Compendium of Cancer Genome Aberrations

HAEM5:Acute myeloid leukaemia with CEBPA mutation: Difference between revisions

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==WHO Essential and Desirable Genetic Diagnostic Criteria==
==WHO Essential and Desirable Genetic Diagnostic Criteria==
<span style="color:#0070C0">(''Instructions: The table will have the diagnostic criteria from the WHO book <u>autocompleted</u>; remove any <u>non</u>-genetics related criteria. If applicable, add text about other classification'' ''systems that define this entity and specify how the genetics-related criteria differ.'')</span>
{| class="wikitable"
{| class="wikitable"
|+
|+
|WHO Essential Criteria (Genetics)*
|WHO Essential Criteria (Genetics)*
|>= 20% blasts with a myeloid immunophenotype in the bone marrow or blood; presence of biallelic mutations in ''CEBPA'', or a single mutation located in the bZIP region; absence of criteria allowing for classification into other AMLs with defining genetic abnormalities; not fulling diagnostic criteria for myeloid neoplasm post cytotoxic therapy.
|
|-
|-
|WHO Desirable Criteria (Genetics)*
|WHO Desirable Criteria (Genetics)*
|NA
|
|-
|-
|Other Classification
|Other Classification
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<nowiki>*</nowiki>Note: These are only the genetic/genomic criteria. Additional diagnostic criteria can be found in the [https://tumourclassification.iarc.who.int/home <u>WHO Classification of Tumours</u>].
<nowiki>*</nowiki>Note: These are only the genetic/genomic criteria. Additional diagnostic criteria can be found in the [https://tumourclassification.iarc.who.int/home <u>WHO Classification of Tumours</u>].
==Related Terminology==
==Related Terminology==
<span style="color:#0070C0">(''Instructions: The table will have the related terminology from the WHO <u>autocompleted</u>.)''</span>
{| class="wikitable"
{| class="wikitable"
|+
|+
|Acceptable
|Acceptable
|acute myeloid leukaemia with biallelic mutation of ''CEBPA.''
|
|-
|-
|Not Recommended
|Not Recommended
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None.
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"
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''DUX4'' has many homologous genes; an alternate translocation in a minority of cases is t(10;19), but this is usually indistinguishable from t(4;19) by short-read sequencing (add references).
''DUX4'' has many homologous genes; an alternate translocation in a minority of cases is t(10;19), but this is usually indistinguishable from t(4;19) by short-read sequencing (add references).
|-
|<span class="blue-text">EXAMPLE:</span> ''ALK''
|<span class="blue-text">EXAMPLE:</span> ''ELM4::ALK''
Other fusion partners include ''KIF5B, NPM1, STRN, TFG, TPM3, CLTC, KLC1''
|<span class="blue-text">EXAMPLE:</span> Fusions result in constitutive activation of the ''ALK'' tyrosine kinase. The most common ''ALK'' fusion is ''EML4::ALK'', with breakpoints in intron 19 of ''ALK''. At the transcript level, a variable (5’) partner gene is fused to 3’ ''ALK'' at exon 20. Rarely, ''ALK'' fusions contain exon 19 due to breakpoints in intron 18.
|<span class="blue-text">EXAMPLE:</span> N/A
|<span class="blue-text">EXAMPLE:</span> Rare (Lung adenocarcinoma)
|<span class="blue-text">EXAMPLE:</span> T
|
|<span class="blue-text">EXAMPLE:</span>
Both balanced and unbalanced forms are observed by FISH (add references).
|-
|<span class="blue-text">EXAMPLE:</span> ''ABL1''
|<span class="blue-text">EXAMPLE:</span> N/A
|<span class="blue-text">EXAMPLE:</span> Intragenic deletion of exons 2–7 in ''EGFR'' removes the ligand-binding domain, resulting in a constitutively active tyrosine kinase with downstream activation of multiple oncogenic pathways.
