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Adding CNS Tumor information
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==Recurrent Genomic Alterations in AML Detected by Chromosomal Microarray (Literature Review)==
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==Recurrent Genomic Alterations in Pediatric and Adult CNS Detected by Chromosomal Microarray (Literature Review)==
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Table 1 - A comprehensive list of CNAs and CN-LOH detectable by CMA testing with strong diagnostic, prognostic and treatment implications in AML.  Table derived from Xu et al., 2018 [PMID 30344013] with permission from Cancer Genetics.
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Table 1 - Pediatric Central Nervous System Tumors.  Table derived from Ligon et al., 2018 [   ] with permission from Cancer Genetics.
 
{| class="wikitable"
 
{| class="wikitable"
 
|-
 
|-
! Chromosome
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! TUMOR
! AML Subtype
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! SUBTYPES
! Abnormality Type (Amplification, Loss, CN-LOH)
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! BROAD ABERRATIONS (>10Mb)
! Region
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! FOCAL ABERRATIONS (>10Mb)
! Relevant Genes (if known)
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! CLINICAL FEATURES
! Clinical Significance
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! REFERENCES
! Level of Evidence
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|-
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! GLIOMAS
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|-
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| Low grade glioma, WHO grade I
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| Pilocytic astrocytoma/pilomyxoid astrocytoma
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| Some tumors show polysomy 7; other polysomies more common in adult PA
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| '''Fusions:''' KIAA1549-BRAF fusion (via 3'BRAF duplication), other BRAF partners reported; NTRK fusions (rare); FGFR1 fusions (rare); '''Mutations:''' BRAF V600E (particularly extra-cerebellar tumors); FGFR1 (midline PA); NF1 (esp. germline), other MAPK pathway mutations '''Loss:''' NF1 in optic pathway PA
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| Classic PA are cerebellar (most commonly associated with BRAF duplication); PA in patients with germline NF1 alterations often develop as optic gliomas;Surgical resection can be curative; PMA generally more aggressive than PA; BRAF fusions and BRAF mutations generally are mutually exclusive
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| PMID:19016743; PMCID:2761618; PMID:18716556 PMID:25461780  PMID:25664944; PMID:26378811 PMCID:3429698; PMID:23817572; PMID:23583981 PMID:18974108; PMID:23278243; PMID:21274720
 
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| 1
   
| AML including NK-AML
 
| AML including NK-AML
 
| CN-LOH
 
| CN-LOH