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Acute myeloid leukemia(AML)

MedGen UID:
9730
Concept ID:
C0023467
Neoplastic Process
Synonyms: Acute granulocytic leukemia; Acute myelogenous leukemia; Acute myeloid leukemia, adult; Acute non-lymphocytic leukemia; AML; AML adult; Familial Acute Myelocytic Leukemia; Leukemia, acute myelogenous, somatic; Leukemia, acute myeloid, somatic
SNOMED CT: Acute myeloid leukemia (91861009); AML - Acute myeloblastic leukemia (91861009); Acute myelocytic leukemia (91861009); Acute non-lymphocytic leukemia (1162928000); Acute myelogenous leukemia (1162928000); Acute granulocytic leukemia (1162928000); Acute myelocytic leukemia (1162928000); Acute myeloid leukemia (1162928000); AML - Acute myeloid leukemia (91861009); Acute myeloid leukemia, disease (91861009)
 
Genes (locations): CEBPA (19q13.11); CHIC2 (4q12); DNMT3A (2p23.3); ETV6 (12p13.2); FLT3 (13q12.2); GATA2 (3q21.3); JAK2 (9p24.1); KIT (4q12); KRAS (12p12.1); LPP (3q27.3-28); MLLT10 (10p12.31); NPM1 (5q35.1); NUP214 (9q34.13); PICALM (11q14.2); RUNX1 (21q22.12); SH3GL1 (19p13.3); TERT (5p15.33)
 
HPO: HP:0004808
Monarch Initiative: MONDO:0018874
OMIM®: 601626
Orphanet: ORPHA519

Definition

A clonal expansion of myeloid blasts in the bone marrow, blood or other tissues. The classification of acute myeloid leukemias (AMLs) encompasses four major categories: 1) AML with recurrent genetic abnormalities; 2) AML with multilineage dysplasia; 3) Therapy-related AML; 4) AML not otherwise specified. The required bone marrow or peripheral blood blast percentage for the diagnosis of AML is 20% (WHO classification) [from NCBI]

Additional descriptions

From GeneReviews
CEBPA-associated familial acute myeloid leukemia (AML) is defined as the presence of a heterozygous germline CEBPA pathogenic variant in an individual with AML and/or family in which more than one individual has AML. In contrast, sporadic CEBPA-associated AML is defined as AML in which a CEBPA pathogenic variant(s) is identified in leukemic cells but not in the non-leukemic cells. In the majority of individuals, the age of onset of familial AML appears to be earlier than sporadic AML; disease onset has been reported in persons as young as age 1.8 years and up to age 50 years. The prognosis of CEBPA-associated familial AML appears to be favorable compared with sporadic CEBPA-associated AML. Individuals with CEBPA-associated familial AML who have been cured of their initial disease may be at greater risk of developing additional independent leukemic episodes, in addition to the risk of relapse from preexisting clones.
From MedlinePlus Genetics
Familial acute myeloid leukemia with mutated CEBPA is one form of a cancer of the blood-forming tissue (bone marrow) called acute myeloid leukemia. In normal bone marrow, early blood cells called hematopoietic stem cells develop into several types of blood cells: white blood cells (leukocytes) that protect the body from infection; red blood cells (erythrocytes) that carry oxygen; and platelets (thrombocytes), which are involved in blood clotting. In acute myeloid leukemia, the bone marrow makes large numbers of abnormal, immature white blood cells called myeloid blasts. Instead of developing into normal white blood cells, the myeloid blasts develop into cancerous leukemia cells. The large number of abnormal cells in the bone marrow interferes with the production of functional white blood cells, red blood cells, and platelets.

People with familial acute myeloid leukemia with mutated CEBPA have a shortage of white blood cells (leukopenia), leading to increased susceptibility to infections. A low number of red blood cells (anemia) also occurs in this disorder, resulting in fatigue and weakness. Affected individuals also have a reduction in the amount of platelets (thrombocytopenia), which can result in easy bruising and abnormal bleeding. Other symptoms of familial acute myeloid leukemia with mutated CEBPA may include fever and weight loss.

