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Correlation of MTAP immunohistochemical deficiency with CDKN2A homozygous deletion and clinicopathological features in pleomorphic xanthoastrocytoma
Pleomorphic xanthoastrocytoma (PXA) is a rare tumor ranging from World Health Organization (WHO) grades 2–3 and can potentially recur and metastasize throughout the central nervous system (CNS). Cyclin-dependent kinase inhibitor 2A/B (CDKN2A/B) deletion is a frequent genomic alteration of PXA. Methy...
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Published in: | Brain tumor pathology 2023, Vol.40 (1), p.15-25 |
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description | Pleomorphic xanthoastrocytoma (PXA) is a rare tumor ranging from World Health Organization (WHO) grades 2–3 and can potentially recur and metastasize throughout the central nervous system (CNS).
Cyclin-dependent kinase inhibitor 2A/B (CDKN2A/B)
deletion is a frequent genomic alteration of PXA. Methylthioadenosine phosphorylase (MTAP) immunohistochemistry is a promising surrogate marker for
CDKN2A
homozygous deletion in different cancers but has not been examined in PXA. Therefore, we performed
CDKN2A
fluorescence in situ hybridization and MTAP immunohistochemistry on specimens from 23 patients with CNS WHO grades 2 (
n
= 10) and 3 (
n
= 13) PXAs, including specimens from primary and recurrent tumors, and determined whether MTAP immunohistochemistry correlated with
CDKN2A
homozygous deletion and clinicopathological features.
CDKN2A
homozygous deletion was detected in 30% (3/10) and 76.9% (10/13) of CNS WHO grades 2 and 3 PXAs, respectively. In addition, MTAP loss was inconsistent with
CDKN2A
homozygous deletion (sensitivity = 86.7%, specificity = 100%). Furthermore,
CDKN2A
homozygous deletion was correlated with WHO grade (p = 0.026) and the Ki-67 labeling index (p = 0.037). Therefore, MTAP immunostaining can be a suitable surrogate marker for
CDKN2A
homozygous deletions in PXAs, and
CDKN2A
homozygous deletions may be an important prognostic factor for PXAs. |
doi_str_mv | 10.1007/s10014-022-00447-0 |
format | article |
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Cyclin-dependent kinase inhibitor 2A/B (CDKN2A/B)
deletion is a frequent genomic alteration of PXA. Methylthioadenosine phosphorylase (MTAP) immunohistochemistry is a promising surrogate marker for
CDKN2A
homozygous deletion in different cancers but has not been examined in PXA. Therefore, we performed
CDKN2A
fluorescence in situ hybridization and MTAP immunohistochemistry on specimens from 23 patients with CNS WHO grades 2 (
n
= 10) and 3 (
n
= 13) PXAs, including specimens from primary and recurrent tumors, and determined whether MTAP immunohistochemistry correlated with
CDKN2A
homozygous deletion and clinicopathological features.
CDKN2A
homozygous deletion was detected in 30% (3/10) and 76.9% (10/13) of CNS WHO grades 2 and 3 PXAs, respectively. In addition, MTAP loss was inconsistent with
CDKN2A
homozygous deletion (sensitivity = 86.7%, specificity = 100%). Furthermore,
CDKN2A
homozygous deletion was correlated with WHO grade (p = 0.026) and the Ki-67 labeling index (p = 0.037). Therefore, MTAP immunostaining can be a suitable surrogate marker for
CDKN2A
homozygous deletions in PXAs, and
CDKN2A
homozygous deletions may be an important prognostic factor for PXAs.</description><identifier>ISSN: 1433-7398</identifier><identifier>EISSN: 1861-387X</identifier><identifier>DOI: 10.1007/s10014-022-00447-0</identifier><identifier>PMID: 36550382</identifier><language>eng</language><publisher>Singapore: Springer Nature Singapore</publisher><subject>Cancer Research ; Cloning ; DNA methylation ; Kinases ; Medical prognosis ; Medicine ; Medicine & Public Health ; Mesothelioma ; Mutation ; Neurology ; Neurosurgery ; Oncology ; Original Article ; Pathology ; Patients ; Proteins ; Statistical analysis ; Survival analysis ; Tumors</subject><ispartof>Brain tumor pathology, 2023, Vol.40 (1), p.15-25</ispartof><rights>The Author(s), under exclusive licence to The Japan Society of Brain Tumor Pathology 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 The Japan Society of Brain Tumor Pathology.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c399t-c6bd1590e4a52a65ba8fdd1b6483545cb60977e0a7f6372cb5de72100020f2993</citedby><cites>FETCH-LOGICAL-c399t-c6bd1590e4a52a65ba8fdd1b6483545cb60977e0a7f6372cb5de72100020f2993</cites><orcidid>0000-0002-5446-1318</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27903,27904</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/36550382$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Lou, Lei</creatorcontrib><creatorcontrib>Li, Jiajun</creatorcontrib><creatorcontrib>Qin, Manman</creatorcontrib><creatorcontrib>Tian, Xiaoxi</creatorcontrib><creatorcontrib>Guo, Wenli</creatorcontrib><creatorcontrib>Li, Yuehong</creatorcontrib><title>Correlation of MTAP immunohistochemical deficiency with CDKN2A homozygous deletion and clinicopathological features in pleomorphic xanthoastrocytoma</title><title>Brain tumor pathology</title><addtitle>Brain Tumor Pathol</addtitle><addtitle>Brain Tumor Pathol</addtitle><description>Pleomorphic xanthoastrocytoma (PXA) is a rare tumor ranging from World Health Organization (WHO) grades 2–3 and can potentially recur and metastasize throughout the central nervous system (CNS).
