ARID1A mutation associated with recurrence and shorter progression-free survival in atypical meningiomas
Purpose The oncologic outcomes for atypical meningiomas can be poor. Generally, patients that have had a prior recurrence have a substantially elevated risk of a future recurrence. Additionally, certain tumor genomic profiles have been shown as markers of poor prognosis. We sought to characterize th...
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| Veröffentlicht in: | Journal of cancer research and clinical oncology 2023-07, Vol.149 (8), p.5165-5172 |
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| creator | Chaluts, Danielle Dullea, Jonathan T. Ali, Muhammad Vasan, Vikram Devarajan, Alex Rutland, John W. Gill, Corey M. Ellis, Ethan Kinoshita, Yayoi McBride, Russell B. Bederson, Joshua Donovan, Michael Sebra, Robert Umphlett, Melissa Shrivastava, Raj K. |
| description | Purpose
The oncologic outcomes for atypical meningiomas can be poor. Generally, patients that have had a prior recurrence have a substantially elevated risk of a future recurrence. Additionally, certain tumor genomic profiles have been shown as markers of poor prognosis. We sought to characterize the genomic differences between primary and recurrent tumors as well as assess if those differences had implications on recurrence.
Methods
We identified primary and recurrent gross totally resected WHO grade II meningiomas with > 30 days of post-surgical follow-up at our institution. For genes with a prevalence of > 5% in the cohort, we compared the mutational prevalence in primary and recurrent tumors. For a gene of interest, we assessed the time to radiographic recurrence using adjusted cox-regression.
Results
We identified 88 meningiomas (77 primary, 16 recurrent) with a median follow-up of 5.33 years. Mutations in
ARID1A
found in association with recurrent tumors (7/16 recurrent tumors vs 5/72 primary tumors,
p |
| doi_str_mv | 10.1007/s00432-022-04442-y |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_2734616032</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2734616032</sourcerecordid><originalsourceid>FETCH-LOGICAL-c375t-c34c12e4d6f1cc05654285c7447659e41e2b320db1b58f6d25c0ee419801dda13</originalsourceid><addsrcrecordid>eNp9kUtrGzEUhUVpSFy3f6CLIuimm0l09ZrJ0iRtGggEQrIWsuaOLeOZcXVnHPzvI9dOA11kodfVd44uOox9BXEOQpQXJIRWshAyD621LHYf2AT2JVDKfGQTASUURoI9Y5-IViKfTSlP2ZmySldCwoQtZw-31zDj7Tj4IfYd90R9iH7Amj_HYckThjEl7AJy39Wcln0aMPFN6hcJibKkaBIipzFt49avecwew24TQ9632MVuEfvW02d20vg14ZfjOmVPv34-Xv0u7u5vbq9md0VQpRnyrANI1LVtIARhrNGyMqHUurTmEjWgnCsp6jnMTdXYWpogMJcvKwF17UFN2Y-Db-7wz4g0uDZSwPXad9iP5GSptAUrlMzo9__QVT-mLnfnZKVKq6U1e0oeqJB6ooSN26TY-rRzINw-B3fIweUc3N8c3C6Lvh2tx3mL9T_J68dnQB0AylfdAtPb2-_YvgCAo5PN</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2837642652</pqid></control><display><type>article</type><title>ARID1A mutation associated with recurrence and shorter progression-free survival in atypical meningiomas</title><source>MEDLINE</source><source>Springer Nature - Complete Springer Journals</source><creator>Chaluts, Danielle ; Dullea, Jonathan T. ; Ali, Muhammad ; Vasan, Vikram ; Devarajan, Alex ; Rutland, John W. ; Gill, Corey M. ; Ellis, Ethan ; Kinoshita, Yayoi ; McBride, Russell B. ; Bederson, Joshua ; Donovan, Michael ; Sebra, Robert ; Umphlett, Melissa ; Shrivastava, Raj K.</creator><creatorcontrib>Chaluts, Danielle ; Dullea, Jonathan T. ; Ali, Muhammad ; Vasan, Vikram ; Devarajan, Alex ; Rutland, John W. ; Gill, Corey M. ; Ellis, Ethan ; Kinoshita, Yayoi ; McBride, Russell B. ; Bederson, Joshua ; Donovan, Michael ; Sebra, Robert ; Umphlett, Melissa ; Shrivastava, Raj K.</creatorcontrib><description>Purpose
The oncologic outcomes for atypical meningiomas can be poor. Generally, patients that have had a prior recurrence have a substantially elevated risk of a future recurrence. Additionally, certain tumor genomic profiles have been shown as markers of poor prognosis. We sought to characterize the genomic differences between primary and recurrent tumors as well as assess if those differences had implications on recurrence.