While acute myeloid leukemia is generally a disease of older adults, familial acute myeloid leukemia with mutated CEBPA often begins earlier in life, and it has been reported to occur as early as age 4. Between 50 and 65 percent of affected individuals survive their disease, compared with 25 to 40 percent of those with other forms of acute myeloid leukemia. However, people with familial acute myeloid leukemia with mutated CEBPA have a higher risk of having a new primary occurrence of this disorder after successful treatment of the initial occurrence.  https://medlineplus.gov/genetics/condition/familial-acute-myeloid-leukemia-with-mutated-cebpa
From MedlinePlus Genetics
Core binding factor acute myeloid leukemia (CBF-AML) is one form of a cancer of the blood-forming tissue (bone marrow) called acute myeloid leukemia. In normal bone marrow, early blood cells called hematopoietic stem cells develop into several types of blood cells: white blood cells (leukocytes) that protect the body from infection, red blood cells (erythrocytes) that carry oxygen, and platelets (thrombocytes) that are involved in blood clotting. In acute myeloid leukemia, the bone marrow makes large numbers of abnormal, immature white blood cells called myeloid blasts. Instead of developing into normal white blood cells, the myeloid blasts develop into cancerous leukemia cells. The large number of abnormal cells in the bone marrow interferes with the production of functional white blood cells, red blood cells, and platelets.

People with CBF-AML have a shortage of all types of mature blood cells: a shortage of white blood cells (leukopenia) leads to increased susceptibility to infections, a low number of red blood cells (anemia) causes fatigue and weakness, and a reduction in the amount of platelets (thrombocytopenia) can result in easy bruising and abnormal bleeding. Other symptoms of CBF-AML may include fever and weight loss.

While acute myeloid leukemia is generally a disease of older adults, CBF-AML often begins in young adulthood and can occur in childhood. Compared to other forms of acute myeloid leukemia, CBF-AML has a relatively good prognosis: about 90 percent of individuals with CBF-AML recover from their disease following treatment, compared with 25 to 40 percent of those with other forms of acute myeloid leukemia. However, the disease recurs in approximately half of them after successful treatment of the initial occurrence.  https://medlineplus.gov/genetics/condition/core-binding-factor-acute-myeloid-leukemia
From MedlinePlus Genetics
Cytogenetically normal acute myeloid leukemia (CN-AML) is one form of a cancer of the blood-forming tissue (bone marrow) called acute myeloid leukemia. In normal bone marrow, early blood cells called hematopoietic stem cells develop into several types of blood cells: white blood cells (leukocytes) that protect the body from infection, red blood cells (erythrocytes) that carry oxygen, and platelets (thrombocytes) that are involved in blood clotting. In acute myeloid leukemia, the bone marrow makes large numbers of abnormal, immature white blood cells called myeloid blasts. Instead of developing into normal white blood cells, the myeloid blasts develop into cancerous leukemia cells. The large number of abnormal cells in the bone marrow interferes with the production of functional white blood cells, red blood cells, and platelets.

People with CN-AML have a shortage of all types of mature blood cells: a shortage of white blood cells (leukopenia) leads to increased susceptibility to infections, a low number of red blood cells (anemia) causes fatigue and weakness, and a reduction in the amount of platelets (thrombocytopenia) can result in easy bruising and abnormal bleeding. Other symptoms of CN-AML may include fever and weight loss.

The age at which CN-AML begins ranges from childhood to late adulthood. CN-AML is said to be an intermediate-risk cancer because the prognosis varies: some affected individuals respond well to normal treatment while others may require stronger treatments. The age at which the condition begins and the prognosis are affected by the specific genetic factors involved in the condition.  https://medlineplus.gov/genetics/condition/cytogenetically-normal-acute-myeloid-leukemia

Clinical features

From HPO
Acute myeloid leukemia
MedGen UID:
9730
Concept ID:
C0023467
Neoplastic Process
A clonal expansion of myeloid blasts in the bone marrow, blood or other tissues. The classification of acute myeloid leukemias (AMLs) encompasses four major categories: 1) AML with recurrent genetic abnormalities; 2) AML with multilineage dysplasia; 3) Therapy-related AML; 4) AML not otherwise specified. The required bone marrow or peripheral blood blast percentage for the diagnosis of AML is 20% (WHO classification)

Term Hierarchy

CClinical test,  RResearch test,  OOMIM,  GGeneReviews,  VClinVar  
  • CROGVAcute myeloid leukemia
Follow this link to review classifications for Acute myeloid leukemia in Orphanet.