Cyclin-dependent kinase inhibitor 2A/B (CDKN2A/B)
deletion is a frequent genomic alteration of PXA. Methylthioadenosine phosphorylase (MTAP) immunohistochemistry is a promising surrogate marker for
CDKN2A
homozygous deletion in different cancers but has not been examined in PXA. Therefore, we performed
CDKN2A
fluorescence in situ hybridization and MTAP immunohistochemistry on specimens from 23 patients with CNS WHO grades 2 (
n
= 10) and 3 (
n
= 13) PXAs, including specimens from primary and recurrent tumors, and determined whether MTAP immunohistochemistry correlated with
CDKN2A
homozygous deletion and clinicopathological features.
CDKN2A
homozygous deletion was detected in 30% (3/10) and 76.9% (10/13) of CNS WHO grades 2 and 3 PXAs, respectively. In addition, MTAP loss was inconsistent with
CDKN2A
homozygous deletion (sensitivity = 86.7%, specificity = 100%). Furthermore,
CDKN2A
homozygous deletion was correlated with WHO grade (p = 0.026) and the Ki-67 labeling index (p = 0.037). Therefore, MTAP immunostaining can be a suitable surrogate marker for
CDKN2A
homozygous deletions in PXAs, and
CDKN2A
homozygous deletions may be an important prognostic factor for PXAs.</description><subject>Cancer Research</subject><subject>Cloning</subject><subject>DNA methylation</subject><subject>Kinases</subject><subject>Medical prognosis</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Mesothelioma</subject><subject>Mutation</subject><subject>Neurology</subject><subject>Neurosurgery</subject><subject>Oncology</subject><subject>Original Article</subject><subject>Pathology</subject><subject>Patients</subject><subject>Proteins</subject><subject>Statistical analysis</subject><subject>Survival analysis</subject><subject>Tumors</subject><issn>1433-7398</issn><issn>1861-387X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2023</creationdate><recordtype>article</recordtype><recordid>eNp9kctu1DAUhi0EoqXwAiyQJTZsAr7EcbIcTSkgymVRJHaW45xMXDl2sB3B9Dl4YNyZAhILNrYlf-c79vkRekrJS0qIfJXKSuuKMFYRUteyIvfQKW0bWvFWfr1fzjXnleRde4IepXR9CxFJH6IT3ghBeMtO0c9tiBGczjZ4HEb84WrzGdt5Xn2YbMrBTDBbox0eYLTGgjd7_N3mCW_P339kGzyFOdzsd2FNhXBw0Gg_YOOstyYsOk_Bhd1BMYLOa4SErceLg1IZl8ka_EP7QumUYzD7HGb9GD0YtUvw5G4_Q18uXl9t31aXn968224uK8O7Llem6QcqOgK1Fkw3otftOAy0b-qWi1qYviGdlEC0HBsumenFAJKVoRFGRtZ1_Ay9OHqXGL6tkLKabTLgnPZQfqSYFC0tjo4W9Pk_6HVYoy-vU6yjLRGyzLRQ7EiZGFKKMKol2lnHvaJE3Wamjpmpkpk6ZKZIKXp2p177GYY_Jb9DKgA_Aqlc-R3Ev73_o_0FIxqkig</recordid><startdate>2023</startdate><enddate>2023</enddate><creator>Lou, Lei</creator><creator>Li, Jiajun</creator><creator>Qin, Manman</creator><creator>Tian, Xiaoxi</creator><creator>Guo, Wenli</creator><creator>Li, Yuehong</creator><general>Springer Nature Singapore</general><general>Springer Nature B.V</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</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>K9.</scope><scope>M0S</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PSYQQ</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0002-5446-1318</orcidid></search><sort><creationdate>2023</creationdate><title>Correlation of MTAP immunohistochemical deficiency with CDKN2A homozygous deletion and clinicopathological features in pleomorphic xanthoastrocytoma</title><author>Lou, Lei ; Li, Jiajun ; Qin, Manman ; Tian, Xiaoxi ; Guo, Wenli ; Li, Yuehong</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c399t-c6bd1590e4a52a65ba8fdd1b6483545cb60977e0a7f6372cb5de72100020f2993</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2023</creationdate><topic>Cancer Research</topic><topic>Cloning</topic><topic>DNA methylation</topic><topic>Kinases</topic><topic>Medical prognosis</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Mesothelioma</topic><topic>Mutation</topic><topic>Neurology</topic><topic>Neurosurgery</topic><topic>Oncology</topic><topic>Original