Compendium of Cancer Genome Aberrations

CNS5:Pleomorphic xanthoastrocytoma: Difference between revisions

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==Related Terminology==
== Related Terminology ==


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==Gene Rearrangements==
==Gene Rearrangements ==


{| class="wikitable sortable"
{| class="wikitable sortable"
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!Clinical Relevance Details/Other Notes
!Clinical Relevance Details/Other Notes
|-
|-
|''BRAF''||''BRAF''-''KIAA1549'' (rare), ''RAF1'' fusions, ''NTRK2''/''ALK''/''NTRK1'' (very rare in PXA)||Aberrant MAPK pathway activation (i.e BRAF p.V600E variant)||N/A
|''BRAF''||''BRAF''::''KIAA1549'' (rare), ''RAF1'' fusions, ''NTRK2''/''ALK''/''NTRK1'' (very rare in PXA)||Aberrant MAPK pathway activation (i.e BRAF p.V600E variant)||N/A
|BRAF p.V600E: Common in PXA, Fusions: Rare
|BRAF p.V600E: Common in PXA, Fusions: Rare
|D, P, T
|D, P, T
|Yes (WHO 2021/2025, NCCN 2023)<ref>{{Cite journal|last=d’Amati|first=Antonio|last2=Bargiacchi|first2=Lavinia|last3=Rossi|first3=Sabrina|last4=Carai|first4=Andrea|last5=Bertero|first5=Luca|last6=Barresi|first6=Valeria|last7=Errico|first7=Maria Elena|last8=Buccoliero|first8=Anna Maria|last9=Asioli|first9=Sofia|date=2024-03-13|title=Pediatric CNS tumors and 2021 WHO classification: what do oncologists need from pathologists?|url=https://www.frontiersin.org/journals/molecular-neuroscience/articles/10.3389/fnmol.2024.1268038/full|journal=Frontiers in Molecular Neuroscience|language=English|volume=17|doi=10.3389/fnmol.2024.1268038|issn=1662-5099}}</ref>
|Yes (WHO 2021/2025, NCCN 2023)<ref>{{Cite journal|last=d’Amati|first=Antonio|last2=Bargiacchi|first2=Lavinia|last3=Rossi|first3=Sabrina|last4=Carai|first4=Andrea|last5=Bertero|first5=Luca|last6=Barresi|first6=Valeria|last7=Errico|first7=Maria Elena|last8=Buccoliero|first8=Anna Maria|last9=Asioli|first9=Sofia|date=2024-03-13|title=Pediatric CNS tumors and 2021 WHO classification: what do oncologists need from pathologists?|url=https://www.frontiersin.org/journals/molecular-neuroscience/articles/10.3389/fnmol.2024.1268038/full|journal=Frontiers in Molecular Neuroscience|language=English|volume=17|doi=10.3389/fnmol.2024.1268038|issn=1662-5099}}</ref>
|BRAF p.V600E is diagnostic and predictive; kinase fusions targetable in rare cases<ref name=":0">{{Cite journal|last=Phillips|first=Joanna J.|last2=Gong|first2=Henry|last3=Chen|first3=Katharine|last4=Joseph|first4=Nancy M.|last5=van Ziffle|first5=Jessica|last6=Bastian|first6=Boris C.|last7=Grenert|first7=James P.|last8=Kline|first8=Cassie N.|last9=Mueller|first9=Sabine|date=2019-01|title=The genetic landscape of anaplastic pleomorphic xanthoastrocytoma|url=https://pubmed.ncbi.nlm.nih.gov/30051528|journal=Brain Pathology (Zurich, Switzerland)|volume=29|issue=1|pages=85–96|doi=10.1111/bpa.12639|issn=1750-3639|pmc=7837273|pmid=30051528}}</ref><ref>{{Cite journal|last=Vaubel|first=Rachael A.|last2=Caron|first2=Alissa A.|last3=Yamada|first3=Seiji|last4=Decker|first4=Paul A.|last5=Eckel Passow|first5=Jeanette E.|last6=Rodriguez|first6=Fausto J.|last7=Nageswara Rao|first7=Amulya A.