Conditions with this feature

Acute myeloid leukemia
MedGen UID:
9730
Concept ID:
C0023467
Neoplastic Process
A clonal expansion of myeloid blasts in the bone marrow, blood or other tissues. The classification of acute myeloid leukemias (AMLs) encompasses four major categories: 1) AML with recurrent genetic abnormalities; 2) AML with multilineage dysplasia; 3) Therapy-related AML; 4) AML not otherwise specified. The required bone marrow or peripheral blood blast percentage for the diagnosis of AML is 20% (WHO classification)
Dyskeratosis congenita, X-linked
MedGen UID:
216941
Concept ID:
C1148551
Disease or Syndrome
Dyskeratosis congenita and related telomere biology disorders (DC/TBD) are caused by impaired telomere maintenance resulting in short or very short telomeres. The phenotypic spectrum of telomere biology disorders is broad and includes individuals with classic dyskeratosis congenita (DC) as well as those with very short telomeres and an isolated physical finding. Classic DC is characterized by a triad of dysplastic nails, lacy reticular pigmentation of the upper chest and/or neck, and oral leukoplakia, although this may not be present in all individuals. People with DC/TBD are at increased risk for progressive bone marrow failure (BMF), myelodysplastic syndrome or acute myelogenous leukemia, solid tumors (usually squamous cell carcinoma of the head/neck or anogenital cancer), and pulmonary fibrosis. Other findings can include eye abnormalities (epiphora, blepharitis, sparse eyelashes, ectropion, entropion, trichiasis), taurodontism, liver disease, gastrointestinal telangiectasias, and avascular necrosis of the hips or shoulders. Although most persons with DC/TBD have normal psychomotor development and normal neurologic function, significant developmental delay is present in both forms; additional findings include cerebellar hypoplasia (Hoyeraal Hreidarsson syndrome) and bilateral exudative retinopathy and intracranial calcifications (Revesz syndrome and Coats plus syndrome). Onset and progression of manifestations of DC/TBD vary: at the mild end of the spectrum are those who have only minimal physical findings with normal bone marrow function, and at the severe end are those who have the diagnostic triad and early-onset BMF.
Hereditary thrombocytopenia and hematological cancer predisposition syndrome associated with RUNX1
MedGen UID:
321945
Concept ID:
C1832388
Disease or Syndrome
RUNX1 familial platelet disorder with associated myeloid malignancies (RUNX1-FPDMM) is characterized by prolonged bleeding and/or easy bruising and an increased risk of developing a hematologic malignancy. RUNX1-FPDMM is characterized by thrombocytopenia with normal platelet size; bleeding is often greater than expected due to qualitative platelet dysfunction. Myeloid malignancies are the most common, including acute myelogenous leukemia (and myelodysplastic syndrome. T- and B-cell acute lymphoblastic leukemias and lymphomas have also been reported, as well as skin manifestations (e.g., eczema, psoriasis).
Fanconi anemia complementation group N
MedGen UID:
372133
Concept ID:
C1835817
Disease or Syndrome
Fanconi anemia (FA) is characterized by physical abnormalities, bone marrow failure, and increased risk for malignancy. Physical abnormalities, present in approximately 75% of affected individuals, include one or more of the following: short stature, abnormal skin pigmentation, skeletal malformations of the upper and/or lower limbs, microcephaly, and ophthalmic and genitourinary tract anomalies. Progressive bone marrow failure with pancytopenia typically presents in the first decade, often initially with thrombocytopenia or leukopenia. The incidence of acute myeloid leukemia is 13% by age 50 years. Solid tumors – particularly of the head and neck, skin, and genitourinary tract – are more common in individuals with FA.
Fanconi anemia complementation group D1
MedGen UID:
325420
Concept ID:
C1838457
Disease or Syndrome
Fanconi anemia (FA) is characterized by physical abnormalities, bone marrow failure, and increased risk for malignancy. Physical abnormalities, present in approximately 75% of affected individuals, include one or more of the following: short stature, abnormal skin pigmentation, skeletal malformations of the upper and/or lower limbs, microcephaly, and ophthalmic and genitourinary tract anomalies. Progressive bone marrow failure with pancytopenia typically presents in the first decade, often initially with thrombocytopenia or leukopenia. The incidence of acute myeloid leukemia is 13% by age 50 years. Solid tumors – particularly of the head and neck, skin, and genitourinary tract – are more common in individuals with FA.
Nonimmune chronic idiopathic neutropenia of adults
MedGen UID:
375050
Concept ID:
C1842930
Disease or Syndrome
