Acute myeloid leukaemia with CEBPA mutation
Haematolymphoid Tumours (WHO Classification, 5th ed.)
 | This page is under construction |
editContent Update To WHO 5th Edition Classification Is In Process; Content Below is Based on WHO 4th Edition ClassificationThis page was converted to the new template on 2023-12-07. The original page can be found at HAEM4:Acute Myeloid Leukemia (AML) with Biallelic Mutations of CEBPA.
(General Instructions – The focus of these pages is the clinically significant genetic alterations in each disease type. This is based on up-to-date knowledge from multiple resources such as PubMed and the WHO classification books. The CCGA is meant to be a supplemental resource to the WHO classification books; the CCGA captures in a continually updated wiki-stye manner the current genetics/genomics knowledge of each disease, which evolves more rapidly than books can be revised and published. If the same disease is described in multiple WHO classification books, the genetics-related information for that disease will be consolidated into a single main page that has this template (other pages would only contain a link to this main page). Use HUGO-approved gene names and symbols (italicized when appropriate), HGVS-based nomenclature for variants, as well as generic names of drugs and testing platforms or assays if applicable. Please complete tables whenever possible and do not delete them (add N/A if not applicable in the table and delete the examples); to add (or move) a row or column in a table, click nearby within the table and select the > symbol that appears. Please do not delete or alter the section headings. The use of bullet points alongside short blocks of text rather than only large paragraphs is encouraged. Additional instructions below in italicized blue text should not be included in the final page content. Please also see Author_Instructions and FAQs as well as contact your Associate Editor or Technical Support.)
Primary Author(s)*
Paul Defazio, MSc, Monash Health
WHO Classification of Disease
| Structure | Disease |
|---|---|
| Book | Haematolymphoid Tumours (5th ed.) |
| Category | Myeloid proliferations and neoplasms |
| Family | Acute myeloid leukaemia |
| Type | Acute myeloid leukaemia with defining genetic abnormalities |
| Subtype(s) | Acute myeloid leukaemia with CEBPA mutation |
WHO Essential and Desirable Genetic Diagnostic Criteria
(Instructions: The table will have the diagnostic criteria from the WHO book autocompleted; remove any non-genetics related criteria. If applicable, add text about other classification systems that define this entity and specify how the genetics-related criteria differ.)
| WHO Essential Criteria (Genetics)* | |
| WHO Desirable Criteria (Genetics)* | |
| Other Classification |
*Note: These are only the genetic/genomic criteria. Additional diagnostic criteria can be found in the WHO Classification of Tumours.
Related Terminology
(Instructions: The table will have the related terminology from the WHO autocompleted.)
| Acceptable | |
| Not Recommended |
Gene Rearrangements
Put your text here and fill in the table (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.)
| Driver Gene | Fusion(s) and Common Partner Genes | Molecular Pathogenesis | Typical Chromosomal Alteration(s) | Prevalence -Common >20%, Recurrent 5-20% or Rare <5% (Disease) | Diagnostic, Prognostic, and Therapeutic Significance - D, P, T | Established Clinical Significance Per Guidelines - Yes or No (Source) | Clinical Relevance Details/Other Notes |
|---|---|---|---|---|---|---|---|
| EXAMPLE: ABL1 | EXAMPLE: BCR::ABL1 | EXAMPLE: The pathogenic derivative is the der(22) resulting in fusion of 5’ BCR and 3’ABL1. | EXAMPLE: t(9;22)(q34;q11.2) | EXAMPLE: Common (CML) | EXAMPLE: D, P, T | EXAMPLE: Yes (WHO, NCCN) | EXAMPLE:
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). BCR::ABL1 is generally favorable in CML (add reference). |
| EXAMPLE: CIC | EXAMPLE: CIC::DUX4 | EXAMPLE: Typically, the last exon of CIC is fused to DUX4. The fusion breakpoint in CIC is usually intra-exonic and removes an inhibitory sequence, upregulating PEA3 genes downstream of CIC including ETV1, ETV4, and ETV5. | EXAMPLE: t(4;19)(q25;q13) | EXAMPLE: Common (CIC-rearranged sarcoma) | EXAMPLE: D | EXAMPLE:
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). | |
| EXAMPLE: ALK | EXAMPLE: ELM4::ALK
|
EXAMPLE: 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. | EXAMPLE: N/A | EXAMPLE: Rare (Lung adenocarcinoma) | EXAMPLE: T | EXAMPLE:
Both balanced and unbalanced forms are observed by FISH (add references). | |
| EXAMPLE: ABL1 | EXAMPLE: N/A | EXAMPLE: 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. | EXAMPLE: N/A | EXAMPLE: Recurrent (IDH-wildtype Glioblastoma) | EXAMPLE: D, P, T | ||
editv4:Chromosomal Rearrangements (Gene Fusions)The content below was from the old template. Please incorporate above.