|last8=Lachance|first8=Daniel|last9=Parney|first9=Ian|date=2018-03|title=Recurrent copy number alterations in low-grade and anaplastic pleomorphic xanthoastrocytoma with and without BRAF V600E mutation|url=https://pmc.ncbi.nlm.nih.gov/articles/PMC5807227/|journal=Brain Pathology (Zurich, Switzerland)|volume=28|issue=2|pages=172–182|doi=10.1111/bpa.12495|issn=1750-3639|pmc=5807227|pmid=28181325}}</ref> <ref>{{Cite journal|last=Tian|first=Lei|last2=Sun|first2=Wei|last3=Lou|first3=Lei|last4=Wang|first4=Wenyan|last5=Li|first5=Yanan|last6=Zhou|first6=Huandi|last7=Xiao|first7=Zhiqing|last8=Xue|first8=Xiaoying|date=2025|title=Pleomorphic xanthoastrocytoma with multiple recurrences and continuous malignant progression to bone metastasis: a case report|url=https://pmc.ncbi.nlm.nih.gov/articles/PMC12174448/|journal=Frontiers in Surgery|volume=12|pages=1595199|doi=10.3389/fsurg.2025.1595199|issn=2296-875X|pmc=12174448|pmid=40535548}}</ref><ref>{{Cite journal|last=Di Nunno|first=Vincenzo|last2=Gatto|first2=Lidia|last3=Tosoni|first3=Alicia|last4=Bartolini|first4=Stefania|last5=Franceschi|first5=Enrico|date=2022|title=Implications of BRAF V600E mutation in gliomas: Molecular considerations, prognostic value and treatment evolution|url=https://pmc.ncbi.nlm.nih.gov/articles/PMC9846085/|journal=Frontiers in Oncology|volume=12|pages=1067252|doi=10.3389/fonc.2022.1067252|issn=2234-943X|pmc=9846085|pmid=36686797}}</ref>
|''BRAF'' p.V600E is diagnostic and predictive; kinase fusions targetable in rare cases<ref name=":0">{{Cite journal|last=Phillips|first=Joanna J.|last2=Gong|first2=Henry|last3=Chen|first3=Katharine|last4=Joseph|first4=Nancy M.|last5=van Ziffle|first5=Jessica|last6=Bastian|first6=Boris C.|last7=Grenert|first7=James P.|last8=Kline|first8=Cassie N.|last9=Mueller|first9=Sabine|date=2019-01|title=The genetic landscape of anaplastic pleomorphic xanthoastrocytoma|url=https://pubmed.ncbi.nlm.nih.gov/30051528|journal=Brain Pathology (Zurich, Switzerland)|volume=29|issue=1|pages=85–96|doi=10.1111/bpa.12639|issn=1750-3639|pmc=7837273|pmid=30051528}}</ref><ref>{{Cite journal|last=Vaubel|first=Rachael A.|last2=Caron|first2=Alissa A.|last3=Yamada|first3=Seiji|last4=Decker|first4=Paul A.|last5=Eckel Passow|first5=Jeanette E.|last6=Rodriguez|first6=Fausto J.|last7=Nageswara Rao|first7=Amulya A.|last8=Lachance|first8=Daniel|last9=Parney|first9=Ian|date=2018-03|title=Recurrent copy number alterations in low-grade and anaplastic pleomorphic xanthoastrocytoma with and without BRAF V600E mutation|url=https://pmc.ncbi.nlm.nih.gov/articles/PMC5807227/|journal=Brain Pathology (Zurich, Switzerland)|volume=28|issue=2|pages=172–182|doi=10.1111/bpa.12495|issn=1750-3639|pmc=5807227|pmid=28181325}}</ref> <ref>{{Cite journal|last=Tian|first=Lei|last2=Sun|first2=Wei|last3=Lou|first3=Lei|last4=Wang|first4=Wenyan|last5=Li|first5=Yanan|last6=Zhou|first6=Huandi|last7=Xiao|first7=Zhiqing|last8=Xue|first8=Xiaoying|date=2025|title=Pleomorphic xanthoastrocytoma with multiple recurrences and continuous malignant progression to bone metastasis: a case report|url=https://pmc.ncbi.nlm.nih.gov/articles/PMC12174448/|journal=Frontiers in Surgery|volume=12|pages=1595199|doi=10.3389/fsurg.2025.1595199|issn=2296-875X|pmc=12174448|pmid=40535548}}</ref><ref>{{Cite journal|last=Di Nunno|first=Vincenzo|last2=Gatto|first2=Lidia|last3=Tosoni|first3=Alicia|last4=Bartolini|first4=Stefania|last5=Franceschi|first5=Enrico|date=2022|title=Implications of BRAF V600E mutation in gliomas: Molecular considerations, prognostic value and treatment evolution|url=https://pmc.ncbi.nlm.nih.gov/articles/PMC9846085/|journal=Frontiers in Oncology|volume=12|pages=1067252|doi=10.3389/fonc.2022.1067252|issn=2234-943X|pmc=9846085|pmid=36686797}}</ref>
|-
|-
|''CDKN2A''/''B''
|''CDKN2A''/''B''
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|D, P
|D, P
|Yes (WHO, NCCN—context specific)
|Yes (WHO, NCCN—context specific)
|Co-occurrence with BRAF p.V600E supports PXA diagnosis
|Co-occurrence with ''BRAF'' p.V600E supports PXA diagnosis
|-
|-
|TERT
|''TERT''
|N/A
|N/A


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<br />
<br />
|-
|-
|NTRK2, ALK, RAF1
|''NTRK2'', ''ALK'', ''RAF1''
|Fusions: NACC2-NTRK2, BEND5-NTRK2, PPP1CB-ALK, etc.
