. Three patients are still alive at 7.4, 8.3 and 8.5 years after diagnosis.
Cox proportional-hazards regression identified independent prognostic factors for OS, female (
p
= 0.019), MGMT methylation (
p
< 0.0001) and IDH1 mutation (
p
= 0.023), and for PFS, MGMT methylation (
p
= 0.001) and IDH1 mutation (
p
= 0.018).
Kaplan-Meier survival analysis showed that MGMT
methylated
/IDH1
+ve
was associated with a significantly longer OS 66.8 months (95 % CI: 0.0–167.8) and PFS 16.9 months (95 % CI: 11.1–22.7) when compared with MGMT
methylated
/IDH1
-ve
OS 15.5 months (95 % CI: 11.6–19.4) and PFS 9.4 months (95 % CI: 8–10.8) (log-rank,
P
= 0.000) and MGMT
unmethylated
/IDH1
-ve
OS 11.1 months (95 % CI: 8.5–13.7) and PFS 6.3 months (95 % CI: 4.4–8.3) (log-rank,
p
= 0.000).
Conclusions
While the importance of MGMT methylation is well established, we demonstrate that the combination of MGMT
methylated
/IDH1
+ve
is associated with considerably longer OS and PFS in this series of chemoradiotherapy-treated glioblastoma tumours. The long-term cognitive function and quality of life in these long-term survivors warrant investigation.</description><identifier>ISSN: 0001-6268</identifier><identifier>EISSN: 0942-0940</identifier><identifier>DOI: 10.1007/s00701-016-2928-8</identifier><identifier>PMID: 27526690</identifier><language>eng</language><publisher>Vienna: Springer Vienna</publisher><subject>Adolescent ; Adult ; Aged ; Biomarkers, Tumor - genetics ; Brain Neoplasms - drug therapy ; Brain Neoplasms - genetics ; Brain Neoplasms - radiotherapy ; Clinical Article - Brain Tumors ; Disease-Free Survival ; DNA Methylation ; DNA Modification Methylases - genetics ; DNA Repair Enzymes - genetics ; Female ; Glioblastoma - drug therapy ; Glioblastoma - genetics ; Glioblastoma - radiotherapy ; Humans ; Interventional Radiology ; Isocitrate Dehydrogenase - genetics ; Male ; Medicine ; Medicine & Public Health ; Middle Aged ; Minimally Invasive Surgery ; Mutation ; Neurology ; Neuroradiology ; Neurosurgery ; Promoter Regions, Genetic ; Surgical Orthopedics ; Tumor Suppressor Proteins - genetics</subject><ispartof>Acta neurochirurgica, 2016-10, Vol.158 (10), p.1943-1953</ispartof><rights>Springer-Verlag Wien 2016</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c405t-3d291d22665ef1f0343a435d61f526f2665af5fe6b603ba44f2c443a5f6a7dd03</citedby><cites>FETCH-LOGICAL-c405t-3d291d22665ef1f0343a435d61f526f2665af5fe6b603ba44f2c443a5f6a7dd03</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s00701-016-2928-8$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s00701-016-2928-8$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27901,27902,41464,42533,51294</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/27526690$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Millward, Christopher P.</creatorcontrib><creatorcontrib>Brodbelt, Andrew R.</creatorcontrib><creatorcontrib>Haylock, Brian</creatorcontrib><creatorcontrib>Zakaria, Rasheed</creatorcontrib><creatorcontrib>Baborie, Atik</creatorcontrib><creatorcontrib>Crooks, Daniel</creatorcontrib><creatorcontrib>Husband, David</creatorcontrib><creatorcontrib>Shenoy, Aditya</creatorcontrib><creatorcontrib>Wong, Helen</creatorcontrib><creatorcontrib>Jenkinson, Michael D.</creatorcontrib><title>The impact of MGMT methylation and IDH-1 mutation on long-term outcome for glioblastoma treated with chemoradiotherapy</title><title>Acta neurochirurgica</title><addtitle>Acta Neurochir</addtitle><addtitle>Acta Neurochir (Wien)</addtitle><description>Background
Increasingly, biomarkers have been identified that correlate with improved overall and progression-free survival (OS and PFS) in glioblastoma, including MGMT methylation status and mutations in the IDH1 gene. In this study, we investigated the clinical and biological factors associated with long-term survival in glioblastoma patients treated with chemoradiotherapy.
