Compendium of Cancer Genome Aberrations

CNS5:Diffuse astrocytoma, MYB- or MYBL1-altered: Difference between revisions

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==Primary Author(s)*==
==Primary Author(s)*==


Put your text here
Scott C. Smith, PhD, FACMG; SUNY Upstate Medical University


__TOC__
__TOC__
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==Cancer Category/Type==
==Cancer Category/Type==


Put your text here
WHO Classification of Tumours of the Central Nervous System (5th Edition)


==Cancer Sub-Classification / Subtype==
==Cancer Sub-Classification / Subtype==


Put your text here
Diffuse Astrocytoma, MYB- or MYBL1-Altered


==Definition / Description of Disease==
==Definition / Description of Disease==


Put your text here
Diffuse astrocytoma, ''MYB'' or ''MYBL1''-altered is one of several newly recognized tumor types in the 5<sup>th</sup> edition of the ''WHO Classification of Tumors of the Central Nervous System''. The newly recognized classifications were in response to advances in understanding of paediatric-type gliomas, facilitated by an increased molecular characterisation of these tumours. Diffuse astrocytoma, MYB or MYBL1-altered is a subset of diffuse low-grade glioma with amplifications, structural variants, and fusions involving the ''MYB'' and ''MYBL1'' protooncogenes. Diffuse astrocytoma, MYB or MYBL1-altered subtypes are without characteristic histological features of angiocentric glioma<ref>{{Cite journal|last=Slegers|first=Rutger Juriaan|last2=Blumcke|first2=Ingmar|date=2020-03-09|title=Low-grade developmental and epilepsy associated brain tumors: a critical update 2020|url=https://pubmed.ncbi.nlm.nih.gov/32151273|journal=Acta Neuropathologica Communications|volume=8|issue=1|pages=27|doi=10.1186/s40478-020-00904-x|issn=2051-5960|pmc=7063704|pmid=32151273}}</ref><ref>{{Cite journal|last=Bandopadhayay|first=Pratiti|last2=Ramkissoon|first2=Lori A.|last3=Jain|first3=Payal|last4=Bergthold|first4=Guillaume|last5=Wala|first5=Jeremiah|last6=Zeid|first6=Rhamy|last7=Schumacher|first7=Steven E.|last8=Urbanski|first8=Laura|last9=O'Rourke|first9=Ryan|date=2016-03|title=MYB-QKI rearrangements in angiocentric glioma drive tumorigenicity through a tripartite mechanism|url=https://pubmed.ncbi.nlm.nih.gov/26829751|journal=Nature Genetics|volume=48|issue=3|pages=273–282|doi=10.1038/ng.3500|issn=1546-1718|pmc=4767685|pmid=26829751}}</ref>. A related group of diffuse gliomas, the isomorphic glioma, occur predominantly in adults and are typically well-differentiated, low to moderately cellular, comprised of astrocytes with rounded nuclei and regular chromatin structures, and have low proliferative indices<ref>{{Cite journal|last=Wefers|first=Annika K.|last2=Stichel|first2=Damian|last3=Schrimpf|first3=Daniel|last4=Coras|first4=Roland|last5=Pages|first5=Mélanie|last6=Tauziède-Espariat|first6=Arnault|last7=Varlet|first7=Pascale|last8=Schwarz|first8=Daniel|last9=Söylemezoglu|first9=Figen|date=2020-01|title=Isomorphic diffuse glioma is a morphologically and molecularly distinct tumour entity with recurrent gene fusions of MYBL1 or MYB and a benign disease course|url=https://pubmed.ncbi.nlm.nih.gov/31563982|journal=Acta Neuropathologica|volume=139|issue=1|pages=193–209|doi=10.1007/s00401-019-02078-w|issn=1432-0533|pmc=7477753|pmid=31563982}}</ref><ref>{{Cite journal|last=Chiang|first=Jason|last2=Harreld|first2=Julie H.