Methods
We identified primary and recurrent gross totally resected WHO grade II meningiomas with > 30 days of post-surgical follow-up at our institution. For genes with a prevalence of > 5% in the cohort, we compared the mutational prevalence in primary and recurrent tumors. For a gene of interest, we assessed the time to radiographic recurrence using adjusted cox-regression.
Results
We identified 88 meningiomas (77 primary, 16 recurrent) with a median follow-up of 5.33 years. Mutations in
ARID1A
found in association with recurrent tumors (7/16 recurrent tumors vs 5/72 primary tumors,
p <
0.001). In the whole cohort, mutations in
ARID1A
were not associated with alterations in time to recurrence after adjusting for recurrence status (
p =
0.713). When restricted to primary tumors,
ARID1A
is associated with a 625% increase in the hazard of recurrence (HR = 7.26 [1.42–37.0];
p =
0.017).
Conclusion
We demonstrate mutations in
ARID1A
, a chromatin remodeling gene, in a higher prevalence in recurrent tumors. We further demonstrate that when mutations in
ARID1A
are present in primary atypical meningiomas, these tumors tend to have worse prognosis. Further prospective study may validate
ARID1A
as a prognostic marker.</description><identifier>ISSN: 0171-5216</identifier><identifier>EISSN: 1432-1335</identifier><identifier>DOI: 10.1007/s00432-022-04442-y</identifier><identifier>PMID: 36348021</identifier><language>eng</language><publisher>Berlin/Heidelberg: Springer Berlin Heidelberg</publisher><subject>Brain cancer ; Cancer Research ; Chromatin remodeling ; DNA-Binding Proteins - genetics ; Genomics ; Hematology ; Humans ; Internal Medicine ; Medical prognosis ; Medicine ; Medicine & Public Health ; Meningeal Neoplasms - genetics ; Meningeal Neoplasms - surgery ; Meningioma - surgery ; Mutation ; Neoplasm Recurrence, Local - epidemiology ; Neoplasm Recurrence, Local - genetics ; Oncology ; Prognosis ; Progression-Free Survival ; Prospective Studies ; Retrospective Studies ; Transcription Factors - genetics ; Tumors</subject><ispartof>Journal of cancer research and clinical oncology, 2023-07, Vol.149 (8), p.5165-5172</ispartof><rights>The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature 2022. Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law.</rights><rights>2022. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c375t-c34c12e4d6f1cc05654285c7447659e41e2b320db1b58f6d25c0ee419801dda13</citedby><cites>FETCH-LOGICAL-c375t-c34c12e4d6f1cc05654285c7447659e41e2b320db1b58f6d25c0ee419801dda13</cites><orcidid>0000-0002-8018-1213</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s00432-022-04442-y$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s00432-022-04442-y$$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/36348021$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Chaluts, Danielle</creatorcontrib><creatorcontrib>Dullea, Jonathan T.</creatorcontrib><creatorcontrib>Ali, Muhammad</creatorcontrib><creatorcontrib>Vasan, Vikram</creatorcontrib><creatorcontrib>Devarajan, Alex</creatorcontrib><creatorcontrib>Rutland, John W.</creatorcontrib><creatorcontrib>Gill, Corey M.</creatorcontrib><creatorcontrib>Ellis, Ethan</creatorcontrib><creatorcontrib>Kinoshita, Yayoi</creatorcontrib><creatorcontrib>McBride, Russell B.</creatorcontrib><creatorcontrib>Bederson, Joshua</creatorcontrib><creatorcontrib>Donovan, Michael</creatorcontrib><creatorcontrib>Sebra, Robert</creatorcontrib><creatorcontrib>Umphlett, Melissa</creatorcontrib><creatorcontrib>Shrivastava, Raj K.</creatorcontrib><title>ARID1A mutation associated with recurrence and shorter progression-free survival in atypical meningiomas</title><title>Journal of cancer research and clinical oncology</title><addtitle>J Cancer Res Clin Oncol</addtitle><addtitle>J Cancer Res Clin Oncol</addtitle><description>Purpose
The oncologic outcomes for atypical meningiomas can be poor. Generally, patients that have had a prior recurrence have a substantially elevated risk of a future recurrence. Additionally, certain tumor genomic profiles have been shown as markers of poor prognosis. We sought to characterize the genomic differences between primary and recurrent tumors as well as assess if those differences had implications on recurrence.