|Fusions: ''NACC2-NTRK2, BEND5-NTRK2, PPP1CB-ALK,'' etc.
|MAPK pathway activation via kinase fusions
|MAPK pathway activation via kinase fusions
|Variable; not associated with classic chr alterations
|Variable; not associated with classic chr alterations
|Rare (<5%)<ref>{{Cite journal|last=Galbraith|first=Kristyn|last2=Serrano|first2=Jonathan|last3=Shen|first3=Guomiao|last4=Tran|first4=Ivy|last5=Slocum|first5=Cheyanne C.|last6=Ketchum|first6=Courtney|last7=Abdullaev|first7=Zied|last8=Turakulov|first8=Rust|last9=Bale|first9=Tejus|date=2024-01-02|title=Impact of Rare and Multiple Concurrent Gene Fusions on Diagnostic DNA Methylation Classifier in Brain Tumors|url=https://pubmed.ncbi.nlm.nih.gov/37870438|journal=Molecular cancer research: MCR|volume=22|issue=1|pages=21–28|doi=10.1158/1541-7786.MCR-23-0627|issn=1557-3125|pmc=10942665|pmid=37870438}}</ref>
|Rare (<5%)<ref>{{Cite journal|last=Galbraith|first=Kristyn|last2=Serrano|first2=Jonathan|last3=Shen|first3=Guomiao|last4=Tran|first4=Ivy|last5=Slocum|first5=Cheyanne C.|last6=Ketchum|first6=Courtney|last7=Abdullaev|first7=Zied|last8=Turakulov|first8=Rust|last9=Bale|first9=Tejus|date=2024-01-02|title=Impact of Rare and Multiple Concurrent Gene Fusions on Diagnostic DNA Methylation Classifier in Brain Tumors|url=https://pubmed.ncbi.nlm.nih.gov/37870438|journal=Molecular cancer research: MCR|volume=22|issue=1|pages=21–28|doi=10.1158/1541-7786.MCR-23-0627|issn=1557-3125|pmc=10942665|pmid=37870438}}</ref>
|D
|D
|Context-dependent ( e.g. For patients with CNS tumors who harbor NTRK fusions, TRK inhibitors such as larotrectinib or repotrectinib are considered a preferred therapy, regardless of histology, if other options are limited) NCCN CNS Cancer guidelines
|Context-dependent (e.g. For patients with CNS tumors who harbor NTRK fusions, TRK inhibitors such as larotrectinib or repotrectinib are considered a preferred therapy, regardless of histology, if other options are limited) NCCN CNS Cancer guidelines
|Reported in individual cases; more common in glioneuronal/low-grade gliomas
|Reported in individual cases
|}
|}
==Individual Region Genomic Gain/Loss/LOH==
==Individual Region Genomic Gain/Loss/LOH==
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|Homozygous loss, LOH
|Homozygous loss, LOH
|9p21.3; chr9:21,900,000-22,300,000 (GRCh38; ~400Kb)
|9p21.3; chr9:21,900,000-22,300,000 (GRCh38; ~400Kb)
|CDKN2A, CDKN2B
|''CDKN2A'', ''CDKN2B''
|D, P
|D, P
|Yes (WHO CNS5, NCCN)
|Yes (WHO CNS5, NCCN)
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|Gain
|Gain
|Chr7 whole arm or segmental (varies)
|Chr7 whole arm or segmental (varies)
|EGFR not typically amplified)
|''EGFR'' not typically amplified
|D
|D