Method
Demographic and clinical data were collected for all patients with glioblastoma diagnosed between May 2004 and September 2007, treated with chemoradiotherapy and with associated tissue samples available for biomarker analysis. MGMT methylation was determined by pyrosequencing. IDH1 mutation was identified by R132H immunohistochemistry. Univariate Cox regression analysis of factors associated with survival and Kaplan-Meier survival analysis was performed using the SPSS statistics package.
Results
One hundred patients were included in the study. Median follow-up was 12.2 months (range 1.6–102.4). Median OS was 12.1 months (95 % CI: 10.8–13.3) and median PFS was 8.2 months (95 % CI: 6.8–9.5). The 2-, 3- and 5-year survival was 18, 9 and 6 % respectively. Three patients are still alive at 7.4, 8.3 and 8.5 years after diagnosis.
Cox proportional-hazards regression identified independent prognostic factors for OS, female (
p
= 0.019), MGMT methylation (
p
< 0.0001) and IDH1 mutation (
p
= 0.023), and for PFS, MGMT methylation (
p
= 0.001) and IDH1 mutation (
p
= 0.018).
Kaplan-Meier survival analysis showed that MGMT
methylated
/IDH1
+ve
was associated with a significantly longer OS 66.8 months (95 % CI: 0.0–167.8) and PFS 16.9 months (95 % CI: 11.1–22.7) when compared with MGMT
methylated
/IDH1
-ve
OS 15.5 months (95 % CI: 11.6–19.4) and PFS 9.4 months (95 % CI: 8–10.8) (log-rank,
P
= 0.000) and MGMT
unmethylated
/IDH1
-ve
OS 11.1 months (95 % CI: 8.5–13.7) and PFS 6.3 months (95 % CI: 4.4–8.3) (log-rank,
p
= 0.000).
Conclusions
While the importance of MGMT methylation is well established, we demonstrate that the combination of MGMT
methylated
/IDH1
+ve
is associated with considerably longer OS and PFS in this series of chemoradiotherapy-treated glioblastoma tumours. The long-term cognitive function and quality of life in these long-term survivors warrant investigation.</description><subject>Adolescent</subject><subject>Adult</subject><subject>Aged</subject><subject>Biomarkers, Tumor - genetics</subject><subject>Brain Neoplasms - drug therapy</subject><subject>Brain Neoplasms - genetics</subject><subject>Brain Neoplasms - radiotherapy</subject><subject>Clinical Article - Brain Tumors</subject><subject>Disease-Free Survival</subject><subject>DNA Methylation</subject><subject>DNA Modification Methylases - genetics</subject><subject>DNA Repair Enzymes - genetics</subject><subject>Female</subject><subject>Glioblastoma - drug therapy</subject><subject>Glioblastoma - genetics</subject><subject>Glioblastoma - radiotherapy</subject><subject>Humans</subject><subject>Interventional Radiology</subject><subject>Isocitrate Dehydrogenase - genetics</subject><subject>Male</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Middle Aged</subject><subject>Minimally Invasive Surgery</subject><subject>Mutation</subject><subject>Neurology</subject><subject>Neuroradiology</subject><subject>Neurosurgery</subject><subject>Promoter Regions, Genetic</subject><subject>Surgical Orthopedics</subject><subject>Tumor Suppressor Proteins - genetics</subject><issn>0001-6268</issn><issn>0942-0940</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNqNkc9rHSEQx6W05FfzB-QShF56sVVX3d1jSdIkkJDLy1l8q77dsK6v6ia8_z7z2DSUQqEgo46fmXHmi9AZo98YpfX3DIYyQpkivOUNaT6gI9oKTsDQj3Cm8Kq4ag7Rcc5PcOO1qA7QIa8lV6qlR-h51Ts8hK3pCo4e31_fr3Bwpd-Npgxxwmay-PbyhjAc5rK4YI1x2pDiUsBxLl0MDvuY8GYc4no0ucRgcEnOFGfxy1B63PUuxGTsEEvvktnuPqNP3ozZnb7tJ-jx59Xq4obcPVzfXvy4I52gspDK8pZZDn-VzjNPK1EZUUmrmIcG_N5vvPROrRWt1kYIzzsBjPTK1NbS6gR9XfJuU_w1u1x0GHLnxtFMLs5Zs4bXLcyPVv-DUglz5TWgX_5Cn-KcJmgEKNYqKQVnQLGF6lLMOTmvt2kIJu00o3qvn17001Bf7_XTDcScv2We18HZ94jfggHAFyDD07Rx6Y_S_8z6CrkopKc</recordid><startdate>20161001</startdate><enddate>20161001</enddate><creator>Millward, Christopher P.</creator><creator>Brodbelt, Andrew R.