|last3=Tinkle|first3=Christopher L.|last4=Moreira|first4=Daniel C.|last5=Li|first5=Xiaoyu|last6=Acharya|first6=Sahaja|last7=Qaddoumi|first7=Ibrahim|last8=Ellison|first8=David W.|date=2019-12|title=A single-center study of the clinicopathologic correlates of gliomas with a MYB or MYBL1 alteration|url=https://pubmed.ncbi.nlm.nih.gov/31595312|journal=Acta Neuropathologica|volume=138|issue=6|pages=1091–1092|doi=10.1007/s00401-019-02081-1|issn=1432-0533|pmc=7467132|pmid=31595312}}</ref>. These adult diffuse gliomas exhibit alterations of ''MYBL1'' rather than ''MYB'' . Gene fusions with multiple partners characterize the pediatric ''MYB'' or ''MYBL1-''altered gliomas<ref>{{Cite journal|last=Ramkissoon|first=Lori A.|last2=Horowitz|first2=Peleg M.|last3=Craig|first3=Justin M.|last4=Ramkissoon|first4=Shakti H.|last5=Rich|first5=Benjamin E.|last6=Schumacher|first6=Steven E.|last7=McKenna|first7=Aaron|last8=Lawrence|first8=Michael S.|last9=Bergthold|first9=Guillaume|date=2013-05-14|title=Genomic analysis of diffuse pediatric low-grade gliomas identifies recurrent oncogenic truncating rearrangements in the transcription factor MYBL1|url=https://pubmed.ncbi.nlm.nih.gov/23633565|journal=Proceedings of the National Academy of Sciences of the United States of America|volume=110|issue=20|pages=8188–8193|doi=10.1073/pnas.1300252110|issn=1091-6490|pmc=3657784|pmid=23633565}}</ref><ref>{{Cite journal|last=Barinfeld|first=Orit|last2=Zahavi|first2=Alon|last3=Weiss|first3=Shirel|last4=Toledano|first4=Helen|last5=Michowiz|first5=Shalom|last6=Goldenberg-Cohen|first6=Nitza|date=2022|title=Genetic Alteration Analysis of IDH1, IDH2, CDKN2A, MYB and MYBL1 in Pediatric Low-Grade Gliomas|url=https://pubmed.ncbi.nlm.nih.gov/35574540|journal=Frontiers in Surgery|volume=9|pages=880048|doi=10.3389/fsurg.2022.880048|issn=2296-875X|pmc=9096721|pmid=35574540}}</ref>. The most frequently identified fusion is with ''QKI''<ref>{{Cite journal|last=Suh|first=Ye Yoon|last2=Lee|first2=Kwanghoon|last3=Shim|first3=Yu-Mi|last4=Phi|first4=Ji Hoon|last5=Park|first5=Chul-Kee|last6=Kim|first6=Seung-Ki|last7=Choi|first7=Seung Hong|last8=Yun|first8=Hongseok|last9=Park|first9=Sung-Hye|date=2023-02-21|title=MYB/MYBL1::QKI fusion-positive diffuse glioma|url=https://pubmed.ncbi.nlm.nih.gov/36592415|journal=Journal of Neuropathology and Experimental Neurology|volume=82|issue=3|pages=250–260|doi=10.1093/jnen/nlac123|issn=1554-6578|pmc=9941827|pmid=36592415}}</ref><ref>{{Cite journal|last=Jain|first=Payal|last2=Resnick|first2=Adam C.|date=2017-03-04|title=MYB-QKI drives childhood brain tumors via tripartite mechanism|url=https://pubmed.ncbi.nlm.nih.gov/27973981|journal=Cell Cycle (Georgetown, Tex.)|volume=16|issue=5|pages=390–391|doi=10.1080/15384101.2016.1260990|issn=1551-4005|pmc=5351923|pmid=27973981}}</ref>''.'' The ''MYB'' or ''MYBL1-''altered diffuse gliomas in both children and adults are generally indolent and behave in a WHO grade 1 fashion.
 