|No (however, frequently mentioned in literature as a recurrent copy number change in PXA<ref>{{Cite journal|last=Vaubel|first=Rachael|last2=Zschernack|first2=Valentina|last3=Tran|first3=Quynh T.|last4=Jenkins|first4=Sarah|last5=Caron|first5=Alissa|last6=Milosevic|first6=Dragana|last7=Smadbeck|first7=James|last8=Vasmatzis|first8=George|last9=Kandels|first9=Daniela|date=2021-01|title=Biology and grading of pleomorphic xanthoastrocytoma-what have we learned about it?|url=https://pmc.ncbi.nlm.nih.gov/articles/PMC8018001/|journal=Brain Pathology (Zurich, Switzerland)|volume=31|issue=1|pages=20–32|doi=10.1111/bpa.12874|issn=1750-3639|pmc=8018001|pmid=32619305}}</ref>
|No (however, frequently mentioned in literature as a recurrent copy number change in PXA)<ref>{{Cite journal|last=Vaubel|first=Rachael|last2=Zschernack|first2=Valentina|last3=Tran|first3=Quynh T.|last4=Jenkins|first4=Sarah|last5=Caron|first5=Alissa|last6=Milosevic|first6=Dragana|last7=Smadbeck|first7=James|last8=Vasmatzis|first8=George|last9=Kandels|first9=Daniela|date=2021-01|title=Biology and grading of pleomorphic xanthoastrocytoma-what have we learned about it?|url=https://pmc.ncbi.nlm.nih.gov/articles/PMC8018001/|journal=Brain Pathology (Zurich, Switzerland)|volume=31|issue=1|pages=20–32|doi=10.1111/bpa.12874|issn=1750-3639|pmc=8018001|pmid=32619305}}</ref>
|Trisomy, supports diagnosis; also seen in other gliomas
|Trisomy, supports diagnosis; also seen in other gliomas
|-
|-
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|Loss
|Loss
|Whole chr22 (varied cytoband, arm)
|Whole chr22 (varied cytoband, arm)
|NF2, others
|''NF2'', others
|D
|D
|No (not guideline-specific, recurrent in PXA)
|No (not guideline-specific, recurrent in PXA)
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|Copy-neutral
|Copy-neutral
|Varies (mainly 9p21)
|Varies (mainly 9p21)
|CDKN2A, CDKN2B
|''CDKN2A, CDKN2B''
|D, P
|D, P
|Yes (NCCN)
|Yes (NCCN)
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|Includes polyploidy, subclones, mosaicism; complexity increases at recurrence/progression<ref name=":1" />
|Includes polyploidy, subclones, mosaicism; complexity increases at recurrence/progression<ref name=":1" />
|-
|-
|Pleomorphic xanthoastrocytoma (PXA) not identified as a high‑TMB or focal amplifications. No MSI‑driven marker in PXA. Global mutation pattern in PXA dominated by MAPK activation (BRAF or kinase fusions) plus CDKN2A/B loss
|Global mutation pattern in PXA dominated by MAPK activation (''BRAF'' or kinase fusions) plus ''CDKN2A/B'' loss
|CDKN2A/B loss and loss of p16/p14ARF tumor suppressors; cell cycle dysregulation
|CDKN2A/B loss and loss of p16/p14ARF tumor suppressors; cell cycle dysregulation
|Common  
|Common  
|P,D
|P,D
|Yes
|Yes
|CDKN2A/B loss defining feature of PXA; not associated with grade or BRAF status; central to PXA biology
|''CDKN2A/B'' loss defining feature of PXA; not associated with grade or ''BRAF'' status; central to PXA biology
Pleomorphic xanthoastrocytoma (PXA) not identified as a high‑TMB tumour type. No MSI‑driven marker in PXA.
