Acute myeloid leukaemia with NPM1 mutation
Haematolymphoid Tumours (WHO Classification, 5th ed.)
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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 Mutated NPM1.
(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)*
Xinjie Xu, PhD, FACMG
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 NPM1 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.
Rare gene fusions involving NPM1 genes (NPM1-MLF1 and NPM1–HAUS1) have been reported in patients with AML and are associated with cytoplasmic accumulation of NPM1[1][2][3].
| 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)
- Diagnosis based on identification of genetic lesion of NPM1 by immunohistochemical and /or molecular testing.
- Mutated NPM1 is associated with a favorable prognosis in AML patients who do not have FLT3-internal tandem duplication (FLT3-ITD) mutations and with normal karyotype[4][5][6][7]. A more recent study found that NPM1-positive/FLT3-ITD-negative genotype predicts favorable outcomes in AML patients younger than 65 years, but not in those older than 65 years[8]. Besides FLT3-ITD, the prognostic impact of NPM1 mutations in AML can be modified by the presence of other concurrent mutations. In NPM1 mutated AML, concurrent mutations have been found in DNMT3A (54%), NRAS (19%), TET2 (16%) and PTPN11 (15%)[5]. DNMT3A missense mutations predicted shorter overall survival and higher cumulative incidence of relapse when stratified by NPM1 mutation status, whereas 'NRAS truncation mutations do not correlate with clinical outcome[9]. NRAS codon Gly12 and Gly13 mutations predict better overall survival in AML patients with concurrent NPM1 and DNMT3A mutations[5].
- Minimal residual disease (MRD) monitoring of AML patients after chemotherapy provides important prognostic information[10][11]. Because NPM1 mutations are very stable over the course of disease, they are an excellent marker for monitoring minimal residual disease (MRD) for NPM1 mutated AML patients[3][12]. Indeed, several studies have suggested that MRD accessed by NPM1 mutation level using PCR-based methods is a strong independent predictor of higher relapse risk[7][13].
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.
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.
trisomy 8, deletion 9q
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.
- Studies investigating the methods by which NPM1 mutations lead to leukemogenesis show that NPM1 mutation alone is not sufficient to cause AML[14].
- AML associated NPM1 mutations are generally frame-shift alterations at codons Trp288 and Trp290 with the most common alterations being 4-bp insertions that disrupt the NPM nucleolar-localization signal and generate a leucine-rich nuclear export signal, thus leading to abnormal cytoplasmic accumulation of NPM. In addition, a small subset of AML cases with NPM cytoplasmic localization by immunohistochemical staining did not harbor detectable NPM1 mutations[1], raising the possibility of alternative mechanisms for ectopic NPM expression.
- In a study of 52 primary AML patients with cytoplasmic NPM1 (NPM1c), 98% of the subjects had exon 12 mutations; over 55 unique mutations have been identified in exon 12[14][15]. Most mutations consist of a 4-base-pair insertion with >95% of mutations occurring between nucleotides 960 and 961 NM_002520[15]. The most common mutation (“type A”) involve duplication of TCTG (nucleotides 956-959 NM_002520), resulting in an insertion at position 960 NM_002520[15]. Type B and D mutations, which are also relatively common, both involve 4-base-pair insertions at position 960 NM_002520 [21]. NPM1 mutations cause increased nuclear exporting of NPM1 protein, compared to wild-type NPM1, hence increased cytoplasmic localization of the protein – ‘cytoplasmic NPM1’ (NPM1c)[14][16].
| Gene | Mutation | Oncogene/Tumor Suppressor/Other | Presumed Mechanism (LOF/GOF/Other; Driver/Passenger) | Prevalence (COSMIC/TCGA/Other) |
|---|---|---|---|---|
| EXAMPLE: TP53 | EXAMPLE: R273H | EXAMPLE: Tumor Suppressor | EXAMPLE: LOF | EXAMPLE: 20% |
Other Mutations
- In NPM1 mutated AML, concurrent mutations have been found in DNMT3A (54%), NRAS (19%), TET2 (16%) and PTPN11 (15%)[5].
