Compendium of Cancer Genome Aberrations

CNS5:Pleomorphic xanthoastrocytoma: Difference between revisions

[unchecked revision][unchecked revision]
← Older editNewer edit →
VisualWikitext
Wkhan (talk | contribs)
15 edits
No edit summary
Line 3: Line 3:
[[CNS5:Table_of_Contents|Central Nervous System Tumours (WHO Classification, 5th ed.)]]
[[CNS5:Table_of_Contents|Central Nervous System Tumours (WHO Classification, 5th ed.)]]


{{Under Construction}}
<span style="color:#0070C0">(''General Instructions – The focus of these pages is the clinically significant genetic alterations in each disease type. This is based on up-to-date knowledge from multiple resources such as PubMed and the WHO classification books. The CCGA is meant to be a supplemental resource to the WHO classification books; the CCGA captures in a continually updated wiki-stye manner the current genetics/genomics knowledge of each disease, which evolves more rapidly than books can be revised and published. If the same disease is described in multiple WHO classification books, the genetics-related information for that disease will be consolidated into a single main page that has this template (other pages would only contain a link to this main page).'' </span>
 
<span style="color:#0070C0">(''General Instructions – The focus of these pages is the clinically significant genetic alterations in each disease type. This is based on up-to-date knowledge from multiple resources such as PubMed and the WHO classification books. The CCGA is meant to be a supplemental resource to the WHO classification books; the CCGA captures in a continually updated wiki-stye manner the current genetics/genomics knowledge of each disease, which evolves more rapidly than books can be revised and published. If the same disease is described in multiple WHO classification books, the genetics-related information for that disease will be consolidated into a single main page that has this template (other pages would only contain a link to this main page). Use [https://www.genenames.org/ <u>HUGO-approved gene names and symbols</u>] (italicized when appropriate), [https://varnomen.hgvs.org/ <u>HGVS-based nomenclature for variants</u>], as well as generic names of drugs and testing platforms or assays if applicable. Please complete tables whenever possible and do not delete them (add N/A if not applicable in the table and delete the examples); to add (or move) a row or column in a table, click nearby within the table and select the > symbol that appears. Please do not delete or alter the section headings. The use of bullet points alongside short blocks of text rather than only large paragraphs is encouraged. Additional instructions below in italicized blue text should not be included in the final page content. Please also see'' </span><u>''[[Author_Instructions]]''</u><span style="color:#0070C0"> ''and [[Frequently Asked Questions (FAQs)|<u>FAQs</u>]] as well as contact your [[Leadership|<u>Associate Editor</u>]] or [mailto:CCGA@cancergenomics.org <u>Technical Support</u>].)''</span>
==Primary Author(s)*==
==Primary Author(s)*==
Wahab A. Khan, PhD, FACMG, Dartmouth Health <span style="color:#0070C0"> </span>
Wahab A. Khan, PhD, FACMG, Dartmouth Health <span style="color:#0070C0"> </span>
Line 30: Line 28:
|}
|}


==Related Terminology==
== Related Terminology - Pleomorphic xanthoastrocytoma (PXA) ==


{| class="wikitable"
{| class="wikitable"
Line 41: Line 39:
|}
|}


==Gene Rearrangements==
==Gene Rearrangements ==
Put your text here and fill in the table <span style="color:#0070C0">(''Instructions: Details on clinical significance such as prognosis and other important information can be provided in the notes section. Please include references throughout the table. Do not delete the table.'')</span>
 
{| class="wikitable sortable"
{| class="wikitable sortable"
|-
|-
Line 71: Line 69:
|Telomerase activation (mainly in anaplastic PXA)
|Telomerase activation (mainly in anaplastic PXA)
|TERT promoter mutations/amplifications
|TERT promoter mutations/amplifications
|'''Recurrent (15–47% in anaplastic) PMID: 30051528'''
|Recurrent (15–47% in anaplastic)<ref>{{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>
|P (poor; recurrence risk)
|P (poor; recurrence risk)
|Yes (WHO, NCCN-context specefic)
|Yes (WHO, NCCN-context specefic)
Line 82: Line 80:
|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%) PMID: 37870438'''
|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
Line 88: Line 86:
|}
|}
==Individual Region Genomic Gain/Loss/LOH==
==Individual Region Genomic Gain/Loss/LOH==
Put your text here and fill in the table <span style="color:#0070C0">(''Instructions: Includes aberrations not involving gene rearrangements. Details on clinical significance such as prognosis and other important information can be provided in the notes section. Can refer to CGC workgroup tables as linked on the homepage if applicable. Please include references throughout the table. Do not delete the table.'') </span>
 
