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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  
 
| PMID:19016743; PMCID:2761618; PMID:18716556 PMID:25461780  PMID:25664944; PMID:26378811 PMCID:3429698; PMID:23817572; PMID:23583981 PMID:18974108; PMID:23278243; PMID:21274720  
 
|-
 
|-
| AML including NK-AML
  −
| CN-LOH
  −
| 1p
   
|  
 
|  
| D
+
| Angiocentric glioma
| 3
+
| Aberrations involving 6q24-q25
 +
| '''Fusions:''' MYB-QKI rearrangement/deletion (classic histology); '''Rearrangement:''' MYB alone (atypical histology); '''Amplification:''' MYB (atypical histology)
 +
| Generally indolent tumors; surgical resection can be curative
 +
| PMID:26829751; PMID:23633565; PMID:26778052 PMID:23583981
 
|-
 
|-
| 2
  −
| AML
  −
| CN-LOH
  −
| 2p
  −
| ''DNMT3A''
  −
| D
  −
| 3
  −
|-
  −
| 3
  −
| NK-AML, sAML
  −
| Loss
  −
| 3p14.1
  −
| ''FOXP1''
  −
| D
  −
| 3
  −
|-
  −
| 4
  −
| sAML, pAML
  −
| CN-LOH
  −
| 4q24
  −
| ''TET2''
  −
| D
  −
| 3
  −
|-
  −
| 4
  −
| AML, NK-AML, sAML
  −
| Loss
  −
| 4q24
  −
| ''TET2''
  −
| D, P
  −
| 3
  −
|-
  −
| 5
  −
| pAML, sAML
  −
| Loss
  −
| 5q
  −
|
  −
| D
  −
| 1
  −
|-
  −
| 6
  −
| AML including NK-AML
  −
| CN-LOH
  −
| 6p
  −
|
  −
| D
  −
| 3
  −
|-
  −
| 7
  −
| AML including NK-AML
  −
| CN-LOH
  −
| 7q
  −
| ''EZH2''
  −
| D
  −
| 3
  −
|-
  −
| 7
  −
| NK-AML, pAML, sAML
  −
| Loss
  −
| 7q
  −
| ''EZH2, CUX1''
  −
| D
  −
| 1
  −
|-
  −
| 8
  −
| AML with complex karyotype
  −
| Amplification
  −
| 8q24
  −
| ''MYC''
  −
| D, P
  −
| 3
  −
|-
  −
| 9
  −
| NK-AML, sAML
  −
| CN-LOH
  −
| 9p
  −
| ''JAK2''
  −
| D
  −
| 3
  −
|-
  −
| 11*
  −
| AML with complex karyotype
  −
| Amplification
  −
| 11q23
  −
| ''MLL (KMT2A)''
  −
| D, P
  −
| 3
  −
|-
  −
| 11*
  −
| AML
  −
| CN-LOH
  −
| 11p
  −
| ''WT1''
  −
| D
  −
| 3
  −
|-
  −
| 11
  −
| pAML, sAML, NK-AML
  −
| CN-LOH
  −
| 11q
  −
| ''CBL''
  −
| D
  −
| 3
  −
|-
  −
| 12
  −
| AML, NK-AML, AML with complex karyotype, sAML
  −
| Loss
  −
| 12p13.2
  −
| ''ETV6''
  −
| D
  −
| 3
  −
|-
  −
| 13*
  −
| pAML, NK-AML, ''NPM1'' mutated AML, FLT3-ITD positive AML, sAML
  −
| CN-LOH
  −
| 13q
  −
| ''FLT3''
  −
| D, P
  −
| 2
  −
|-
  −
| 16
  −
| NK-AML, AML with complex karyotype, pAML, sAML
  −
| Loss
  −
| 16q
  −
| ''CBFB''
  −
| D
  −
| 3
  −
|-
  −
| 17
  −
| AML, NK-AML, pAML, sAML
  −
| CN-LOH
  −
| 17p
  −
| ''TP53''
  −
| D
  −
| 3
  −
|-
  −
| 17
  −
| sAML, NK-AML, AML with complex karyotype, ''de novo'' AML
  −
| Loss
  −
| 17p
  −
| ''TP53''
  −
| D, P
  −
| 1
  −
|-
  −
| 17
  −
| NK-AML, pAML
  −
| Loss
  −
| 17q11.2
  −
| ''NF1, SUZ12''
  −
| D, P
  −
| 3
  −
|-
  −
| 19*
  −
| AML, NK-AML, sAML
  −
| CN-LOH
  −
| 19q
  −
| ''CEBPA''
  −
| D
  −
| 3
  −
|-
  −
| 20
  −
| sAML
  −
| Loss
  −
| 20q
  −
|
  −
| D
  −
| 3
  −
|-
  −
| 21*
  −
| pAML, AML with complex karyotype
  −
| Amplification
  −
| 21q22
  −
| ''ERG, ETS2''
  −
| D, P, T
  −
| 3
  −
|-
  −
| 21*
  −
| AML, NK-AML, sAML
  −
| CN-LOH
  −
| 21q
  −
| ''RUNX1''
  −
| D
  −
| 3
  −
|-
  −
| 21*
  −
| sAML
  −
| Loss
  −
| 21q22.12
  −
| ''RUNX1''
  −
| D
  −
| 3
  −
|-
  −
|}
  −
D = diagnostic significance; P = prognostic significance; T = therapeutic significance. Classification of levels of evidence: Level 1 = WHO classification or professional practice guidelines; Level 2 = well-powered studies with consensus from experts in the field; Level 3 = multiple small studies without any contradicting data; Level 4 = individual small studies, case reports, preclinical studies.
  −
  −
Abrreviations: CMA = chromosomal microarray; CNA = copy number aberration; CN-LOH = copy-neutral loss-of-heterozygosity; AML = acute myeloid leukemia; NK-AML = normal karyotype AML; pAML = primary AML; and sAML = secondary AML.
  −
  −
The * indicates CNAs and CN-LOH regions that are predominantly seen in AML.
  −
  −
==Reference==
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  −
1. Xu X, Bryke C, Sukhanova M, Huxley E, Dash DP, Dixon-Mciver A, Fang M, Griepp PT, Hodge JC, Iqbal A, Jeffries S, Kanagal-Shamanna R, Quintero-Rivera F, Shetty S, Slovak ML, Yenamandra A, Lennon PA, Raca G. (2018). Assessing copy number abnormalities and copy-neutral loss-of-heterozygosity across the genome as best practice in diagnostic evaluation of acute myeloid leukemia: An evidence-based review from the cancer genomics consortium (CGC) myeloid neoplasms working group. Cancer Genet [Epub ahead of print], PMID 30344013.