|<span class="blue-text">EXAMPLE:</span> N/A
|<span class="blue-text">EXAMPLE:</span> Recurrent (IDH-wildtype Glioblastoma)
|<span class="blue-text">EXAMPLE:</span> D, P, T
|
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<blockquote class="blockedit">{{Box-round|title=v4:Chromosomal Rearrangements (Gene Fusions)|The content below was from the old template. Please incorporate above.}}</blockquote>
None
{| class="wikitable sortable"
|-
!Chromosomal Rearrangement!!Genes in Fusion (5’ or 3’ Segments)!!Pathogenic Derivative!!Prevalence
|-
|<span class="blue-text">EXAMPLE:</span> t(9;22)(q34;q11.2)||<span class="blue-text">EXAMPLE:</span> 3'ABL1 / 5'BCR||<span class="blue-text">EXAMPLE:</span> der(22)||<span class="blue-text">EXAMPLE:</span> 5%
|-
|<span class="blue-text">EXAMPLE:</span> t(8;21)(q22;q22)||<span class="blue-text">EXAMPLE:</span> 5'RUNX1 / 3'RUNXT1||<span class="blue-text">EXAMPLE:</span> der(8)||<span class="blue-text">EXAMPLE:</span> 5%
|}
<blockquote class="blockedit">
<center><span style="color:Maroon">'''End of V4 Section'''</span>
----
</blockquote>
<blockquote class="blockedit">{{Box-round|title=v4:Clinical Significance (Diagnosis, Prognosis and Therapeutic Implications).|Please incorporate this section into the relevant tables found in:
* Chromosomal Rearrangements (Gene Fusions)
* Individual Region Genomic Gain/Loss/LOH
* Characteristic Chromosomal Patterns
* Gene Mutations (SNV/INDEL)}}</blockquote>
Patients with biallelic ''CEBPA'' mutations and a normal karyotype have a more favorable prognosis than those with monoallelic or no ''CEBPA'' mutations, with higher complete remission rates and longer disease-free survival, relapse-free survival, event-free survival, and overall survival<ref name=":0">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. Revised 4th Edition. IARC Press: Lyon, France, p142-144.</ref>.
Patients with abnormal karyotypes (but not complex karyotypes) and biallelic ''CEBPA'' mutations also have longer disease-free survival, event-free survival, and overall survival when compared to patients with monoallelic or no ''CEBPA'' mutations<ref name=":0" />.
<blockquote class="blockedit">
<center><span style="color:Maroon">'''End of V4 Section'''</span>
----
</blockquote>
==Individual Region Genomic Gain/Loss/LOH==
==Individual Region Genomic Gain/Loss/LOH==




None.
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"
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<blockquote class="blockedit">{{Box-round|title=v4:Genomic Gain/Loss/LOH|The content below was from the old template. Please incorporate above.}}</blockquote>
None
{| class="wikitable sortable"
|-
!Chromosome Number!!Gain/Loss/Amp/LOH!!Region
|-
|<span class="blue-text">EXAMPLE:</span> 8||<span class="blue-text">EXAMPLE:</span> Gain||<span class="blue-text">EXAMPLE:</span> chr8:0-1000000
|-
|<span class="blue-text">EXAMPLE:</span> 7||<span class="blue-text">EXAMPLE:</span> Loss||<span class="blue-text">EXAMPLE:</span> chr7:0-1000000
|}
<blockquote class="blockedit">
<center><span style="color:Maroon">'''End of V4 Section'''</span>
----
</blockquote>
==Characteristic Chromosomal or Other Global Mutational Patterns==
==Characteristic Chromosomal or Other Global Mutational Patterns==




None.
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"
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|}
<blockquote class="blockedit">{{Box-round|title=v4:Characteristic Chromosomal Aberrations / Patterns|The content below was from the old template. Please incorporate above.}}</blockquote>
None
<blockquote class="blockedit">
<center><span style="color:Maroon">'''End of V4 Section'''</span>
----
</blockquote>
==Gene Mutations (SNV/INDEL)==
==Gene Mutations (SNV/INDEL)==




Patients with biallelic ''CEBPA'' mutations and a normal karyotype have a more favorable prognosis than those with monoallelic or no ''CEBPA'' mutations, with higher complete remission rates and longer disease-free survival, relapse-free survival, event-free survival, and overall survival<ref name=":0">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. Revised 4th Edition. IARC Press: Lyon, France, p142-144.</ref>.