==Synonyms / Terminology==
 
Put your text here
 
==Epidemiology / Prevalence==
 
Put your text here


==Clinical Features==
==Clinical Features==


Put your text here and fill in the table
Medically refractory epilepsy since childhood.
{| class="wikitable"
{| class="wikitable"
|'''Signs and Symptoms'''
|'''Signs and Symptoms'''
|EXAMPLE Asymptomatic (incidental finding on complete blood counts)
|History of epilepsy or seizure
 
Magnetic resonance imaging (MRI): well-delineated, occasionally infiltrative-appearing, non-enhancing T1-hypointense, T2-fluid attenuated inversion recovery-hyperintense lesion without restricted diffusion<ref>{{Cite journal|last=Fabbri|first=Viscardo Paolo|last2=Caporalini|first2=Chiara|last3=Asioli|first3=Sofia|last4=Buccoliero|first4=Annamaria|date=2022-12|title=Paediatric-type diffuse low-grade gliomas: a clinically and biologically distinct group of tumours with a favourable outcome|url=https://pubmed.ncbi.nlm.nih.gov/36534420|journal=Pathologica|volume=114|issue=6|pages=410–421|doi=10.32074/1591-951X-828|issn=1591-951X|pmc=9763978|pmid=36534420}}</ref>
EXAMPLE B-symptoms (weight loss, fever, night sweats)
 
EXAMPLE Fatigue
 
EXAMPLE Lymphadenopathy (uncommon)
|-
|-
|'''Laboratory Findings'''
|'''Laboratory Findings'''
|EXAMPLE Cytopenias
|Genetics: Negative for ''IDH1'' p.R132H, ''BRAF'' p.V600E; positive for ''MYBL1'' or ''MYB'' rearrangement, amplification, or copy number change
 
EXAMPLE Lymphocytosis (low level)
|}
|}


==Sites of Involvement==
==Sites of Involvement==


Put your text here
Supratentorial (adult), cortical and subcortical regions of the cerebral cortex (pediatric)<ref>{{Cite journal|last=Fabbri|first=Viscardo Paolo|last2=Caporalini|first2=Chiara|last3=Asioli|first3=Sofia|last4=Buccoliero|first4=Annamaria|date=2022-12|title=Paediatric-type diffuse low-grade gliomas: a clinically and biologically distinct group of tumours with a favourable outcome|url=https://pubmed.ncbi.nlm.nih.gov/36534420|journal=Pathologica|volume=114|issue=6|pages=410–421|doi=10.32074/1591-951X-828|issn=1591-951X|pmc=9763978|pmid=36534420}}</ref>


==Morphologic Features==
==Morphologic Features==


Put your text here
Histomorphology: minimally to moderately hypercellular tumor; diffuse infiltration by monomorphic cells with ovoid to elongated nuclei, scant cytoplasm, fibrillary background<ref>{{Cite journal|last=Fabbri|first=Viscardo Paolo|last2=Caporalini|first2=Chiara|last3=Asioli|first3=Sofia|last4=Buccoliero|first4=Annamaria|date=2022-12|title=Paediatric-type diffuse low-grade gliomas: a clinically and biologically distinct group of tumours with a favourable outcome|url=https://pubmed.ncbi.nlm.nih.gov/36534420|journal=Pathologica|volume=114|issue=6|pages=410–421|doi=10.32074/1591-951X-828|issn=1591-951X|pmc=9763978|pmid=36534420}}</ref><ref>{{Cite journal|last=Suh|first=Ye Yoon|last2=Lee|first2=Kwanghoon|last3=Shim|first3=Yu-Mi|last4=Phi|first4=Ji Hoon|last5=Park|first5=Chul-Kee|last6=Kim|first6=Seung-Ki|last7=Choi|first7=Seung Hong|last8=Yun|first8=Hongseok|last9=Park|first9=Sung-Hye|date=2023-02-21|title=MYB/MYBL1::QKI fusion-positive diffuse glioma|url=https://pubmed.ncbi.nlm.nih.gov/36592415|journal=Journal of Neuropathology and Experimental Neurology|volume=82|issue=3|pages=250–260|doi=10.1093/jnen/nlac123|issn=1554-6578|pmc=9941827|pmid=36592415}}</ref>


==Immunophenotype==
==Immunophenotype==


Put your text here and fill in the table
Positivity for GFAP, below 1% Ki-67 index, negative for OLIG2 and IDH1 R132H<ref>{{Cite journal|last=Wefers|first=Annika K.|last2=Stichel|first2=Damian|last3=Schrimpf|first3=Daniel|last4=Coras|first4=Roland|last5=Pages|first5=Mélanie|last6=Tauziède-Espariat|first6=Arnault|last7=Varlet|first7=Pascale|last8=Schwarz|first8=Daniel|last9=Söylemezoglu|first9=Figen|date=2020-01|title=Isomorphic diffuse glioma is a morphologically and molecularly distinct tumour entity with recurrent gene fusions of MYBL1 or MYB and a benign disease course|url=https://pubmed.ncbi.nlm.nih.gov/31563982|journal=Acta Neuropathologica|volume=139|issue=1|pages=193–209|doi=10.1007/s00401-019-02078-w|issn=1432-0533|pmc=7477753|pmid=31563982}}</ref>