{| class="wikitable sortable"
{| class="wikitable sortable"
|-
|-
Line 102: Line 100:
|D, P
|D, P
|Yes (WHO CNS5, NCCN)
|Yes (WHO CNS5, NCCN)
|'''Defining PXA feature; occurs in >85% of cases (PMID: 28181325)'''
|Defining PXA feature; occurs in >85% of cases<ref name=":1" />
|-
|-
|7
|7
Line 109: Line 107:
|EGFR not typically amplified)
|EGFR not typically amplified)
|D
|D
|No (however, frequently mentioned in literature as a recurrent copy number change in PXA (PMID:
|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
|-
|-
Line 126: Line 124:
|P
|P
|No
|No
|Seen in a subset, less common ((PMID: 28181325)
|Seen in a subset, less common
|-
|-
|LOH
|LOH
Line 137: Line 135:
|}
|}
==Characteristic Chromosomal or Other Global Mutational Patterns==
==Characteristic Chromosomal or Other Global Mutational Patterns==
Put your text here and fill in the table <span style="color:#0070C0">(I''nstructions: Included in this category are alterations such as hyperdiploid; gain of odd number chromosomes including typically chromosome 1, 3, 5, 7, 11, and 17; co-deletion of 1p and 19q; complex karyotypes without characteristic genetic findings; chromothripsis; microsatellite instability; homologous recombination deficiency; mutational signature pattern; etc. Details on clinical significance such as prognosis and other important information can be provided in the notes section. Please include references throughout the table. Do not delete the table.'')</span>
 
{| class="wikitable sortable"
{| class="wikitable sortable"
|-
|-
Line 148: Line 146:
!Clinical Relevance Details/Other Notes
!Clinical Relevance Details/Other Notes
|-
|-
|<span class="blue-text">EXAMPLE:</span>
|Common chromosome gains: +7, +5, +2, +12, +20, +21, +15
Co-deletion of 1p and 18q
|Variable; chromosomal hyperdiploidy
|<span class="blue-text">EXAMPLE:</span> See chromosomal rearrangements table as this pattern is due to an unbalanced derivative translocation associated with oligodendroglioma (add reference).
|Recurrent (17-20%)
|<span class="blue-text">EXAMPLE:</span> Common (Oligodendroglioma)
|P
|<span class="blue-text">EXAMPLE:</span> D, P
|No
|
|Whole chromosome gains common; gains of +12 and +21 more common in BRAF V600E tumors; may indicate genomic instability<ref name=":1">Vaubel RA, Caron AA, Yamada S, Decker PA, Eckel Passow JE, Rodriguez FJ, Nageswara Rao AA, Lachance D, Parney I, Jenkins R, Giannini C. Recurrent copy number alterations in low-grade and anaplastic pleomorphic xanthoastrocytoma with and without BRAF V600E mutation. Brain Pathol. 2018 Mar;28(2):172-182. doi: 10.1111/bpa.12495. Epub 2017 Apr 2. PMID: 28181325; PMCID: PMC5807227.</ref>
|
|-
|Whole chromosome loss or cnLOH most commonly involved chromosomes 22, 14, 13, and 10
|Variable gene losses
|Recurrent
|P
|No
|Seen in subset; trend toward anaplastic cases<ref name=":1" />
|-
|-
|<span class="blue-text">EXAMPLE:</span>
|Complex karyotype with multiple CNVs
Microsatellite instability - hypermutated
|Chromosomal instability (CIN)
|
|Common
|<span class="blue-text">EXAMPLE:</span> Common (Endometrial carcinoma)
|P
|<span class="blue-text">EXAMPLE:</span> P, T
|No
|
|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
|
|CDKN2A/B loss and loss of p16/p14ARF tumor suppressors; cell cycle dysregulation
|
|Common
|
|P,D
|
|Yes
|
|CDKN2A/B loss defining feature of PXA; not associated with grade or BRAF status; central to PXA biology
|}
|}
==Gene Mutations (SNV/INDEL)==
==Gene Mutations (SNV/INDEL)==
Put your text here and fill in the table <span style="color:#0070C0">(''Instructions: This table is not meant to be an exhaustive list; please include only genes/alterations that are recurrent or common as well either disease defining and/or clinically significant. If a gene has multiple mechanisms depending on the type or site of the alteration, add multiple entries in the table. For clinical significance, denote associations with FDA-approved therapy (not an extensive list of applicable drugs) and NCCN or other national guidelines if applicable; Can also refer to CGC workgroup tables as linked on the homepage if applicable as well as any high impact papers or reviews of gene mutations in this entity. Details on clinical significance such as prognosis and other important information such as concomitant and mutually exclusive mutations can be provided in the notes section. Please include references throughout the table. Do not delete the table.'') </span>
<span style="color:#0070C0">''This table is not meant to be an exhaustive list''</span>
{| class="wikitable sortable"
{| class="wikitable sortable"
|-
|-
Line 189: Line 192:
|D, P, T
|D, P, T
|Yes (WHO CNS5, NCCN)  
|Yes (WHO CNS5, NCCN)  
|Specific for PXA, actionable with BRAF/MEK inhibitors; rarely found in diffuse astrocytomas. Favorable prognostic marker (PMID: 35545827).
|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
Line 198: Line 201:
|P
|P
|Yes (WHO CNS5)
|Yes (WHO CNS5)
|Associated with anaplastic progression, poor recurrence-free survival, and adverse prognosis in high-grade PXA (PMID: 35545827)
|Associated with anaplastic progression, poor recurrence-free survival, and adverse prognosis in high-grade PXA<ref name=":2" />
|-
|-
|IDH1/IDH2
|IDH1/IDH2
Line 206: Line 209:
|D
|D
|Yes (WHO CNS5 for differential diagnosis)
|Yes (WHO CNS5 for differential diagnosis)
|Absence confirms classic PXA; if present, suggests diffuse astrocytoma not PXA (PMID: 26414224)
|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
Line 214: Line 217:
|T
|T
|Yes (FDA/NCCN for fusion-positive CNS tumors, not PXA-specific)
|Yes (FDA/NCCN for fusion-positive CNS tumors, not PXA-specific)
|'''Targetable by TRK/ALK inhibitors (larotrectinib, entrectinib); found chiefly in pediatric BRAF-wildtype PXAs.(PMID: 40568680)'''
|Targetable by TRK/ALK inhibitors (larotrectinib, entrectinib); found chiefly in pediatric BRAF-wildtype PXAs<ref>Fischer JM, Gilbert AR, Galvan EM, Singh AK, Floyd JR, Shah S. Pleomorphic xanthoastrocytoma with anaplasia and BEND5-NTRK2 fusion in a young adult with a history of cranial radiation for childhood rhabdomyosarcoma. Neurooncol Adv. 2025 Mar 8;7(1):vdaf052. doi: 10.1093/noajnl/vdaf052. PMID: 40568680; PMCID: PMC12188291.</ref>
|-
|
|
|
|
|
|
|
|}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==
Put your text here
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==
Put your text here and fill in the table <span style="color:#0070C0">(''Instructions: Please include references throughout the table. Do not delete the table.)''</span>
 