Methods
We identified primary and recurrent gross totally resected WHO grade II meningiomas with > 30 days of post-surgical follow-up at our institution. For genes with a prevalence of > 5% in the cohort, we compared the mutational prevalence in primary and recurrent tumors. For a gene of interest, we assessed the time to radiographic recurrence using adjusted cox-regression.
Results
We identified 88 meningiomas (77 primary, 16 recurrent) with a median follow-up of 5.33 years. Mutations in
ARID1A
found in association with recurrent tumors (7/16 recurrent tumors vs 5/72 primary tumors,
p <
0.001). In the whole cohort, mutations in
ARID1A
were not associated with alterations in time to recurrence after adjusting for recurrence status (
p =
0.713). When restricted to primary tumors,
ARID1A
is associated with a 625% increase in the hazard of recurrence (HR = 7.26 [1.42–37.0];
p =
0.017).
Conclusion
We demonstrate mutations in
ARID1A
, a chromatin remodeling gene, in a higher prevalence in recurrent tumors. We further demonstrate that when mutations in
ARID1A
are present in primary atypical meningiomas, these tumors tend to have worse prognosis. Further prospective study may validate
ARID1A
as a prognostic marker.</description><subject>Brain cancer</subject><subject>Cancer Research</subject><subject>Chromatin remodeling</subject><subject>DNA-Binding Proteins - genetics</subject><subject>Genomics</subject><subject>Hematology</subject><subject>Humans</subject><subject>Internal Medicine</subject><subject>Medical prognosis</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Meningeal Neoplasms - genetics</subject><subject>Meningeal Neoplasms - surgery</subject><subject>Meningioma - surgery</subject><subject>Mutation</subject><subject>Neoplasm Recurrence, Local - epidemiology</subject><subject>Neoplasm Recurrence, Local - genetics</subject><subject>Oncology</subject><subject>Prognosis</subject><subject>Progression-Free Survival</subject><subject>Prospective Studies</subject><subject>Retrospective Studies</subject><subject>Transcription Factors - genetics</subject><subject>Tumors</subject><issn>0171-5216</issn><issn>1432-1335</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2023</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>BENPR</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNp9kUtrGzEUhUVpSFy3f6CLIuimm0l09ZrJ0iRtGggEQrIWsuaOLeOZcXVnHPzvI9dOA11kodfVd44uOox9BXEOQpQXJIRWshAyD621LHYf2AT2JVDKfGQTASUURoI9Y5-IViKfTSlP2ZmySldCwoQtZw-31zDj7Tj4IfYd90R9iH7Amj_HYckThjEl7AJy39Wcln0aMPFN6hcJibKkaBIipzFt49avecwew24TQ9632MVuEfvW02d20vg14ZfjOmVPv34-Xv0u7u5vbq9md0VQpRnyrANI1LVtIARhrNGyMqHUurTmEjWgnCsp6jnMTdXYWpogMJcvKwF17UFN2Y-Db-7wz4g0uDZSwPXad9iP5GSptAUrlMzo9__QVT-mLnfnZKVKq6U1e0oeqJB6ooSN26TY-rRzINw-B3fIweUc3N8c3C6Lvh2tx3mL9T_J68dnQB0AylfdAtPb2-_YvgCAo5PN</recordid><startdate>20230701</startdate><enddate>20230701</enddate><creator>Chaluts, Danielle</creator><creator>Dullea, Jonathan T.</creator><creator>Ali, Muhammad</creator><creator>Vasan, Vikram</creator><creator>Devarajan, Alex</creator><creator>Rutland, John W.</creator><creator>Gill, Corey M.</creator><creator>Ellis, Ethan</creator><creator>Kinoshita, Yayoi</creator><creator>McBride, Russell B.</creator><creator>Bederson, Joshua</creator><creator>Donovan, Michael</creator><creator>Sebra, Robert</creator><creator>Umphlett, Melissa</creator><creator>Shrivastava, Raj K.