None
| Chromosomal Rearrangement | Genes in Fusion (5’ or 3’ Segments) | Pathogenic Derivative | Prevalence |
|---|---|---|---|
| EXAMPLE: t(9;22)(q34;q11.2) | EXAMPLE: 3'ABL1 / 5'BCR | EXAMPLE: der(22) | EXAMPLE: 5% |
| EXAMPLE: t(8;21)(q22;q22) | EXAMPLE: 5'RUNX1 / 3'RUNXT1 | EXAMPLE: der(8) | EXAMPLE: 5% |
End of V4 Section
editv4: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)
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[1]. 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[1].
End of V4 Section
Individual Region Genomic Gain/Loss/LOH
Put your text here and fill in the table (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.)
| Chr # | Gain, Loss, Amp, LOH | Minimal Region Cytoband and/or Genomic Coordinates [Genome Build; Size] | Relevant Gene(s) | Diagnostic, Prognostic, and Therapeutic Significance - D, P, T | Established Clinical Significance Per Guidelines - Yes or No (Source) | Clinical Relevance Details/Other Notes |
|---|---|---|---|---|---|---|
| EXAMPLE:
7 |
EXAMPLE: Loss | EXAMPLE:
chr7 |
EXAMPLE:
Unknown |
EXAMPLE: D, P | EXAMPLE: No | EXAMPLE:
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 references). |
| EXAMPLE:
8 |
EXAMPLE: Gain | EXAMPLE:
chr8 |
EXAMPLE:
Unknown |
EXAMPLE: D, P | EXAMPLE:
Common recurrent secondary finding for t(8;21) (add references). | |
| EXAMPLE:
17 |
EXAMPLE: Amp | EXAMPLE:
17q12; chr17:39,700,064-39,728,658 [hg38; 28.6 kb] |
EXAMPLE:
ERBB2 |
EXAMPLE: D, P, T | EXAMPLE:
Amplification of ERBB2 is associated with HER2 overexpression in HER2 positive breast cancer (add references). Add criteria for how amplification is defined. | |
editv4:Genomic Gain/Loss/LOHThe content below was from the old template. Please incorporate above.
None
| Chromosome Number | Gain/Loss/Amp/LOH | Region |
|---|---|---|
| EXAMPLE: 8 | EXAMPLE: Gain | EXAMPLE: chr8:0-1000000 |
| EXAMPLE: 7 | EXAMPLE: Loss | EXAMPLE: chr7:0-1000000 |
End of V4 Section
Characteristic Chromosomal or Other Global Mutational Patterns
Put your text here and fill in the table (Instructions: 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.)
| Chromosomal Pattern | Molecular Pathogenesis | Prevalence -
Common >20%, Recurrent 5-20% or Rare <5% (Disease) |
Diagnostic, Prognostic, and Therapeutic Significance - D, P, T | Established Clinical Significance Per Guidelines - Yes or No (Source) | Clinical Relevance Details/Other Notes |
|---|---|---|---|---|---|
| EXAMPLE:
Co-deletion of 1p and 18q |
EXAMPLE: See chromosomal rearrangements table as this pattern is due to an unbalanced derivative translocation associated with oligodendroglioma (add reference). | EXAMPLE: Common (Oligodendroglioma) | EXAMPLE: D, P | ||
| EXAMPLE:
Microsatellite instability - hypermutated |
EXAMPLE: Common (Endometrial carcinoma) | EXAMPLE: P, T | |||
editv4:Characteristic Chromosomal Aberrations / PatternsThe content below was from the old template. Please incorporate above.
