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Acute myeloid leukemia(AML)

MedGen UID:
9730
Concept ID:
C0023467
Neoplastic Process
Synonyms: Acute granulocytic leukemia; Acute myeloblastic leukemia; Acute myelocytic 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); Acute non-lymphocytic leukemia (17788007); Acute myeloid leukemia (413443009); AML - Acute myeloblastic leukemia (91861009); Acute myeloid leukemia - category (413443009); Acute myeloid leukemia, no ICD-O subtype (17788007); Acute myelocytic leukemia (91861009); Acute myeloid leukemia, no International Classification of Diseases for Oncology subtype (17788007); Acute granulocytic leukemia (17788007); Acute myelogenous leukemia (17788007); Acute myeloblastic leukemia (17788007); Acute myelocytic leukemia (17788007); AML - Acute myeloid leukemia (91861009); Acute myeloid leukemia, disease (91861009)
Modes of inheritance:
Autosomal dominant inheritance
MedGen UID:
141047
Concept ID:
C0443147
Intellectual Product
Sources: HPO, OMIM
A mode of inheritance that is observed for traits related to a gene encoded on one of the autosomes (i.e., the human chromosomes 1-22) in which a trait manifests in heterozygotes. In the context of medical genetics, an autosomal dominant disorder is caused when a single copy of the mutant allele is present. Males and females are affected equally, and can both transmit the disorder with a risk of 50% for each child of inheriting the mutant allele.
Somatic mutation
MedGen UID:
107465
Concept ID:
C0544886
Cell or Molecular Dysfunction
Sources: HPO, OMIM
A mode of inheritance in which a trait or disorder results from a de novo mutation occurring after conception, rather than being inherited from a preceding generation.
Somatic mutation (HPO, OMIM)
 
Genes (locations): CBFB (16q22.1); 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
OMIM®: 601626
Orphanet: ORPHA519

Definition

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 GeneReviews]

Additional descriptions

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.\n\nPeople 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.\n\nWhile 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.\n\nPeople 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.\n\nWhile 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.\n\nPeople 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.\n\nThe 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
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.
Acute myeloid leukemia
MedGen UID:
9730
Concept ID:
C0023467
Neoplastic Process
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.
Acute myeloid leukemia
MedGen UID:
9730
Concept ID:
C0023467
Neoplastic Process
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.

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
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.
Dyskeratosis congenita, X-linked
MedGen UID:
216941
Concept ID:
C1148551
Disease or Syndrome
Dyskeratosis congenita (DC), a telomere biology disorder, is characterized by a classic triad of dysplastic nails, lacy reticular pigmentation of the upper chest and/or neck, and oral leukoplakia. The classic triad may not be present in all individuals. People with DC are at increased risk for progressive bone marrow failure (BMF), myelodysplastic syndrome (MDS) or acute myelogenous leukemia (AML), solid tumors (usually squamous cell carcinoma of the head/neck or anogenital cancer), and pulmonary fibrosis. Other findings can include: abnormal pigmentation changes not restricted to the upper chest and neck, eye abnormalities (epiphora, blepharitis, sparse eyelashes, ectropion, entropion, trichiasis), and dental abnormalities (caries, periodontal disease, taurodauntism). Although most persons with DC have normal psychomotor development and normal neurologic function, significant developmental delay is present in the two variants in which additional findings include cerebellar hypoplasia (Hoyeraal Hreidarsson syndrome) and bilateral exudative retinopathy and intracranial calcifications (Revesz syndrome). Onset and progression of manifestations of DC 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.
Familial platelet disorder with associated myeloid malignancy
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).
Myelodysplasia, immunodeficiency, facial dysmorphism, short stature, and psychomotor delay
MedGen UID:
318627
Concept ID:
C1832442
Disease or Syndrome
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.
Neutropenia, nonimmune chronic idiopathic, 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).
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
Myeloproliferative/lymphoproliferative neoplasms, familial (multiple types), susceptibility to
MedGen UID:
895780
Concept ID:
C4225174
Finding
Familial myeloproliferative/lymphoproliferative neoplasms is an autosomal dominant cancer predisposition syndrome characterized by adult-onset of hematologic malignancies mainly affecting the myeloid line. Most patients present with myelodysplastic syndrome (MDS; 614286) and/or acute myeloid leukemia (AML; 601626). Rare lymphoid malignancies, including lymphoma, can also occur. Some mutation carriers, even if unaffected by a hematologic malignancy, may have evidence of immune dysregulation disorders, including asthma, eczema, or juvenile arthritis. The disorder shows incomplete penetrance (summary by Lewinsohn et al., 2016). Patients may show a favorable response to treatment with lenalidomide (summary by Polprasert et al., 2015).
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.
Acute erythroleukemia, familial
MedGen UID:
1648472
Concept ID:
C4746575
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).
Monosomy 7 of bone marrow
MedGen UID:
1731846
Concept ID:
C5435704
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.
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).