{| class="wikitable sortable"
{| class="wikitable sortable"
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!Finding!!Marker
!Finding!!Marker
|-
|-
|Positive (universal)||EXAMPLE CD1
|Positive (universal)||GFAP<span lang="EN-US">Scott C. Smith,
PhD, FACMG; SUNY Upstate Medical University</span>
|-
|-
|Positive (subset)||EXAMPLE CD2
|Positive (subset)||Ki-67 index below 1%
|-
|-
|Negative (universal)||EXAMPLE CD3
|Negative (universal)||OLIG2, IDH1 R132H
|-
|Negative (subset)||EXAMPLE CD4
|}
|}


==Chromosomal Rearrangements (Gene Fusions)==
==Chromosomal Rearrangements (Gene Fusions)==


Put your text here and fill in the table
''MYB'' or ''MYBL1'' rearrangement


''MYB'' or ''MYBL1'' amplification
{| class="wikitable sortable"
{| class="wikitable sortable"
|-
|-
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!Notes
!Notes
|-
|-
|EXAMPLE t(9;22)(q34;q11.2)||EXAMPLE 3'ABL1 / 5'BCR||EXAMPLE der(22)||EXAMPLE 20% (COSMIC)
|6q23.3 rearrangement
EXAMPLE 30% (add reference)
|
|
|
|Yes
|Yes
|
|Multiple potential  partners
|-
|8q13.1 rearrangement
|
|
|
|Yes
|Yes
|
|Multiple potential  partners
|-
|del(6)(q23.3q26); t(6;6)(q23.3;q26)
|''MYB::QKI''
|
|
|Yes
|Yes
|No
|Yes
|Yes
|EXAMPLE
|
 
|Creates fusion oncogenic protein
The t(9;22) is diagnostic of CML in the appropriate morphology and clinical context (add reference). This fusion is responsive to targeted therapy such as Imatinib (Gleevec) (add reference).
|}
|}
==Individual Region Genomic Gain/Loss/LOH==
==Individual Region Genomic Gain/Loss/LOH==


Put your text here and fill in the table
''MYB'' or ''MYBL1'' copy number variation as identified by chromosomal microarray or FISH


{| class="wikitable sortable"
{| class="wikitable sortable"
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!Notes
!Notes
|-
|-
|EXAMPLE
|6
 
|Amp/Loss/Gain
7
|135502446-135540310 [GRCh37]
|EXAMPLE Loss
|6q23.3
|EXAMPLE
 
chr7:1- 159,335,973 [hg38]
|EXAMPLE
 
chr7
|Yes
|Yes
|Yes
|Yes
|No
|Yes<ref>{{Cite journal|last=Trkova|first=Katerina|last2=Sumerauer|first2=David|last3=Krskova|first3=Lenka|last4=Vicha|first4=Ales|last5=Koblizek|first5=Miroslav|last6=Votava|first6=Tomas|last7=Priban|first7=Vladimir|last8=Zapotocky|first8=Michal|date=2023-09|title=DIPG-like MYB-altered diffuse astrocytoma with durable response to intensive chemotherapy|url=https://pubmed.ncbi.nlm.nih.gov/37165121|journal=Child's Nervous System: ChNS: Official Journal of the International Society for Pediatric Neurosurgery|volume=39|issue=9|pages=2509–2513|doi=10.1007/s00381-023-05976-3|issn=1433-0350|pmc=PMC10432314|pmid=37165121}}</ref>
|EXAMPLE
|<ref>{{Cite journal|last=Ramkissoon|first=Lori A.|last2=Horowitz|first2=Peleg M.|last3=Craig|first3=Justin M.|last4=Ramkissoon|first4=Shakti H.|last5=Rich|first5=Benjamin E.|last6=Schumacher|first6=Steven E.|last7=McKenna|first7=Aaron|last8=Lawrence|first8=Michael S.|last9=Bergthold|first9=Guillaume|date=2013-05-14|title=Genomic analysis of diffuse pediatric low-grade gliomas identifies recurrent oncogenic truncating rearrangements in the transcription factor MYBL1|url=https://pubmed.ncbi.nlm.nih.gov/23633565|journal=Proceedings of the National Academy of Sciences of the United States of America|volume=110|issue=20|pages=8188–8193|doi=10.1073/pnas.1300252110|issn=1091-6490|pmc=3657784|pmid=23633565}}</ref><ref>{{Cite journal|last=Bale|first=Tejus A.|last2=Rosenblum|first2=Marc K.|date=2022-07|title=The 2021 WHO Classification of Tumors of the Central Nervous System: An update on pediatric low-grade gliomas and glioneuronal tumors|url=https://pubmed.ncbi.nlm.nih.gov/35218102|journal=Brain Pathology (Zurich, Switzerland)|volume=32|issue=4|pages=e13060|doi=10.1111/bpa.13060|issn=1750-3639|pmc=9245930|pmid=35218102}}</ref><ref>{{Cite journal|last=Trkova|first=Katerina|last2=Sumerauer|first2=David|last3=Krskova|first3=Lenka|last4=Vicha|first4=Ales|last5=Koblizek|first5=Miroslav|last6=Votava|first6=Tomas|last7=Priban|first7=Vladimir|last8=Zapotocky|first8=Michal|date=2023-09|title=DIPG-like MYB-altered diffuse astrocytoma with durable response to intensive chemotherapy|url=https://pubmed.ncbi.nlm.nih.gov/37165121|journal=Child's Nervous System: ChNS: Official Journal of the International Society for Pediatric Neurosurgery|volume=39|issue=9|pages=2509–2513|doi=10.1007/s00381-023-05976-3|issn=1433-0350|pmc=PMC10432314|pmid=37165121}}</ref>
 