Article</topic><topic>Pathology</topic><topic>Patients</topic><topic>Proteins</topic><topic>Statistical analysis</topic><topic>Survival analysis</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Lou, Lei</creatorcontrib><creatorcontrib>Li, Jiajun</creatorcontrib><creatorcontrib>Qin, Manman</creatorcontrib><creatorcontrib>Tian, Xiaoxi</creatorcontrib><creatorcontrib>Guo, Wenli</creatorcontrib><creatorcontrib>Li, Yuehong</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>ProQuest Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</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)</collection><collection>ProQuest Central</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>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</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 One Psychology</collection><collection>MEDLINE - Academic</collection><jtitle>Brain tumor pathology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Lou, Lei</au><au>Li, Jiajun</au><au>Qin, Manman</au><au>Tian, Xiaoxi</au><au>Guo, Wenli</au><au>Li, Yuehong</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Correlation of MTAP immunohistochemical deficiency with CDKN2A homozygous deletion and clinicopathological features in pleomorphic xanthoastrocytoma</atitle><jtitle>Brain tumor pathology</jtitle><stitle>Brain Tumor Pathol</stitle><addtitle>Brain Tumor Pathol</addtitle><date>2023</date><risdate>2023</risdate><volume>40</volume><issue>1</issue><spage>15</spage><epage>25</epage><pages>15-25</pages><issn>1433-7398</issn><eissn>1861-387X</eissn><abstract>Pleomorphic xanthoastrocytoma (PXA) is a rare tumor ranging from World Health Organization (WHO) grades 2–3 and can potentially recur and metastasize throughout the central nervous system (CNS).
Cyclin-dependent kinase inhibitor 2A/B (CDKN2A/B)
deletion is a frequent genomic alteration of PXA. Methylthioadenosine phosphorylase (MTAP) immunohistochemistry is a promising surrogate marker for
CDKN2A
homozygous deletion in different cancers but has not been examined in PXA. Therefore, we performed
CDKN2A
fluorescence in situ hybridization and MTAP immunohistochemistry on specimens from 23 patients with CNS WHO grades 2 (
n
= 10) and 3 (
n
= 13) PXAs, including specimens from primary and recurrent tumors, and determined whether MTAP immunohistochemistry correlated with
CDKN2A
homozygous deletion and clinicopathological features.
CDKN2A
homozygous deletion was detected in 30% (3/10) and 76.9% (10/13) of CNS WHO grades 2 and 3 PXAs, respectively. In addition, MTAP loss was inconsistent with
CDKN2A
homozygous deletion (sensitivity = 86.7%, specificity = 100%). Furthermore,
CDKN2A
homozygous deletion was correlated with WHO grade (p = 0.026) and the Ki-67 labeling index (p = 0.037). Therefore, MTAP immunostaining can be a suitable surrogate marker for
CDKN2A
homozygous deletions in PXAs, and
CDKN2A
homozygous deletions may be an important prognostic factor for PXAs.</abstract><cop>Singapore</cop><pub>Springer Nature Singapore</pub><pmid>36550382</pmid><doi>10.1007/s10014-022-00447-0</doi><tpages>11</tpages><orcidid>https://orcid.org/0000-0002-5446-1318</orcidid></addata></record> |
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subjects | Cancer Research Cloning DNA methylation Kinases Medical prognosis Medicine Medicine & Public Health Mesothelioma Mutation Neurology Neurosurgery Oncology Original Article Pathology Patients Proteins Statistical analysis Survival analysis Tumors |
title | Correlation of MTAP immunohistochemical deficiency with CDKN2A homozygous deletion and clinicopathological features in pleomorphic xanthoastrocytoma |
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