</creator><creator>Haylock, Brian</creator><creator>Zakaria, Rasheed</creator><creator>Baborie, Atik</creator><creator>Crooks, Daniel</creator><creator>Husband, David</creator><creator>Shenoy, Aditya</creator><creator>Wong, Helen</creator><creator>Jenkinson, Michael D.</creator><general>Springer Vienna</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>7TK</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</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>H94</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope></search><sort><creationdate>20161001</creationdate><title>The impact of MGMT methylation and IDH-1 mutation on long-term outcome for glioblastoma treated with chemoradiotherapy</title><author>Millward, Christopher P. ; Brodbelt, Andrew R. ; Haylock, Brian ; Zakaria, Rasheed ; Baborie, Atik ; Crooks, Daniel ; Husband, David ; Shenoy, Aditya ; Wong, Helen ; Jenkinson, Michael D.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c405t-3d291d22665ef1f0343a435d61f526f2665af5fe6b603ba44f2c443a5f6a7dd03</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>Adolescent</topic><topic>Adult</topic><topic>Aged</topic><topic>Biomarkers, Tumor - genetics</topic><topic>Brain Neoplasms - drug therapy</topic><topic>Brain Neoplasms - genetics</topic><topic>Brain Neoplasms - radiotherapy</topic><topic>Clinical Article - Brain Tumors</topic><topic>Disease-Free Survival</topic><topic>DNA Methylation</topic><topic>DNA Modification Methylases - genetics</topic><topic>DNA Repair Enzymes - genetics</topic><topic>Female</topic><topic>Glioblastoma - drug therapy</topic><topic>Glioblastoma - genetics</topic><topic>Glioblastoma - radiotherapy</topic><topic>Humans</topic><topic>Interventional Radiology</topic><topic>Isocitrate Dehydrogenase - genetics</topic><topic>Male</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Middle Aged</topic><topic>Minimally Invasive Surgery</topic><topic>Mutation</topic><topic>Neurology</topic><topic>Neuroradiology</topic><topic>Neurosurgery</topic><topic>Promoter Regions, Genetic</topic><topic>Surgical Orthopedics</topic><topic>Tumor Suppressor Proteins - genetics</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Millward, Christopher P.</creatorcontrib><creatorcontrib>Brodbelt, Andrew R.</creatorcontrib><creatorcontrib>Haylock, Brian</creatorcontrib><creatorcontrib>Zakaria, Rasheed</creatorcontrib><creatorcontrib>Baborie, Atik</creatorcontrib><creatorcontrib>Crooks, Daniel</creatorcontrib><creatorcontrib>Husband, David</creatorcontrib><creatorcontrib>Shenoy, Aditya</creatorcontrib><creatorcontrib>Wong, Helen</creatorcontrib><creatorcontrib>Jenkinson, Michael D.</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Neurosciences Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</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><jtitle>Acta neurochirurgica</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Millward, Christopher P.</au><au>Brodbelt, Andrew R.</au><au>Haylock, Brian</au><au>Zakaria, Rasheed</au><au>Baborie, Atik</au><au>Crooks, Daniel</au><au>Husband, David</au><au>Shenoy, Aditya</au><au>Wong, Helen</au><au>Jenkinson, Michael D.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The impact of MGMT methylation and IDH-1 mutation on long-term outcome for glioblastoma treated with chemoradiotherapy</atitle><jtitle>Acta neurochirurgica</jtitle><stitle>Acta Neurochir</stitle><addtitle>Acta Neurochir (Wien)</addtitle><date>2016-10-01</date><risdate>2016</risdate><volume>158</volume><issue>10</issue><spage>1943</spage><epage>1953</epage><pages>1943-1953</pages><issn>0001-6268</issn><eissn>0942-0940</eissn><abstract>Background
Increasingly, biomarkers have been identified that correlate with improved overall and progression-free survival (OS and PFS) in glioblastoma, including MGMT methylation status and mutations in the IDH1 gene. In this study, we investigated the clinical and biological factors associated with long-term survival in glioblastoma patients treated with chemoradiotherapy.