Presence of monosomy 7 (or 7q deletion) is sufficient for a diagnosis of AML with MDS-related changes when there is ≥20% blasts and no prior therapy (add reference). Monosomy 7/7q deletion is associated with a poor prognosis in AML (add reference).
|-
|-
|EXAMPLE
|8
 
|Amp/Loss/Gain
8
|67474410-67525453 [GRCh37]  
|EXAMPLE Gain
|8q13.1
|EXAMPLE
|Yes
 
|Yes
chr8:1-145,138,636 [hg38]
|Unknown
|EXAMPLE
|<ref>{{Cite journal|last=Ramkissoon|first=Lori A.|last2=Horowitz|first2=Peleg M.|last3=Craig|first3=Justin M.|last4=Ramkissoon|first4=Shakti H.|last5=Rich|first5=Benjamin E.|last6=Schumacher|first6=Steven E.|last7=McKenna|first7=Aaron|last8=Lawrence|first8=Michael S.|last9=Bergthold|first9=Guillaume|date=2013-05-14|title=Genomic analysis of diffuse pediatric low-grade gliomas identifies recurrent oncogenic truncating rearrangements in the transcription factor MYBL1|url=https://pubmed.ncbi.nlm.nih.gov/23633565|journal=Proceedings of the National Academy of Sciences of the United States of America|volume=110|issue=20|pages=8188–8193|doi=10.1073/pnas.1300252110|issn=1091-6490|pmc=3657784|pmid=23633565}}</ref><ref>{{Cite journal|last=Bale|first=Tejus A.|last2=Rosenblum|first2=Marc K.|date=2022-07|title=The 2021 WHO Classification of Tumors of the Central Nervous System: An update on pediatric low-grade gliomas and glioneuronal tumors|url=https://pubmed.ncbi.nlm.nih.gov/35218102|journal=Brain Pathology (Zurich, Switzerland)|volume=32|issue=4|pages=e13060|doi=10.1111/bpa.13060|issn=1750-3639|pmc=9245930|pmid=35218102}}</ref>
 
chr8
|No
|No
|No
|EXAMPLE
 
Common recurrent secondary finding for t(8;21) (add reference).
|}
|}
==Characteristic Chromosomal Patterns==
==Characteristic Chromosomal Patterns==


Put your text here
Possible detection of double minutes or homogeneously stained regions by G-banding for amplification; will require confirmation of being associated with MYB or MYBL (likely by chromosomal microarray)


{| class="wikitable sortable"
{| class="wikitable sortable"
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!Notes
!Notes
|-
|-
|EXAMPLE
|6q23.3 hsr; '' MYB'' amplification <span lang="EN-US">Scott C. Smith,
 