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>
Patients with abnormal karyotypes (but not complex karyotypes) and biallelic ''CEBPA'' mutations also have longer disease-free survival, event-free survival, and overall survival when compared to patients with monoallelic or no ''CEBPA'' mutations<ref name=":0" />. Detection of bi''CEBPA'' should raise possibility of germline mutation. Approximately 5-10%  of bi''CEBPA'' AML cases have a germline N-terminal<ref>{{Cite journal|last=Taskesen|first=Erdogan|last2=Bullinger|first2=Lars|last3=Corbacioglu|first3=Andrea|last4=Sanders|first4=Mathijs A.|last5=Erpelinck|first5=Claudia A. J.|last6=Wouters|first6=Bas J.|last7=van der Poel-van de Luytgaarde|first7=Sonja C.|last8=Damm|first8=Frederik|last9=Krauter|first9=Jürgen|date=2011-02-24|title=Prognostic impact, concurrent genetic mutations, and gene expression features of AML with CEBPA mutations in a cohort of 1182 cytogenetically normal AML patients: further evidence for CEBPA double mutant AML as a distinctive disease entity|url=https://pubmed.ncbi.nlm.nih.gov/21177436|journal=Blood|volume=117|issue=8|pages=2469–2475|doi=10.1182/blood-2010-09-307280|issn=1528-0020|pmid=21177436}}</ref>. In the familia from, AML has very high penetrance and presents relatively early (median aga: 245.5 years)<ref>{{Cite journal|last=Tawana|first=Kiran|last2=Wang|first2=Jun|last3=Renneville|first3=Aline|last4=Bödör|first4=Csaba|last5=Hills|first5=Robert|last6=Loveday|first6=Chey|last7=Savic|first7=Aleksandar|last8=Van Delft|first8=Frederik W.|last9=Treleaven|first9=Jennifer|date=2015-09-03|title=Disease evolution and outcomes in familial AML with germline CEBPA mutations|url=https://pubmed.ncbi.nlm.nih.gov/26162409|journal=Blood|volume=126|issue=10|pages=1214–1223|doi=10.1182/blood-2015-05-647172|issn=1528-0020|pmid=26162409}}</ref>. There are some notable familial AML-Associated ''CEBPA'' germline pathogenic variants: c.68delC, p.Pro23ArgfsTer137<ref>{{Cite journal|last=Smith|first=Matthew L.|last2=Cavenagh|first2=Jamie D.|last3=Lister|first3=T. Andrew|last4=Fitzgibbon|first4=Jude|date=2004-12-02|title=Mutation of CEBPA in familial acute myeloid leukemia|url=https://pubmed.ncbi.nlm.nih.gov/15575056|journal=The New England Journal of Medicine|volume=351|issue=23|pages=2403–2407|doi=10.1056/NEJMoa041331|issn=1533-4406|pmid=15575056}}</ref>; c.68dupC, p.His24AlafsTer84<ref>{{Cite journal|last=Sellick|first=G. S.|last2=Spendlove|first2=H. E.|last3=Catovsky|first3=D.|last4=Pritchard-Jones|first4=K.|last5=Houlston|first5=R. S.|date=2005-07|title=Further evidence that germline CEBPA mutations cause dominant inheritance of acute myeloid leukaemia|url=https://pubmed.ncbi.nlm.nih.gov/15902292|journal=Leukemia|volume=19|issue=7|pages=1276–1278|doi=10.1038/sj.leu.2403788|issn=0887-6924|pmid=15902292}}</ref><ref>{{Cite journal|last=Renneville|first=A.|last2=Mialou|first2=V.|last3=Philippe|first3=N.|last4=Kagialis-Girard|first4=S.|last5=Biggio|first5=V.|last6=Zabot|first6=M.-T.|last7=Thomas|first7=X.|last8=Bertrand|first8=Y.|last9=Preudhomme|first9=C.