|}
|}
==Gene Mutations (SNV/INDEL)==
==Gene Mutations (SNV/INDEL)==
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!Clinical Relevance Details/Other Notes
!Clinical Relevance Details/Other Notes
|-
|-
|BRAF
|''BRAF''


<br />
<br />
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|Specific for PXA, actionable with BRAF/MEK inhibitors; rarely found in diffuse astrocytomas. Favorable prognostic marker<ref name=":2">{{Cite journal|last=Kim|first=Young Zoon|last2=Kim|first2=Chae-Yong|last3=Lim|first3=Do Hoon|date=2022-04|title=The Overview of Practical Guidelines for Gliomas by KSNO, NCCN, and EANO|url=https://pubmed.ncbi.nlm.nih.gov/35545827|journal=Brain Tumor Research and Treatment|volume=10|issue=2|pages=83–93|doi=10.14791/btrt.2022.0001|issn=2288-2405|pmc=9098981|pmid=35545827}}</ref>
|Specific for PXA, actionable with BRAF/MEK inhibitors; rarely found in diffuse astrocytomas. Favorable prognostic marker<ref name=":2">{{Cite journal|last=Kim|first=Young Zoon|last2=Kim|first2=Chae-Yong|last3=Lim|first3=Do Hoon|date=2022-04|title=The Overview of Practical Guidelines for Gliomas by KSNO, NCCN, and EANO|url=https://pubmed.ncbi.nlm.nih.gov/35545827|journal=Brain Tumor Research and Treatment|volume=10|issue=2|pages=83–93|doi=10.14791/btrt.2022.0001|issn=2288-2405|pmc=9098981|pmid=35545827}}</ref>
|-
|-
|TERT
|''TERT''
<br />
<br />
|Promoter mutation
|Promoter mutation
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|Associated with anaplastic progression, poor recurrence-free survival, and adverse prognosis in high-grade PXA<ref name=":2" />
|Associated with anaplastic progression, poor recurrence-free survival, and adverse prognosis in high-grade PXA<ref name=":2" />
|-
|-
|IDH1/IDH2
|''IDH1/IDH2''
|Missense (R132H, etc)
|Missense (R132H, etc)
|Other
|Other
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|Absence confirms classic PXA; if present, suggests diffuse astrocytoma not PXA<ref>Yamada S, Kipp BR, Voss JS, Giannini C, Raghunathan A. Combined "Infiltrating Astrocytoma/Pleomorphic Xanthoastrocytoma" Harboring IDH1 R132H and BRAF V600E Mutations. Am J Surg Pathol. 2016 Feb;40(2):279-84. doi: 10.1097/PAS.0000000000000515. PMID: 26414224.</ref>
|Absence confirms classic PXA; if present, suggests diffuse astrocytoma not PXA<ref>Yamada S, Kipp BR, Voss JS, Giannini C, Raghunathan A. Combined "Infiltrating Astrocytoma/Pleomorphic Xanthoastrocytoma" Harboring IDH1 R132H and BRAF V600E Mutations. Am J Surg Pathol. 2016 Feb;40(2):279-84. doi: 10.1097/PAS.0000000000000515. PMID: 26414224.</ref>
|-
|-
|NTRK2, ALK
|''NTRK2, ALK''
|Kinase gene fusions  
|Kinase gene fusions  
|Oncogene
|Oncogene
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|}Note: A more extensive list of mutations can be found in [https://www.cbioportal.org/ <u>cBioportal</u>], [https://cancer.sanger.ac.uk/cosmic <u>COSMIC</u>], and/or other databases. When applicable, gene-specific pages within the CCGA site directly link to pertinent external content.
|}Note: A more extensive list of mutations can be found in [https://www.cbioportal.org/ <u>cBioportal</u>], [https://cancer.sanger.ac.uk/cosmic <u>COSMIC</u>], and/or other databases. When applicable, gene-specific pages within the CCGA site directly link to pertinent external content.