PhD, FACMG; SUNY Upstate Medical University</span>
Co-deletion of 1p and 18q
|Yes
|No
|No
|Unknown
|Unknown
|
|-
|8q13.1 hsr; ''MYBL1'' amplification<span lang="EN-US">Scott C. Smith,
PhD, FACMG; SUNY Upstate Medical University</span>
|No
|No
|EXAMPLE:
|Unknown
 
|Unknown
See chromosomal rearrangements table as this pattern is due to an unbalanced derivative translocation associated with oligodendroglioma (add reference).
|}
==Gene Mutations (SNV/INDEL)==
 
Put your text here and fill in the table
 
{| class="wikitable sortable"
|-
!Gene; Genetic Alteration!!'''Presumed Mechanism (Tumor Suppressor Gene [TSG] / Oncogene / Other)'''!!'''Prevalence (COSMIC /  TCGA / Other)'''!!'''Concomitant Mutations'''!!'''Mutually Exclusive Mutations'''
!'''Diagnostic Significance (Yes, No or Unknown)'''
!Prognostic Significance (Yes, No or Unknown)
!Therapeutic Significance (Yes, No or Unknown)
!Notes
|-
|EXAMPLE: TP53; Variable LOF mutations
 
EXAMPLE:
 
EGFR; Exon 20 mutations
 
EXAMPLE: BRAF; Activating mutations
|EXAMPLE: TSG
|EXAMPLE: 20% (COSMIC)
 
EXAMPLE: 30% (add Reference)
|EXAMPLE: IDH1 R123H
|EXAMPLE: EGFR amplification
|
|
|
|
|EXAMPLE:  Excludes hairy cell leukemia (HCL) (add reference).
<br />
|}
|}
Note: A more extensive list of mutations can be found in cBioportal (https://www.cbioportal.org/), COSMIC (https://cancer.sanger.ac.uk/cosmic), ICGC (https://dcc.icgc.org/) and/or other databases. When applicable, gene-specific pages within the CCGA site directly link to pertinent external content.
==Epigenomic Alterations==
Put your text here
==Genes and Main Pathways Involved==
==Genes and Main Pathways Involved==
Put your text here and fill in the table
{| class="wikitable sortable"
{| class="wikitable sortable"
|-
|-
!Gene; Genetic Alteration!!Pathway!!Pathophysiologic Outcome
!Gene; Genetic Alteration!!Pathway!!Pathophysiologic Outcome
|-
|-
|EXAMPLE: BRAF and MAP2K1; Activating mutations
|''MYB/MYBL1'' 3’-deletion
|EXAMPLE: MAPK signaling
|MYB/MYBL1 protooncogene
|EXAMPLE: Increased cell growth and proliferation
|Deregulation  of MYB/MYBL1
|-
|EXAMPLE: CDKN2A; Inactivating mutations
|EXAMPLE: Cell cycle regulation
|EXAMPLE: Unregulated cell division
|-
|-
|EXAMPLE:  KMT2C and ARID1A; Inactivating mutations
|''MYB/MYBL1'' amplification
|EXAMPLE: Histone modification, chromatin remodeling
|MYB/MYBL1 protooncogene
|EXAMPLE: Abnormal gene expression program
|Overexpression of MYB/MYBL1
|}
|}
==Genetic Diagnostic Testing Methods==
==Genetic Diagnostic Testing Methods==


Put your text here
Sequencing, PCR, RT-PCR, chromosomal microarray, FISH, possibly detection of double minutes or homogenously stained regions by G-banding
 
==Familial Forms==
 
Put your text here
 
==Additional Information==
 
Put your text here
 
==Links==
 
Put your text placeholder here (use "Link" icon at top of page)


==References==
==References==
<references />
<references />
(use "Cite" icon at top of page)
===EXAMPLE Book===
#Arber DA, et al., (2017). Acute myeloid leukaemia with recurrent genetic abnormalities, in World Health Organization Classification of Tumours of Haematopoietic and Lymphoid Tissues, Revised 4th edition. Swerdlow SH, Campo E, Harris NL, Jaffe ES, Pileri SA, Stein H, Thiele J, Arber DA, Hasserjian RP, Le Beau MM, Orazi A, and Siebert R, Editors. IARC Press: Lyon, France, p129-171.
==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 CCGA coordinators (contact information provided on the homepage).  Additional global feedback or concerns are also welcome.
<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 CCGA coordinators (contact information provided on the homepage).  Additional global feedback or concerns are also welcome.
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