Nonimmune chronic idiopathic neutropenia of adults (NI-CINA) is a relatively mild form of neutropenia diagnosed in adults but predisposing to leukemia in a subset of patients (Papadaki et al., 2002).
Monosomy 7 myelodysplasia and leukemia syndrome 1
MedGen UID:
381529
Concept ID:
C1854978
Disease or Syndrome
Monosomy 7 myelodysplasia and leukemia syndrome-1 (M7MLS1) is an autosomal dominant hematologic disorder with highly variable manifestations. Most patients present in early childhood with pancytopenia and dyspoietic or dysplastic changes in the bone marrow. These abnormalities are almost always associated with monosomy 7 in the bone marrow. In severely affected individuals, the phenotype progresses to frank myelodysplastic syndrome (MDS) or acute myelogenous leukemia (AML). Less severely affected individuals may have transient thrombocytopenia or anemia, or have normal peripheral blood counts with transient bone marrow abnormalities or transient monosomy 7. Germline mutations in the SAMD9L gene, located on chromosome 7q, have a gain-of-function suppressive effect on the cell cycle, resulting in decreased cellular proliferation. It is hypothesized that this germline defect leads to selective pressure favoring somatic loss of the chromosome 7 harboring the mutant allele (adaptation by aneuploidy) (summary by Wong et al., 2018). Monosomy 7 or partial deletion of the long arm of chromosome 7 (7q-) is a frequent cytogenetic finding in the bone marrow of patients with myelodysplasia and acute myelogenous leukemia. Furthermore, monosomy 7 or 7q- is the most frequent abnormality of karyotype in cases of AML that occur after cytotoxic cancer therapy or occupational exposure to mutagens. The age distribution of de novo cases shows peaks in the first and fifth decades. Monosomy 7 is found in about 5% of de novo and 40% of secondary cases of AML. These findings suggest that loss of certain genes at this region is an important event in the development of myelodysplasia (summary by Shannon et al., 1989). Genetic Heterogeneity of Monosomy 7 Myelodysplastic and Leukemia Syndrome See also M7MLS2 (619041), caused by germline mutation in the SAMD9 gene (610457) on chromosome 7q21.
Leukemia, acute myelocytic, with polyposis coli and colon cancer
MedGen UID:
383699
Concept ID:
C1855505
Neoplastic Process
Dohle bodies and leukemia
MedGen UID:
346548
Concept ID:
C1857225
Neoplastic Process
Glioma susceptibility 3
MedGen UID:
442777
Concept ID:
C2751641
Finding
Any malignant glioma in which the cause of the disease is a mutation in the BRCA2 gene.
Deafness-lymphedema-leukemia syndrome
MedGen UID:
481294
Concept ID:
C3279664
Disease or Syndrome
Primary lymphedema with myelodysplasia, also known as Emberger syndrome, is a rare disorder characterized by childhood-onset lymphedema of the lower limbs, with lymphoscintigraphy suggestive of lymphatic vessel hypoplasia, and genital lymphatic abnormalities. Myelodysplasia is usually with monosomy 7. Multiple warts, deafness, and minor anomalies (mild hypotelorism, neck webbing, and slender fingers) may also be present (summary by Mansour et al., 2010).
Fanconi anemia complementation group T
MedGen UID:
896157
Concept ID:
C4084840
Disease or Syndrome
Fanconi anemia (FA) is characterized by physical abnormalities, bone marrow failure, and increased risk for malignancy. Physical abnormalities, present in approximately 75% of affected individuals, include one or more of the following: short stature, abnormal skin pigmentation, skeletal malformations of the upper and/or lower limbs, microcephaly, and ophthalmic and genitourinary tract anomalies. Progressive bone marrow failure with pancytopenia typically presents in the first decade, often initially with thrombocytopenia or leukopenia. The incidence of acute myeloid leukemia is 13% by age 50 years. Solid tumors – particularly of the head and neck, skin, and genitourinary tract – are more common in individuals with FA.
DDX41-related hematologic malignancy predisposition syndrome
MedGen UID:
895780
Concept ID:
C4225174
Finding
DDX41-associated familial myelodysplastic syndrome and acute myeloid leukemia (MDS/AML) is characterized by an increased risk of myeloid neoplasms, lymphoid neoplasms, adult-onset single- or multiple-lineage cytopenias (including aplastic anemia), and red blood cell macrocytosis. The most common myeloid neoplasms include MDS, AML, and therapy-related myeloid neoplasms. Chronic myelomonocytic leukemia, chronic myeloid leukemia, and myeloproliferative neoplasms are less common. Lymphoid neoplasms include non-Hodgkin lymphoma, Hodgkin lymphoma, multiple myeloma, chronic lymphocytic leukemia, and acute lymphoblastic leukemia.
14q32 duplication syndrome
MedGen UID:
896239
Concept ID:
C4225449
Disease or Syndrome