|date=2009-04|title=Another pedigree with familial acute myeloid leukemia and germline CEBPA mutation|url=https://pubmed.ncbi.nlm.nih.gov/18946494|journal=Leukemia|volume=23|issue=4|pages=804–806|doi=10.1038/leu.2008.294|issn=1476-5551|pmid=18946494}}</ref><ref>{{Cite journal|last=Tawana|first=Kiran|last2=Wang|first2=Jun|last3=Renneville|first3=Aline|last4=Bödör|first4=Csaba|last5=Hills|first5=Robert|last6=Loveday|first6=Chey|last7=Savic|first7=Aleksandar|last8=Van Delft|first8=Frederik W.|last9=Treleaven|first9=Jennifer|date=2015-09-03|title=Disease evolution and outcomes in familial AML with germline CEBPA mutations|url=https://pubmed.ncbi.nlm.nih.gov/26162409|journal=Blood|volume=126|issue=10|pages=1214–1223|doi=10.1182/blood-2015-05-647172|issn=1528-0020|pmid=26162409}}</ref>; c.141delC, p.Ala48ProfsTer112<ref name=":1">{{Cite journal|last=Pabst|first=Thomas|last2=Eyholzer|first2=Marianne|last3=Haefliger|first3=Simon|last4=Schardt|first4=Julian|last5=Mueller|first5=Beatrice U.|date=2008-11-01|title=Somatic CEBPA mutations are a frequent second event in families with germline CEBPA mutations and familial acute myeloid leukemia|url=https://pubmed.ncbi.nlm.nih.gov/18768433|journal=Journal of Clinical Oncology: Official Journal of the American Society of Clinical Oncology|volume=26|issue=31|pages=5088–5093|doi=10.1200/JCO.2008.16.5563|issn=1527-7755|pmid=18768433}}</ref>; c.147_165del19, p.Glu50AlafsTer104<ref>{{Cite journal|last=Debeljak|first=Maruša|last2=Kitanovski|first2=Lidija|last3=Pajič|first3=Tadej|last4=Jazbec|first4=Janez|date=2013-07|title=Concordant acute myeloblastic leukemia in monozygotic twins with germline and shared somatic mutations in the gene for CCAAT-enhancer-binding protein α with 13 years difference at onset|url=https://pubmed.ncbi.nlm.nih.gov/23716546|journal=Haematologica|volume=98|issue=7|pages=e73–74|doi=10.3324/haematol.2012.082578|issn=1592-8721|pmc=3696596|pmid=23716546}}</ref>; c.158delG, p.Gly53AlafsTer107<ref name=":4">{{Cite journal|last=Taskesen|first=Erdogan|last2=Bullinger|first2=Lars|last3=Corbacioglu|first3=Andrea|last4=Sanders|first4=Mathijs A.|last5=Erpelinck|first5=Claudia A. J.|last6=Wouters|first6=Bas J.|last7=van der Poel-van de Luytgaarde|first7=Sonja C.|last8=Damm|first8=Frederik|last9=Krauter|first9=Jürgen|date=2011-02-24|title=Prognostic impact, concurrent genetic mutations, and gene expression features of AML with CEBPA mutations in a cohort of 1182 cytogenetically normal AML patients: further evidence for CEBPA double mutant AML as a distinctive disease entity|url=https://pubmed.ncbi.nlm.nih.gov/21177436|journal=Blood|volume=117|issue=8|pages=2469–2475|doi=10.1182/blood-2010-09-307280|issn=1528-0020|pmid=21177436}}</ref>; c.189delC, p.Asp63GlufsTer97<ref name=":4" />; c.314_315insT, p.Phe106LeufsTer2<ref name=":1" />; c.932A>C, p.Gln311Pro<ref>{{Cite journal|last=Pathak|first=Anand|last2=Seipel|first2=Katja|last3=Pemov|first3=Alexander|last4=Dewan|first4=Ramita|last5=Brown|first5=Christina|last6=Ravichandran|first6=Sarangan|last7=Luke|first7=Brian T.