- The most prominent of the complex gene interactions is between NPM1, DNMT3A and FLT3-ITD (internal tandem duplication). The co-occurrence of these various mutations have differing prognostic implications[14].
| Type | Gene/Region/Other |
|---|---|
| Concomitant Mutations | DNMT3A, TET2, IDH1, IDH2, FLT3-ITD |
| Secondary Mutations | Trisomy 8, del (9q) |
| Mutually Exclusive | other AML with recurrent genetic abnormalities |
End of V4 Section
Epigenomic Alterations
Put your text here
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.
- The NPM1 gene encodes nucleophosmin (NPM), which is a multifunctional protein that shuttles between the nucleus and the cytoplasm, and binds many partners in distinct cellular compartments. It is involved in many cellular processes including ribosome biogenesis, maintenance of genomic stability and regulation of cellular proliferation.
- Mutations in NPM1 represent a distinct entity in the World Health Organization (WHO) classification and commonly indicate a better risk prognosis[14]. Predominantly, observed NPM1 variants are sited in exon 12 and cause a frameshift in the C-terminal domain, affecting one or both of the key tryptophan residues in the domain. Such NPM1 mutations result in a ‘functionally stronger’ nuclear export than nuclear import signal (compared to wild-type NPM1) and thus there is cytoplasmic localization of the protein – ‘cytoplasmic NPM1’ (NPM1c)[14][16]. See Figure 3 in [14]. NPM1c sequesters ARF to the cytoplasm; however, unlike the ARF-NPM1 complex in the nucleolus, NPM1c is unable to stabilize ARF in the cytoplasm and consequently ARF becomes unstable and degrades[17]. Without ARF, there is lack of MDM2 inhibition, leading to p53 inactivation by MDM2 and the loss of growth inhibition by p53[14]. In the context of NPM1 mutations, NPM1 haploinsufficiency results in uncontrolled centrosome duplication and consequently supernumerary centrosomes (a potential mechanism for tumor development)[18]. The loss of NPM1 function leads to activation of Myc oncogene (increased oncogene levels), promoting growth and cell proliferation. As expected, in the cytoplasm, NPM1c inhibits caspase-6/-8, promoting growth[14].
End of V4 Section
Genetic Diagnostic Testing Methods
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Familial Forms
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Additional Information
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Links
References
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- ↑ Jump up to: 1.0 1.1 Woolthuis, Carolien M.; et al. (2013). "A single center analysis of nucleophosmin in acute myeloid leukemia: value of combining immunohistochemistry with molecular mutation analysis". Haematologica. 98 (10): 1532–1538. doi:10.3324/haematol.2012.079806. ISSN 1592-8721. PMC 3789457. PMID 23716555.
- ↑ Campregher, Paulo Vidal; et al. (2016). "A novel mechanism of NPM1 cytoplasmic localization in acute myeloid leukemia: the recurrent gene fusion NPM1-HAUS1". Haematologica. 101 (7): e287–290. doi:10.3324/haematol.2015.137364. ISSN 1592-8721. PMC 5004474. PMID 27036161.
- ↑ Jump up to: 3.0 3.1 Falini, B.; et al. (2006). "Aberrant subcellular expression of nucleophosmin and NPM-MLF1 fusion protein in acute myeloid leukaemia carrying t(3;5): a comparison with NPMc+ AML". Leukemia. 20 (2): 368–371. doi:10.1038/sj.leu.2404068. ISSN 0887-6924. PMID 16341033.
- ↑ Falini, Brunangelo; et al. (2009). "Acute myeloid leukemia with mutated NPM1: diagnosis, prognosis and therapeutic perspectives". Current Opinion in Oncology. 21 (6): 573–581. doi:10.1097/CCO.0b013e3283313dfa. ISSN 1531-703X. PMID 19770764.
- ↑ Jump up to: 5.0 5.1 5.2 5.3 Papaemmanuil, Elli; et al. (2016). "Genomic Classification and Prognosis in Acute Myeloid Leukemia". The New England Journal of Medicine. 374 (23): 2209–2221. doi:10.1056/NEJMoa1516192. ISSN 1533-4406. PMC 4979995. PMID 27276561.
- ↑ Schnittger, S.; et al. (2011). "Prognostic impact of FLT3-ITD load in NPM1 mutated acute myeloid leukemia". Leukemia. 25 (8): 1297–1304. doi:10.1038/leu.2011.97. ISSN 1476-5551. PMID 21537333.