A rare chromosomal anomaly syndrome resulting from the partial duplication of the long arm of chromosome 14 that results in a predisposition to a number of adult-onset myeloproliferative neoplasms, including acute myeloid leukaemia, chronic myelomonocytic leukaemia and myeloproliferative neoplasms especially essential thrombocythemia. Progression to myelofibrosis and secondary acute myeloid leukaemia can be observed.
Bone marrow failure syndrome 3
MedGen UID:
934711
Concept ID:
C4310744
Disease or Syndrome
Bone marrow failure syndrome-3 is an autosomal recessive disorder characterized by onset of pancytopenia in early childhood. Patients may have additional variable nonspecific somatic abnormalities, including poor growth, microcephaly, and skin anomalies (summary by Tummala et al., 2016). BMFS3 has a distinct phenotype and may include features that overlap with Shwachman-Diamond syndrome (SDS1; 260400), such as pancreatic insufficiency and short stature, and with dyskeratosis congenita (see, e.g., DKCA1, 127550), such as dental and hair abnormalities and shortened telomeres. In addition, some patients may have joint and skeletal abnormalities, impaired development, and retinal dysplasia (summary by D'Amours et al., 2018). For a discussion of genetic heterogeneity of BMFS, see BMFS1 (614675).
Shwachman-Diamond syndrome 1
MedGen UID:
1640046
Concept ID:
C4692625
Disease or Syndrome
Shwachman-Diamond syndrome (SDS) is characterized by: exocrine pancreatic dysfunction with malabsorption, malnutrition, and growth failure; hematologic abnormalities with single- or multilineage cytopenias and susceptibility to myelodysplasia syndrome (MDS) and acute myelogeneous leukemia (AML); and bone abnormalities. In almost all affected children, persistent or intermittent neutropenia is a common presenting finding, often before the diagnosis of SDS is made. Short stature and recurrent infections are common.
Monosomy 7 myelodysplasia and leukemia syndrome 2
MedGen UID:
1762901
Concept ID:
C5436668
Disease or Syndrome
Monosomy 7 myelodysplasia and leukemia syndrome-2 (M7MLS2) is an autosomal dominant hematologic disorder characterized by onset of pancytopenia, acute myelogenous leukemia (AML), and variable features of myelodysplastic syndrome (MDS) usually in the first decades of life. Bone marrow cells show monosomy 7. Germline mutations in the SAMD9 gene, located on chromosome 7q, have a gain-of-function suppressive effect on the cell cycle, resulting in decreased cellular proliferation. It is hypothesized that this germline defect leads to selective pressure favoring somatic loss of the chromosome 7 harboring the mutant allele (adaptation by aneuploidy) (summary by Wong et al., 2018). For a discussion of genetic heterogeneity of monosomy 7 myelodysplasia and leukemia syndrome, see 252270.
AMED syndrome, digenic
MedGen UID:
1754257
Concept ID:
C5436906
Disease or Syndrome
AMED syndrome (AMEDS) is an autosomal recessive digenic multisystem disorder characterized by global developmental delay with impaired intellectual development, onset of bone marrow failure and myelodysplastic syndrome (MDS) in childhood, and poor overall growth with short stature (summary by Oka et al., 2020). For a discussion of genetic heterogeneity of bone marrow failure syndrome (BMFS), see BMFS1 (614675).
Erythroleukemia, familial, susceptibility to
MedGen UID:
1790819
Concept ID:
C5552985
Finding
Familial erythroleukemia is a leukemic or preleukemic state in which red cell proliferation is the predominant feature. Hematologic characteristics include particularly ineffective and hyperplastic erythropoiesis with megaloblastic components accompanied by myeloblastic proliferation of varying degree (Park et al., 2002). Park et al. (2002) discussed the evolution of the definition of 'erythroleukemia,' which is considered by most to be a subtype of acute myelogenous leukemia (AML; 601626). Controversy about the precise definition of erythroleukemia revolves around the number or percentage of erythroblasts and myeloblasts found in the bone marrow and peripheral circulation. In the French-American-British (FAB) classification system (Bennett et al., 1985), it is known as AML-M6, whereas in the revised World Health Organization (WHO) classification system (Harris et al., 1999), it is known as 'AML, not otherwise categorized' (Zini and D'Onofrio, 2004).
Tumor predisposition syndrome 2
MedGen UID:
1823959
Concept ID:
C5774186
Disease or Syndrome
Tumor predisposition syndrome-2 (TPDS2) is an autosomal recessive cancer predisposition syndrome characterized by the onset of various types of tumors or malignancies in young adulthood. The most common clinical manifestations include acute myeloid leukemia (AML), myelodysplastic syndrome, colorectal adenomatous polyposis and carcinoma, and uveal melanoma, although other tumors and malignancies have been reported (summary by Palles et al., 2022). For a discussion of genetic heterogeneity of TPDS, see TPDS1 (614327).