|last8=Malasky|first8=Michael|last9=Suman|first9=Shalabh|date=2016-07|title=Whole exome sequencing reveals a C-terminal germline variant in CEBPA-associated acute myeloid leukemia: 45-year follow up of a large family|url=https://pubmed.ncbi.nlm.nih.gov/26721895|journal=Haematologica|volume=101|issue=7|pages=846–852|doi=10.3324/haematol.2015.130799|issn=1592-8721|pmc=5004464|pmid=26721895}}</ref>; c.442G>T, p.Glu148Ter<ref>{{Cite journal|last=Mendoza|first=Hadrian|last2=Chen|first2=Po-Han|last3=Pine|first3=Alexander B.|last4=Siddon|first4=Alexa J.|last5=Bale|first5=Allen E.|last6=Gowda|first6=Lohith|last7=Killie|first7=Amy|last8=Richards|first8=Jonica|last9=Varin-Tremblay|first9=Camille|date=2021-05|title=A case of acute myeloid leukemia with unusual germline CEBPA mutation: lessons learned about mutation detection, location, and penetrance|url=https://pubmed.ncbi.nlm.nih.gov/33345654|journal=Leukemia & Lymphoma|volume=62|issue=5|pages=1251–1254|doi=10.1080/10428194.2020.1861276|issn=1029-2403|pmid=33345654}}</ref>.
 
Pathogenic mutations in ''CEBPA'' are predominantly insertion/deletion frameshift mutations in the N-terminal TAD region and in-frame C-terminal bZIP mutations. Patients with biCEBPA and smbZIP-CEBPA are younger and have higher white blood cell counts than those with a single mutation in the N-terminal TAD region<ref name=":5">{{Cite journal|last=Taube|first=Franziska|last2=Georgi|first2=Julia Annabell|last3=Kramer|first3=Michael|last4=Stasik|first4=Sebastian|last5=Middeke|first5=Jan Moritz|last6=Röllig|first6=Christoph|last7=Krug|first7=Utz|last8=Krämer|first8=Alwin|last9=Scholl|first9=Sebastian|date=2022-01-06|title=CEBPA mutations in 4708 patients with acute myeloid leukemia: differential impact of bZIP and TAD mutations on outcome|url=https://pubmed.ncbi.nlm.nih.gov/34320176|journal=Blood|volume=139|issue=1|pages=87–103|doi=10.1182/blood.2020009680|issn=1528-0020|pmid=34320176}}</ref>. No particular mutational hotspots exist but the following table records the most reported mutations in the COSMIC database (frequency based on a count out of 1523 mutations):
{| class="wikitable sortable"
{| class="wikitable sortable"
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!'''Clinical Relevance Details/Other Notes'''
!'''Clinical Relevance Details/Other Notes'''
|-
|-
|''CEBPA''
|<span class="blue-text">EXAMPLE:</span>''EGFR''


<br />
<br />
|c.939_940insAAG, p.K313_V314insK
|<span class="blue-text">EXAMPLE:</span> Exon 18-21 activating mutations
|Oncogene
|<span class="blue-text">EXAMPLE:</span> Oncogene
|Recurrent (AML)
|<span class="blue-text">EXAMPLE:</span> Common (lung cancer)
|D, P, T
|<span class="blue-text">EXAMPLE:</span> T
|Yes (NCCN)
|<span class="blue-text">EXAMPLE:</span> Yes (NCCN)
|AML with ''CEBPA'' mutation is associated with favorable prognosis<ref>{{Cite journal|displayauthors=1|last=Pollyea|first=DA|date=2025|title=NCCN Clinical Practice Guidelines in Oncology: AML.|url=NCCN.org|journal=NCCN|volume=|pages=|via=}}</ref>.
|<span class="blue-text">EXAMPLE:</span> Exons 18, 19, and 21 mutations are targetable for therapy. Exon 20 T790M variants cause resistance to first generation TKI therapy and are targetable by second and third generation TKIs (add references).