None
End of V4 Section
Gene Mutations (SNV/INDEL)
Put your text here and fill in the table (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.)
| Gene | Genetic Alteration | Tumor Suppressor Gene, Oncogene, Other | Prevalence -
Common >20%, Recurrent 5-20% or Rare <5% (Disease) |
Diagnostic, Prognostic, and Therapeutic Significance - D, P, T | Established Clinical Significance Per Guidelines - Yes or No (Source) | Clinical Relevance Details/Other Notes |
|---|---|---|---|---|---|---|
| EXAMPLE:EGFR
|
EXAMPLE: Exon 18-21 activating mutations | EXAMPLE: Oncogene | EXAMPLE: Common (lung cancer) | EXAMPLE: T | EXAMPLE: Yes (NCCN) | EXAMPLE: 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). |
| EXAMPLE: TP53; Variable LOF mutations
|
EXAMPLE: Variable LOF mutations | EXAMPLE: Tumor Supressor Gene | EXAMPLE: Common (breast cancer) | EXAMPLE: P | EXAMPLE: >90% are somatic; rare germline alterations associated with Li-Fraumeni syndrome (add reference). Denotes a poor prognosis in breast cancer. | |
| EXAMPLE: BRAF; Activating mutations | EXAMPLE: Activating mutations | EXAMPLE: Oncogene | EXAMPLE: Common (melanoma) | EXAMPLE: T | ||
Note: A more extensive list of mutations can be found in cBioportal, COSMIC, and/or other databases. When applicable, gene-specific pages within the CCGA site directly link to pertinent external content.
editv4:Gene Mutations (SNV/INDEL)The content below was from the old template. Please incorporate above.
Pathogenic mutations in CEBPA are predominantly insertion/deletion frameshift mutations in the N-terminal TAD region and in-frame C-terminal bZIP mutations. 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):
| Gene | Mutation | Oncogene/Tumor Suppressor/Other | Presumed Mechanism (LOF/GOF/Other; Driver/Passenger) | Prevalence (COSMIC/TCGA/Other) |
|---|---|---|---|---|
| CEBPA | c.939_940insAAG, p.K313_V314insK | Oncogene | LOF | 52 |
| CEBPA | c.68_69insC, p.H24fs*84 | Oncogene | LOF | 43 |
| CEBPA | c.247delC, p.Q83fs*77 | Oncogene | LOF | 32 |
| CEBPA | c.936_937insCAG, p.Q312_K313insQ | Oncogene | LOF | 28 |
| CEBPA | c.912_913insTTG, p.K304_Q305insL | Oncogene | LOF | 24 |
Other Mutations
Concurrent mutations in NPM1 and FLT3 are seen less frequently in individuals with biallelic CEBPA mutations than in those with no or monoallelic mutations[2]. Conversely, mutations in GATA2 appear to occur more often in CEBPA single- and double-mutants[3]. The prognostic significance of these concomitant mutations is, however, unclear. Biallelic CEBPA mutations appear to confer a positive prognostic effect regardless of concomitant mutations.
| Type | Gene/Region/Other |
|---|---|
| Concomitant Mutations | NPM1, FLT3, GATA2 |
| Secondary Mutations | None |
| Mutually Exclusive | None |
End of V4 Section
Epigenomic Alterations
None
Genes and Main Pathways Involved
Put your text here and fill in the table (Instructions: Please include references throughout the table. Do not delete the table.)
| Gene; Genetic Alteration | Pathway | Pathophysiologic Outcome |
|---|---|---|
| EXAMPLE: BRAF and MAP2K1; Activating mutations | EXAMPLE: MAPK signaling | EXAMPLE: Increased cell growth and proliferation |
| EXAMPLE: CDKN2A; Inactivating mutations | EXAMPLE: Cell cycle regulation | EXAMPLE: Unregulated cell division |
| EXAMPLE: KMT2C and ARID1A; Inactivating mutations | EXAMPLE: Histone modification, chromatin remodeling | EXAMPLE: Abnormal gene expression program |
editv4:Genes and Main Pathways InvolvedThe content below was from the old template. Please incorporate above.
CEBPA, located on chromosome 19 band q13.1, encodes a transcription factor of the basic region leucine zipper (bZIP) family. It is involved in the coordination of myeloid differentiation and cellular growth arrest. Alternative translation initiation sites result in protein isoforms of different lengths.