{| class="wikitable sortable"
{| class="wikitable sortable"
|-
|-
!Gene; Genetic Alteration!!Pathway!!Pathophysiologic Outcome
!Gene; Genetic Alteration!!Pathway!!Pathophysiologic Outcome
|-
|-
|<span class="blue-text">EXAMPLE:</span> ''BRAF'' and ''MAP2K1''; Activating mutations
|''BRAF'' and ''MAP2K1''; Activating mutations
|<span class="blue-text">EXAMPLE:</span> MAPK signaling
|MAPK signaling
|<span class="blue-text">EXAMPLE:</span> Increased cell growth and proliferation
|Increased cell growth and proliferation
|-
|-
|<span class="blue-text">EXAMPLE:</span> ''CDKN2A''; Inactivating mutations
|''CDKN2A''; Inactivating mutations
|<span class="blue-text">EXAMPLE:</span> Cell cycle regulation
|Cell cycle regulation
|<span class="blue-text">EXAMPLE:</span> Unregulated cell division
|Unregulated cell division
|-
|-
|<span class="blue-text">EXAMPLE:</span> ''KMT2C'' and ''ARID1A''; Inactivating mutations
|TERT promoter mutations or amplification
|<span class="blue-text">EXAMPLE:</span> Histone modification, chromatin remodeling
|TERT – Telomere maintenance pathway
|<span class="blue-text">EXAMPLE:</span> Abnormal gene expression program
|Activate telomerase and support immortalization via the telomere maintenance pathway
|-
|
|
|
|}
|}
==Genetic Diagnostic Testing Methods==
==Genetic Diagnostic Testing Methods==
Put your text here <span style="color:#0070C0">(''Instructions: Include recommended testing type(s) to identify the clinically significant genetic alterations.'')</span>
Diagnostic workup for suspected PXA typically includes BRAF mutation testing, robust assessment of CDKN2A/B deletion (preferably via SNP-microarray or NGS/ddPCR), and DNA methylation profiling, with extended NGS/fusion testing where needed<ref>https://www.frontiersin.org/journals/molecular-neuroscience/articles/10.3389/fnmol.2024.1268038/full</ref>
==Familial Forms==
==Familial Forms==
Put your text here <span style="color:#0070C0">(''Instructions: Include associated hereditary conditions/syndromes that cause this entity or are caused by this entity.'') </span>
For most PXAs, no inherited/familial cause is identified, and they are considered sporadic tumors.  
==Additional Information==
==Additional Information==
Put your text here
PXA belongs to a specific DNA methylation class characterized by BRAF pathway activation (usually BRAF p.V600E) and near‑universal CDKN2A/B homozygous deletion, and is typically IDH1/2‑ and H3‑wildtype; methylation profiling is increasingly used to confirm this integrated molecular diagnosis and to distinguish PXA from pilocytic astrocytoma and epithelioid glioblastoma<ref>{{Cite journal|last=Dampier|first=Christopher H.|last2=Shah|first2=Niharika|last3=Galbraith|first3=Kristyn|last4=Ebrahimi|first4=Azadeh|last5=Neto|first5=Osorio Lopes Abath|last6=Abdullaev|first6=Zied|last7=Alexandrescu|first7=Sanda|last8=Andreiuolo|first8=Felipe|last9=Armstrong|first9=Terri|date=2025|title=Molecular, histologic, and clinical characterization of methylation class pleomorphic xanthoastrocytoma: An analysis of 469 tumors|url=https://pubmed.ncbi.nlm.nih.gov/40735274|journal=Neuro-Oncology Advances|volume=7|issue=1|pages=vdaf089|doi=10.1093/noajnl/vdaf089|issn=2632-2498|pmc=12305539|pmid=40735274}}</ref>.
 