- ↑ Jump up to: 7.0 7.1 Schnittger, Susanne; et al. (2009). "Minimal residual disease levels assessed by NPM1 mutation-specific RQ-PCR provide important prognostic information in AML". Blood. 114 (11): 2220–2231. doi:10.1182/blood-2009-03-213389. ISSN 1528-0020. PMID 19587375.
- ↑ Ostronoff, Fabiana; et al. (2015). "Prognostic significance of NPM1 mutations in the absence of FLT3-internal tandem duplication in older patients with acute myeloid leukemia: a SWOG and UK National Cancer Research Institute/Medical Research Council report". Journal of Clinical Oncology: Official Journal of the American Society of Clinical Oncology. 33 (10): 1157–1164. doi:10.1200/JCO.2014.58.0571. ISSN 1527-7755. PMC 4372852. PMID 25713434.
- ↑ Gale, Rosemary E.; et al. (2015). "Simpson's Paradox and the Impact of Different DNMT3A Mutations on Outcome in Younger Adults With Acute Myeloid Leukemia". Journal of Clinical Oncology: Official Journal of the American Society of Clinical Oncology. 33 (18): 2072–2083. doi:10.1200/JCO.2014.59.2022. ISSN 1527-7755. PMID 25964253.
- ↑ Grimwade, David; et al. (2014). "Defining minimal residual disease in acute myeloid leukemia: which platforms are ready for "prime time"?". Blood. 124 (23): 3345–3355. doi:10.1182/blood-2014-05-577593. ISSN 1528-0020. PMID 25049280.
- ↑ Hourigan, Christopher S.; et al. (2013). "Minimal residual disease in acute myeloid leukaemia". Nature Reviews. Clinical Oncology. 10 (8): 460–471. doi:10.1038/nrclinonc.2013.100. ISSN 1759-4782. PMC 4163748. PMID 23799371.
- ↑ Falini, B.; et al. (2009). "Altered nucleophosmin transport in acute myeloid leukaemia with mutated NPM1: molecular basis and clinical implications". Leukemia. 23 (10): 1731–1743. doi:10.1038/leu.2009.124. ISSN 1476-5551. PMID 19516275.
- ↑ Ivey, Adam; et al. (2016). "Assessment of Minimal Residual Disease in Standard-Risk AML". The New England Journal of Medicine. 374 (5): 422–433. doi:10.1056/NEJMoa1507471. ISSN 1533-4406. PMID 26789727.
- ↑ Jump up to: 14.0 14.1 14.2 14.3 14.4 14.5 14.6 14.7 14.8 Heath, E. M.; et al. (2017). "Biological and clinical consequences of NPM1 mutations in AML". Leukemia. 31 (4): 798–807. doi:10.1038/leu.2017.30. ISSN 1476-5551. PMID 28111462.
- ↑ Jump up to: 15.0 15.1 15.2 Falini, Brunangelo; et al. (2005). "Cytoplasmic nucleophosmin in acute myelogenous leukemia with a normal karyotype". The New England Journal of Medicine. 352 (3): 254–266. doi:10.1056/NEJMoa041974. ISSN 1533-4406. PMID 15659725.
- ↑ Jump up to: 16.0 16.1 Falini, Brunangelo; et al. (2006). "Immunohistochemistry predicts nucleophosmin (NPM) mutations in acute myeloid leukemia". Blood. 108 (6): 1999–2005. doi:10.1182/blood-2006-03-007013. ISSN 0006-4971. PMID 16720834.
- ↑ Colombo, Emanuela; et al. (2006). "Delocalization and destabilization of the Arf tumor suppressor by the leukemia-associated NPM mutant". Cancer Research. 66 (6): 3044–3050. doi:10.1158/0008-5472.CAN-05-2378. ISSN 0008-5472. PMID 16540653.
- ↑ Sportoletti, Paolo; et al. (2008). "Npm1 is a haploinsufficient suppressor of myeloid and lymphoid malignancies in the mouse". Blood. 111 (7): 3859–3862. doi:10.1182/blood-2007-06-098251. ISSN 0006-4971. PMC 2275037. PMID 18212245.
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 CCGA coordinators (contact information provided on the homepage). Additional global feedback or concerns are also welcome.
Edited by: Fabiola Quintero-Rivera 8/3/2018
*Citation of this Page: “Acute myeloid leukaemia with NPM1 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_NPM1_mutation.