CEPBA works in a tissue-specific manner to direct cellular differentiation by activating lineage-specific gene promoters. Interactions with the basal transcriptional apparatus (TBP/TFIIB), histone acetylators (CBP/p300), and chromatin-remodelling complexes (SWI/SNF) have all been implicated in lineage-specific gene activation by CEBPA. In the haematopoietic system there appears to be interplay between CEBPA and GATA factors[4]. CEBPA knockout mice show a complete lack of granulocytes while blasts accumulate in the bone marrow, suggesting an early block of myeloid maturation[5]. In the context of haematopoietic differentiation, evidence suggests CEBPA plays a role in regulating the expression of genes encoding growth factor receptors (e.g. granulocyte colony-stimulating factor) and secondary granule proteins (e.g. lactoferrin)[6][7]. It has also been implicated, along with NFI-A, in mediating miR-223 expression[8]. Studies indicate that CEBPA is not required for differentiation of granulocytes beyond the granulocyte-monocyte progenitor (GMP) stage, and that CEBPA controls stem-cell renewal with expression of Bmi-1 elevated in 'CEBPA knockouts[9]. Proliferation arrest also appears to be an important aspect of CEBPA function via interaction with CDK2/CDK4, upregulation of the p21 (WAF-1/CIP-1/SDI-1) protein and the SWI/SNF complex, and inhibition of the E2F complex[10][11][12][13][14]. This E2F inhibition leads to c-myc downregulation, which is required for granulocytic regulation[15]. Mutations in the C-terminal region of CEBPA abrogate CEBPA-E2F complex function[16]. The precise mechanism by which CEBPA mutants inhibit granulocytic differentiation in the context of AML is still unclear.
End of V4 Section
Genetic Diagnostic Testing Methods
Sanger sequencing, Next Generation Sequencing
Familial Forms
Familial mutations of CEBPA have been described in several families[17][18][19]. Typically, these are N-terminal mutations that are later joined by a somatic C-terminal mutation on the opposite allele leading to AML.
Additional Information
Put your text here
Links
References
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- ↑ Jump up to: 1.0 1.1 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.
- ↑ Taskesen, Erdogan; et al. (2011). "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". Blood. 117 (8): 2469–2475. doi:10.1182/blood-2010-09-307280. ISSN 1528-0020. PMID 21177436.
- ↑ Green, Claire L.; et al. (2013). "GATA2 mutations in sporadic and familial acute myeloid leukaemia patients with CEBPA mutations". British Journal of Haematology. 161 (5): 701–705. doi:10.1111/bjh.12317. ISSN 1365-2141. PMID 23560626.
- ↑ McNagny, K. M.; et al. (1998). "Regulation of eosinophil-specific gene expression by a C/EBP-Ets complex and GATA-1". The EMBO journal. 17 (13): 3669–3680. doi:10.1093/emboj/17.13.3669. ISSN 0261-4189. PMC 1170703. PMID 9649437.
- ↑ Zhang, D. E.; et al. (1997). "Absence of granulocyte colony-stimulating factor signaling and neutrophil development in CCAAT enhancer binding protein alpha-deficient mice". Proceedings of the National Academy of Sciences of the United States of America. 94 (2): 569–574. doi:10.1073/pnas.94.2.569. ISSN 0027-8424. PMC 19554. PMID 9012825.CS1 maint: PMC format (link)
- ↑ Radomska, H. S.; et al. (1998). "CCAAT/enhancer binding protein alpha is a regulatory switch sufficient for induction of granulocytic development from bipotential myeloid progenitors". Molecular and Cellular Biology. 18 (7): 4301–4314. doi:10.1128/mcb.18.7.4301. ISSN 0270-7306. PMC 109014. PMID 9632814.CS1 maint: PMC format (link)
- ↑ Zhang, P.; et al. (1998). "Upregulation of interleukin 6 and granulocyte colony-stimulating factor receptors by transcription factor CCAAT enhancer binding protein alpha (C/EBP alpha) is critical for granulopoiesis". The Journal of Experimental Medicine. 188 (6): 1173–1184. doi:10.1084/jem.188.6.1173. ISSN 0022-1007. PMC 2212540. PMID 9743535.
- ↑ Fazi, Francesco; et al. (2005). "A minicircuitry comprised of microRNA-223 and transcription factors NFI-A and C/EBPalpha regulates human granulopoiesis". Cell. 123 (5): 819–831. doi:10.1016/j.cell.2005.09.023. ISSN 0092-8674. PMID 16325577.