==Epigenomic Alterations==
==Epigenomic Alterations==
Dominant epigenomic themes in Pleomorphic xanthoastrocytoma (PXA) are: a distinct methylation class tied to MAPK activation and CDKN2A/B loss, progressive promoter hypermethylation in anaplastic transformation, frequent MGMT promoter methylation, and a relative absence of the H3/ATRX-driven epigenetic programs seen in other glioma subtypes<ref>{{Cite journal|last=Martínez|first=Ramón|last2=Carmona|first2=F. Javier|last3=Vizoso|first3=Miguel|last4=Rohde|first4=Veit|last5=Kirsch|first5=Matthias|last6=Schackert|first6=Gabriele|last7=Ropero|first7=Santiago|last8=Paulus|first8=Werner|last9=Barrantes|first9=Alonso|date=2014-03-20|title=DNA methylation alterations in grade II- and anaplastic pleomorphic xanthoastrocytoma|url=https://pubmed.ncbi.nlm.nih.gov/24650279|journal=BMC cancer|volume=14|pages=213|doi=10.1186/1471-2407-14-213|issn=1471-2407|pmc=4000050|pmid=24650279}}</ref><ref>{{Cite journal|last=Tang|first=Karen|last2=Kurland|first2=David|last3=Vasudevaraja|first3=Varshini|last4=Serrano|first4=Jonathan|last5=Delorenzo|first5=Michael|last6=Radmanesh|first6=Alireza|last7=Thomas|first7=Cheddhi|last8=Spino|first8=Marissa|last9=Gardner|first9=Sharon|date=2020-08-01|title=Exploring DNA Methylation for Prognosis and Analyzing the Tumor Microenvironment in Pleomorphic Xanthoastrocytoma|url=https://pmc.ncbi.nlm.nih.gov/articles/PMC8453609/|journal=Journal of Neuropathology and Experimental Neurology|volume=79|issue=8|pages=880–890|doi=10.1093/jnen/nlaa051|issn=1554-6578|pmc=8453609|pmid=32594172}}</ref>.
Dominant epigenomic themes in Pleomorphic xanthoastrocytoma (PXA) are: a distinct methylation class tied to MAPK activation and CDKN2A/B loss, progressive promoter hypermethylation in anaplastic transformation, frequent ''MGMT'' promoter methylation, and a relative absence of the H3/ATRX-driven epigenetic programs seen in other glioma subtypes<ref>{{Cite journal|last=Martínez|first=Ramón|last2=Carmona|first2=F. Javier|last3=Vizoso|first3=Miguel|last4=Rohde|first4=Veit|last5=Kirsch|first5=Matthias|last6=Schackert|first6=Gabriele|last7=Ropero|first7=Santiago|last8=Paulus|first8=Werner|last9=Barrantes|first9=Alonso|date=2014-03-20|title=DNA methylation alterations in grade II- and anaplastic pleomorphic xanthoastrocytoma|url=https://pubmed.ncbi.nlm.nih.gov/24650279|journal=BMC cancer|volume=14|pages=213|doi=10.1186/1471-2407-14-213|issn=1471-2407|pmc=4000050|pmid=24650279}}</ref><ref>{{Cite journal|last=Tang|first=Karen|last2=Kurland|first2=David|last3=Vasudevaraja|first3=Varshini|last4=Serrano|first4=Jonathan|last5=Delorenzo|first5=Michael|last6=Radmanesh|first6=Alireza|last7=Thomas|first7=Cheddhi|last8=Spino|first8=Marissa|last9=Gardner|first9=Sharon|date=2020-08-01|title=Exploring DNA Methylation for Prognosis and Analyzing the Tumor Microenvironment in Pleomorphic Xanthoastrocytoma|url=https://pmc.ncbi.nlm.nih.gov/articles/PMC8453609/|journal=Journal of Neuropathology and Experimental Neurology|volume=79|issue=8|pages=880–890|doi=10.1093/jnen/nlaa051|issn=1554-6578|pmc=8453609|pmid=32594172}}</ref>.


==Genes and Main Pathways Involved==
==Genes and Main Pathways Involved==
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|Unregulated cell division
|Unregulated cell division
|-
|-
|TERT promoter mutations or amplification
|''TERT'' promoter mutations or amplification
|TERT – Telomere maintenance pathway
|TERT – Telomere maintenance pathway
|Activate telomerase and support immortalization via the telomere maintenance pathway
|Activate telomerase and support immortalization via the telomere maintenance pathway
Line 250: Line 251:
[https://www.cancer.gov/rare-brain-spine-tumor/tumors/pleomorphic-xanthroastrocytoma Pleomorphic Xanthoastrocytoma (PXA) and Other BRAF-Altered Tumors: Diagnosis and Treatment - NCI]
[https://www.cancer.gov/rare-brain-spine-tumor/tumors/pleomorphic-xanthroastrocytoma Pleomorphic Xanthoastrocytoma (PXA) and Other BRAF-Altered Tumors: Diagnosis and Treatment - NCI]
==References==
==References==
<references />


==Notes==
==Notes==
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[[Category:DISEASE]]
[[Category:DISEASE]]
[[Category:Diseases P]]
[[Category:Diseases P]]
<references />
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