CNS5:Pleomorphic xanthoastrocytoma: Difference between revisions

Wkhan (talk | contribs)
Wkhan (talk | contribs)
Line 148: Line 148:
!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>
|
|-
|-
|<span class="blue-text">EXAMPLE:</span>
|Whole chromosome loss or cnLOH most commonly involved chromosomes 22, 14, 13, and 10
Microsatellite instability - hypermutated
|Variable gene losses
|
|Recurrent
|<span class="blue-text">EXAMPLE:</span> Common (Endometrial carcinoma)
|P
|<span class="blue-text">EXAMPLE:</span> P, T
|No
|
|Seen in subset; trend toward anaplastic cases<ref name=":1" />
|
|-
|-
|
|Complex karyotype with multiple CNVs
|
|Chromosomal instability (CIN)
|
|Common
|
|P
|
|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)==