 
 
AML with CEBPA mutation constitutes ~5% pf pediatric AML and 5-11% adult AML<ref>{{Cite journal|last=Tarlock|first=Katherine|last2=Lamble|first2=Adam J.|last3=Wang|first3=Yi-Cheng|last4=Gerbing|first4=Robert B.|last5=Ries|first5=Rhonda E.|last6=Loken|first6=Michael R.|last7=Brodersen|first7=Lisa Eidenschink|last8=Pardo|first8=Laura|last9=Leonti|first9=Amanda|date=2021-09-30|title=CEBPA-bZip mutations are associated with favorable prognosis in de novo AML: a report from the Children's Oncology Group|url=https://pubmed.ncbi.nlm.nih.gov/33951732|journal=Blood|volume=138|issue=13|pages=1137–1147|doi=10.1182/blood.2020009652|issn=1528-0020|pmc=8570058|pmid=33951732}}</ref><ref>{{Cite journal|last=Wakita|first=Satoshi|last2=Sakaguchi|first2=Masahiro|last3=Oh|first3=Iekuni|last4=Kako|first4=Shinichi|last5=Toya|first5=Takashi|last6=Najima|first6=Yuho|last7=Doki|first7=Noriko|last8=Kanda|first8=Junya|last9=Kuroda|first9=Junya|date=2022-01-11|title=Prognostic impact of CEBPA bZIP domain mutation in acute myeloid leukemia|url=https://pubmed.ncbi.nlm.nih.gov/34448807|journal=Blood Advances|volume=6|issue=1|pages=238–247|doi=10.1182/bloodadvances.2021004292|issn=2473-9537|pmc=8753195|pmid=34448807}}</ref><ref name=":5" />.
|-
|-
|''CEBPA''
|<span class="blue-text">EXAMPLE:</span> ''TP53''; Variable LOF mutations
<br />
<br />
|c.68_69insC, p.H24fs*84
|<span class="blue-text">EXAMPLE:</span> Variable LOF mutations
|Oncogene
|<span class="blue-text">EXAMPLE:</span> Tumor Supressor Gene
|Recurrent (AML)
|<span class="blue-text">EXAMPLE:</span> Common (breast cancer)
|D, P, T
|<span class="blue-text">EXAMPLE:</span> P
|Yes (NCCN)
|
|
|<span class="blue-text">EXAMPLE:</span> >90% are somatic; rare germline alterations associated with Li-Fraumeni syndrome (add reference). Denotes a poor prognosis in breast cancer.
|-
|-
|''CEBPA''
|<span class="blue-text">EXAMPLE:</span> ''BRAF''; Activating mutations
|c.247delC, p.Q83fs*77
|<span class="blue-text">EXAMPLE:</span> Activating mutations
|Oncogene
|<span class="blue-text">EXAMPLE:</span> Oncogene
|Recurrent (AML)
|<span class="blue-text">EXAMPLE:</span> Common (melanoma)
|D, P, T
|<span class="blue-text">EXAMPLE:</span> T
|Yes (NCCN)
|
|
|-
|''CEBPA''
|c.936_937insCAG, p.Q312_K313insQ
|Oncogene
|Recurrent (AML)
|D, P, T
|Yes (NCCN)
|
|-
|''CEBPA''
|c.912_913insTTG, p.K304_Q305insL
|Oncogene
|Recurrent (AML)
|D, P, T
|Yes (NCCN)
|
|-
|
|
|Oncogene
|Recurrent (AML)
|D, P, T
|Yes (NCCN)
|
|-
|
|
|Oncogene
|Recurrent (AML)
|D, P, T
|Yes (NCCN)
|
|
|-
|-
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|}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.
<br />


<blockquote class="blockedit">{{Box-round|title=v4:Gene Mutations (SNV/INDEL)|The content below was from the old template. Please incorporate above.}}</blockquote>
<blockquote class="blockedit">{{Box-round|title=v4:Gene Mutations (SNV/INDEL)|The content below was from the old template. Please incorporate above.}}</blockquote>
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