</creator><general>Springer Berlin Heidelberg</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>7TO</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>H94</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>MBDVC</scope><scope>PHGZM</scope><scope>PHGZT</scope><scope>PJZUB</scope><scope>PKEHL</scope><scope>PPXIY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>Q9U</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0002-8018-1213</orcidid></search><sort><creationdate>20230701</creationdate><title>ARID1A mutation associated with recurrence and shorter progression-free survival in atypical meningiomas</title><author>Chaluts, Danielle ; Dullea, Jonathan T. ; Ali, Muhammad ; Vasan, Vikram ; Devarajan, Alex ; Rutland, John W. ; Gill, Corey M. ; Ellis, Ethan ; Kinoshita, Yayoi ; McBride, Russell B. ; Bederson, Joshua ; Donovan, Michael ; Sebra, Robert ; Umphlett, Melissa ; Shrivastava, Raj K.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c375t-c34c12e4d6f1cc05654285c7447659e41e2b320db1b58f6d25c0ee419801dda13</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2023</creationdate><topic>Brain cancer</topic><topic>Cancer Research</topic><topic>Chromatin remodeling</topic><topic>DNA-Binding Proteins - genetics</topic><topic>Genomics</topic><topic>Hematology</topic><topic>Humans</topic><topic>Internal Medicine</topic><topic>Medical prognosis</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Meningeal Neoplasms - genetics</topic><topic>Meningeal Neoplasms - surgery</topic><topic>Meningioma - surgery</topic><topic>Mutation</topic><topic>Neoplasm Recurrence, Local - epidemiology</topic><topic>Neoplasm Recurrence, Local - genetics</topic><topic>Oncology</topic><topic>Prognosis</topic><topic>Progression-Free Survival</topic><topic>Prospective Studies</topic><topic>Retrospective Studies</topic><topic>Transcription Factors - genetics</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Chaluts, Danielle</creatorcontrib><creatorcontrib>Dullea, Jonathan T.</creatorcontrib><creatorcontrib>Ali, Muhammad</creatorcontrib><creatorcontrib>Vasan, Vikram</creatorcontrib><creatorcontrib>Devarajan, Alex</creatorcontrib><creatorcontrib>Rutland, John W.</creatorcontrib><creatorcontrib>Gill, Corey M.</creatorcontrib><creatorcontrib>Ellis, Ethan</creatorcontrib><creatorcontrib>Kinoshita, Yayoi</creatorcontrib><creatorcontrib>McBride, Russell B.</creatorcontrib><creatorcontrib>Bederson, Joshua</creatorcontrib><creatorcontrib>Donovan, Michael</creatorcontrib><creatorcontrib>Sebra, Robert</creatorcontrib><creatorcontrib>Umphlett, Melissa</creatorcontrib><creatorcontrib>Shrivastava, Raj K.</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>Oncogenes and Growth Factors 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>Public Health Database</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Research Library (Alumni Edition)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>Research Library Prep</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>Research Library</collection><collection>Research Library (Corporate)</collection><collection>ProQuest Central (New)</collection><collection>ProQuest One Academic (New)</collection><collection>ProQuest Health & Medical Research Collection</collection><collection>ProQuest One Academic Middle East (New)</collection><collection>ProQuest One Health & Nursing</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 Basic</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of cancer research and clinical oncology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Chaluts, Danielle</au><au>Dullea, Jonathan T.</au><au>Ali, Muhammad</au><au>Vasan, Vikram</au><au>Devarajan, Alex</au><au>Rutland, John W.</au><au>Gill, Corey M.