- ↑ Zhang, Pu; et al. (2004). "Enhancement of hematopoietic stem cell repopulating capacity and self-renewal in the absence of the transcription factor C/EBP alpha". Immunity. 21 (6): 853–863. doi:10.1016/j.immuni.2004.11.006. ISSN 1074-7613. PMID 15589173.
- ↑ Pedersen, T. A.; et al. (2001). "Cooperation between C/EBPalpha TBP/TFIIB and SWI/SNF recruiting domains is required for adipocyte differentiation". Genes & Development. 15 (23): 3208–3216. doi:10.1101/gad.209901. ISSN 0890-9369. PMC 312836. PMID 11731483.CS1 maint: PMC format (link)
- ↑ Slomiany, B. A.; et al. (2000). "C/EBPalpha inhibits cell growth via direct repression of E2F-DP-mediated transcription". Molecular and Cellular Biology. 20 (16): 5986–5997. doi:10.1128/mcb.20.16.5986-5997.2000. ISSN 0270-7306. PMC 86075. PMID 10913181.CS1 maint: PMC format (link)
- ↑ Timchenko, N. A.; et al. (1996). "CCAAT/enhancer-binding protein alpha (C/EBP alpha) inhibits cell proliferation through the p21 (WAF-1/CIP-1/SDI-1) protein". Genes & Development. 10 (7): 804–815. doi:10.1101/gad.10.7.804. ISSN 0890-9369. PMID 8846917.
- ↑ Wang, H.; et al. (2001). "C/EBPalpha arrests cell proliferation through direct inhibition of Cdk2 and Cdk4". Molecular Cell. 8 (4): 817–828. doi:10.1016/s1097-2765(01)00366-5. ISSN 1097-2765. PMID 11684017.
- ↑ Wang, Qian-Fei; et al. (2003). "Cell cycle inhibition mediated by the outer surface of the C/EBPalpha basic region is required but not sufficient for granulopoiesis". Oncogene. 22 (17): 2548–2557. doi:10.1038/sj.onc.1206360. ISSN 0950-9232. PMID 12730669.
- ↑ Johansen, L. M.; et al. (2001). "c-Myc is a critical target for c/EBPalpha in granulopoiesis". Molecular and Cellular Biology. 21 (11): 3789–3806. doi:10.1128/MCB.21.11.3789-3806.2001. ISSN 0270-7306. PMC 87031. PMID 11340171.CS1 maint: PMC format (link)
- ↑ Porse, B. T.; et al. (2001). "E2F repression by C/EBPalpha is required for adipogenesis and granulopoiesis in vivo". Cell. 107 (2): 247–258. doi:10.1016/s0092-8674(01)00516-5. ISSN 0092-8674. PMID 11672531.
- ↑ Smith, Matthew L.; et al. (2004). "Mutation of CEBPA in familial acute myeloid leukemia". The New England Journal of Medicine. 351 (23): 2403–2407. doi:10.1056/NEJMoa041331. ISSN 1533-4406. PMID 15575056.
- ↑ Nanri, Tomoko; et al. (2010). "A family harboring a germ-line N-terminal C/EBPalpha mutation and development of acute myeloid leukemia with an additional somatic C-terminal C/EBPalpha mutation". Genes, Chromosomes & Cancer. 49 (3): 237–241. doi:10.1002/gcc.20734. ISSN 1098-2264. PMID 19953636.
- ↑ Sellick, G. S.; et al. (2005). "Further evidence that germline CEBPA mutations cause dominant inheritance of acute myeloid leukaemia". Leukemia. 19 (7): 1276–1278. doi:10.1038/sj.leu.2403788. ISSN 0887-6924. PMID 15902292.
Notes
*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 Associate Editor or other CCGA representative. When pages have a major update, the new author will be acknowledged at the beginning of the page, and those who contributed previously will be acknowledged below as a prior author.
Prior Author(s):
*Citation of this Page: “Acute myeloid leukaemia with CEBPA mutation”. Compendium of Cancer Genome Aberrations (CCGA), Cancer Genomics Consortium (CGC), updated 02/11/2025, https://ccga.io/index.php/HAEM5:Acute_myeloid_leukaemia_with_CEBPA_mutation.