Method
Demographic and clinical data were collected for all patients with glioblastoma diagnosed between May 2004 and September 2007, treated with chemoradiotherapy and with associated tissue samples available for biomarker analysis. MGMT methylation was determined by pyrosequencing. IDH1 mutation was identified by R132H immunohistochemistry. Univariate Cox regression analysis of factors associated with survival and Kaplan-Meier survival analysis was performed using the SPSS statistics package.
Results
One hundred patients were included in the study. Median follow-up was 12.2 months (range 1.6–102.4). Median OS was 12.1 months (95 % CI: 10.8–13.3) and median PFS was 8.2 months (95 % CI: 6.8–9.5). The 2-, 3- and 5-year survival was 18, 9 and 6 % respectively. Three patients are still alive at 7.4, 8.3 and 8.5 years after diagnosis.
Cox proportional-hazards regression identified independent prognostic factors for OS, female (
p
= 0.019), MGMT methylation (
p
< 0.0001) and IDH1 mutation (
p
= 0.023), and for PFS, MGMT methylation (
p
= 0.001) and IDH1 mutation (
p
= 0.018).
Kaplan-Meier survival analysis showed that MGMT
methylated
/IDH1
+ve
was associated with a significantly longer OS 66.8 months (95 % CI: 0.0–167.8) and PFS 16.9 months (95 % CI: 11.1–22.7) when compared with MGMT
methylated
/IDH1
-ve
OS 15.5 months (95 % CI: 11.6–19.4) and PFS 9.4 months (95 % CI: 8–10.8) (log-rank,
P
= 0.000) and MGMT
unmethylated
/IDH1
-ve
OS 11.1 months (95 % CI: 8.5–13.7) and PFS 6.3 months (95 % CI: 4.4–8.3) (log-rank,
p
= 0.000).
Conclusions
While the importance of MGMT methylation is well established, we demonstrate that the combination of MGMT
methylated
/IDH1
+ve
is associated with considerably longer OS and PFS in this series of chemoradiotherapy-treated glioblastoma tumours. The long-term cognitive function and quality of life in these long-term survivors warrant investigation.</abstract><cop>Vienna</cop><pub>Springer Vienna</pub><pmid>27526690</pmid><doi>10.1007/s00701-016-2928-8</doi><tpages>11</tpages></addata></record> |
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| source | MEDLINE; Springer Nature - Complete Springer Journals |
| subjects | Adolescent Adult Aged Biomarkers, Tumor - genetics Brain Neoplasms - drug therapy Brain Neoplasms - genetics Brain Neoplasms - radiotherapy Clinical Article - Brain Tumors Disease-Free Survival DNA Methylation DNA Modification Methylases - genetics DNA Repair Enzymes - genetics Female Glioblastoma - drug therapy Glioblastoma - genetics Glioblastoma - radiotherapy Humans Interventional Radiology Isocitrate Dehydrogenase - genetics Male Medicine Medicine & Public Health Middle Aged Minimally Invasive Surgery Mutation Neurology Neuroradiology Neurosurgery Promoter Regions, Genetic Surgical Orthopedics Tumor Suppressor Proteins - genetics |
| title | The impact of MGMT methylation and IDH-1 mutation on long-term outcome for glioblastoma treated with chemoradiotherapy |
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