==Links==
==Links==
Put a link here or anywhere appropriate in this page <span style="color:#0070C0">(''Instructions: Highlight the text to which you want to add a link in this section or elsewhere, select the "Link" icon at the top of the wiki page, and search the name of the internal page to which you want to link this text, or enter an external internet address by including the "<nowiki>http://www</nowiki>." portion.'')</span>
[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 />
(use the "Cite" icon at the top of the page) <span style="color:#0070C0">(''Instructions: Add each reference into the text above by clicking where you want to insert the reference, selecting the “Cite” icon at the top of the wiki page, and using the “Automatic” tab option to search by PMID to select the reference to insert. If a PMID is not available, such as for a book, please use the “Cite” icon, select “Manual” and then “Basic Form”, and include the entire reference. To insert the same reference again later in the page, select the “Cite” icon and “Re-use” to find the reference; DO NOT insert the same reference twice using the “Automatic” tab as it will be treated as two separate references. The reference list in this section will be automatically generated and sorted''</span><span style="color:#0070C0">''.''</span><span style="color:#0070C0">)</span>
 
==Notes==
==Notes==
<nowiki>*</nowiki>Primary authors will typically be those that initially create and complete the content of a page.  If a subsequent user modifies the content and feels the effort put forth is of high enough significance to warrant listing in the authorship section, please contact the [[Leadership|''<u>Associate Editor</u>'']] or other CCGA representative.  When pages have a major update, the new author will be acknowledged at the beginning of the page, and those who contributed previously will be acknowledged below as a prior author.
Khan WA: “Pleomorphic xanthoastrocytoma”. Compendium of Cancer Genome Aberrations (CCGA), Cancer Genomics Consortium (CGC), updated {{REVISIONMONTH}}/{{REVISIONDAY}}/{{REVISIONYEAR}}, <nowiki>https://ccga.io/index.php/CNS5:Pleomorphic xanthoastrocytoma</nowiki>.
 
Prior Author(s):
<nowiki>*</nowiki>''Citation of this Page'': “Pleomorphic xanthoastrocytoma”. Compendium of Cancer Genome Aberrations (CCGA), Cancer Genomics Consortium (CGC), updated {{REVISIONMONTH}}/{{REVISIONDAY}}/{{REVISIONYEAR}}, <nowiki>https://ccga.io/index.php/CNS5:Pleomorphic xanthoastrocytoma</nowiki>.
[[Category:CNS5]]
[[Category:CNS5]]
[[Category:DISEASE]]
[[Category:DISEASE]]
[[Category:Diseases P]]
[[Category:Diseases P]]
<references />
Retrieved from "https://test.ccga.io/index.php/CNS5:Pleomorphic_xanthoastrocytoma"