</au><au>Ellis, Ethan</au><au>Kinoshita, Yayoi</au><au>McBride, Russell B.</au><au>Bederson, Joshua</au><au>Donovan, Michael</au><au>Sebra, Robert</au><au>Umphlett, Melissa</au><au>Shrivastava, Raj K.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>ARID1A mutation associated with recurrence and shorter progression-free survival in atypical meningiomas</atitle><jtitle>Journal of cancer research and clinical oncology</jtitle><stitle>J Cancer Res Clin Oncol</stitle><addtitle>J Cancer Res Clin Oncol</addtitle><date>2023-07-01</date><risdate>2023</risdate><volume>149</volume><issue>8</issue><spage>5165</spage><epage>5172</epage><pages>5165-5172</pages><issn>0171-5216</issn><eissn>1432-1335</eissn><abstract>Purpose
The oncologic outcomes for atypical meningiomas can be poor. Generally, patients that have had a prior recurrence have a substantially elevated risk of a future recurrence. Additionally, certain tumor genomic profiles have been shown as markers of poor prognosis. We sought to characterize the genomic differences between primary and recurrent tumors as well as assess if those differences had implications on recurrence.
Methods
We identified primary and recurrent gross totally resected WHO grade II meningiomas with > 30 days of post-surgical follow-up at our institution. For genes with a prevalence of > 5% in the cohort, we compared the mutational prevalence in primary and recurrent tumors. For a gene of interest, we assessed the time to radiographic recurrence using adjusted cox-regression.
Results
We identified 88 meningiomas (77 primary, 16 recurrent) with a median follow-up of 5.33 years. Mutations in
ARID1A
found in association with recurrent tumors (7/16 recurrent tumors vs 5/72 primary tumors,
p <
0.001). In the whole cohort, mutations in
ARID1A
were not associated with alterations in time to recurrence after adjusting for recurrence status (
p =
0.713). When restricted to primary tumors,
ARID1A
is associated with a 625% increase in the hazard of recurrence (HR = 7.26 [1.42–37.0];
p =
0.017).
Conclusion
We demonstrate mutations in
ARID1A
, a chromatin remodeling gene, in a higher prevalence in recurrent tumors. We further demonstrate that when mutations in
ARID1A
are present in primary atypical meningiomas, these tumors tend to have worse prognosis. Further prospective study may validate
ARID1A
as a prognostic marker.</abstract><cop>Berlin/Heidelberg</cop><pub>Springer Berlin Heidelberg</pub><pmid>36348021</pmid><doi>10.1007/s00432-022-04442-y</doi><tpages>8</tpages><orcidid>https://orcid.org/0000-0002-8018-1213</orcidid></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0171-5216 |
| ispartof | Journal of cancer research and clinical oncology, 2023-07, Vol.149 (8), p.5165-5172 |
| issn | 0171-5216 1432-1335 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_2734616032 |
| source | MEDLINE; Springer Nature - Complete Springer Journals |
| subjects | Brain cancer Cancer Research Chromatin remodeling DNA-Binding Proteins - genetics Genomics Hematology Humans Internal Medicine Medical prognosis Medicine Medicine & Public Health Meningeal Neoplasms - genetics Meningeal Neoplasms - surgery Meningioma - surgery Mutation Neoplasm Recurrence, Local - epidemiology Neoplasm Recurrence, Local - genetics Oncology Prognosis Progression-Free Survival Prospective Studies Retrospective Studies Transcription Factors - genetics Tumors |
| title | ARID1A mutation associated with recurrence and shorter progression-free survival in atypical meningiomas |
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