Professional guidelines

PubMed

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NCCN Clinical Practice Guidelines in Oncology (NCCN Guidelines®) Acute Lymphoblastic Leukemia, 2024

NCCN Clinical Practice Guidelines in Oncology (NCCN Guidelines®) Acute Myeloid Leukemia, 2023

Recent clinical studies

Etiology

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Therapy

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Prognosis

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Clinical prediction guides

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Golub TR, Slonim DK, Tamayo P, Huard C, Gaasenbeek M, Mesirov JP, Coller H, Loh ML, Downing JR, Caligiuri MA, Bloomfield CD, Lander ES
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Recent systematic reviews

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Heuser M, Fernandez C, Hauch O, Klibanov OM, Chaudhary T, Rives V
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Stemler J, de Jonge N, Skoetz N, Sinkó J, Brüggemann RJ, Busca A, Ben-Ami R, Ráčil Z, Piechotta V, Lewis R, Cornely OA
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Smith TJ, Bohlke K, Lyman GH, Carson KR, Crawford J, Cross SJ, Goldberg JM, Khatcheressian JL, Leighl NB, Perkins CL, Somlo G, Wade JL, Wozniak AJ, Armitage JO; American Society of Clinical Oncology
J Clin Oncol 2015 Oct 1;33(28):3199-212. Epub 2015 Jul 13 doi: 10.1200/JCO.2015.62.3488. PMID: 26169616

Supplemental Content

Table of contents

    Clinical resources

    Practice guidelines

    • PubMed
      See practice and clinical guidelines in PubMed. The search results may include broader topics and may not capture all published guidelines. See the FAQ for details.
    • Bookshelf
      See practice and clinical guidelines in NCBI Bookshelf. The search results may include broader topics and may not capture all published guidelines. See the FAQ for details.

    Curated

    • NCCN, 2024
      NCCN Clinical Practice Guidelines in Oncology (NCCN Guidelines®) Acute Lymphoblastic Leukemia, 2024
    • NCCN, 2023
      NCCN Clinical Practice Guidelines in Oncology (NCCN Guidelines®) Acute Myeloid Leukemia, 2023
    • NCCN, 2011
      NCCN Task Force report: Evaluating the clinical utility of tumor markers in oncology.

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