Professional guidelines

PubMed

Fey MF, Buske C; ESMO Guidelines Working Group.
Ann Oncol 2013 Oct;24 Suppl 6:vi138-43. Epub 2013 Aug 22 doi: 10.1093/annonc/mdt320. PMID: 23970018
Febbo PG, Ladanyi M, Aldape KD, De Marzo AM, Hammond ME, Hayes DF, Iafrate AJ, Kelley RK, Marcucci G, Ogino S, Pao W, Sgroi DC, Birkeland ML
J Natl Compr Canc Netw 2011 Nov;9 Suppl 5:S1-32; quiz S33. doi: 10.6004/jnccn.2011.0137. PMID: 22138009

Recent clinical studies

Etiology

Heuser M, Smith BD, Fiedler W, Sekeres MA, Montesinos P, Leber B, Merchant A, Papayannidis C, Pérez-Simón JA, Hoang CJ, O'Brien T, Ma WW, Zeremski M, O'Connell A, Chan G, Cortes JE
Ann Hematol 2021 May;100(5):1181-1194. Epub 2021 Mar 19 doi: 10.1007/s00277-021-04465-4. PMID: 33740113Free PMC Article
Zhou J, Yiying Quah J, Ng Y, Chooi JY, Hui-Min Toh S, Lin B, Zea Tan T, Hosoi H, Osato M, Seet Q, Ooi LAG, Lindmark B, McHale M, Chng WJ
Haematologica 2020 Sep 1;105(9):2286-2297. doi: 10.3324/haematol.2019.230482. [Epub ahead of print] PMID: 33054053Free PMC Article
Rea B, Aggarwal N, Yatsenko SA, Bailey N, Liu YC
Mod Pathol 2020 Apr;33(4):566-575. Epub 2019 Nov 4 doi: 10.1038/s41379-019-0396-4. PMID: 31685963
Mast KJ, Taub JW, Alonzo TA, Gamis AS, Mosse CA, Mathew P, Berman JN, Wang YC, Jones HM, Campana D, Coustan-Smith E, Raimondi SC, Hirsch B, Hitzler JK, Head DR
Arch Pathol Lab Med 2020 Apr;144(4):466-472. Epub 2019 Aug 20 doi: 10.5858/arpa.2018-0526-OA. PMID: 31429606Free PMC Article
Weinberg OK, Hasserjian RP, Baraban E, Ok CY, Geyer JT, Philip JKSS, Kurzer JH, Rogers HJ, Nardi V, Stone RM, Garcia JS, Hsi ED, Bagg A, Wang SA, Orazi A, Arber DA
Mod Pathol 2019 Sep;32(9):1373-1385. Epub 2019 Apr 18 doi: 10.1038/s41379-019-0263-3. PMID: 31000771

Diagnosis

Maral S, Albayrak M, Sahin O, Ozturk HBA, Han U, Falay M
J Oncol Pharm Pract 2021 Mar;27(2):464-469. Epub 2020 Jun 17 doi: 10.1177/1078155220932352. PMID: 33620259
Rea B, Aggarwal N, Yatsenko SA, Bailey N, Liu YC
Mod Pathol 2020 Apr;33(4):566-575. Epub 2019 Nov 4 doi: 10.1038/s41379-019-0396-4. PMID: 31685963
Mast KJ, Taub JW, Alonzo TA, Gamis AS, Mosse CA, Mathew P, Berman JN, Wang YC, Jones HM, Campana D, Coustan-Smith E, Raimondi SC, Hirsch B, Hitzler JK, Head DR
Arch Pathol Lab Med 2020 Apr;144(4):466-472. Epub 2019 Aug 20 doi: 10.5858/arpa.2018-0526-OA. PMID: 31429606Free PMC Article
Liu F, Knight T, Su Y, Edwards H, Wang G, Wang Y, Taub JW, Lin H, Sun L, Ge Y
Target Oncol 2019 Jun;14(3):351-364. doi: 10.1007/s11523-019-00638-4. PMID: 31115744
Weinberg OK, Hasserjian RP, Baraban E, Ok CY, Geyer JT, Philip JKSS, Kurzer JH, Rogers HJ, Nardi V, Stone RM, Garcia JS, Hsi ED, Bagg A, Wang SA, Orazi A, Arber DA
Mod Pathol 2019 Sep;32(9):1373-1385. Epub 2019 Apr 18 doi: 10.1038/s41379-019-0263-3. PMID: 31000771

Therapy

Heuser M, Smith BD, Fiedler W, Sekeres MA, Montesinos P, Leber B, Merchant A, Papayannidis C, Pérez-Simón JA, Hoang CJ, O'Brien T, Ma WW, Zeremski M, O'Connell A, Chan G, Cortes JE
Ann Hematol 2021 May;100(5):1181-1194. Epub 2021 Mar 19 doi: 10.1007/s00277-021-04465-4. PMID: 33740113Free PMC Article
Maral S, Albayrak M, Sahin O, Ozturk HBA, Han U, Falay M
J Oncol Pharm Pract 2021 Mar;27(2):464-469. Epub 2020 Jun 17 doi: 10.1177/1078155220932352. PMID: 33620259
Yee K, Papayannidis C, Vey N, Dickinson MJ, Kelly KR, Assouline S, Kasner M, Seiter K, Drummond MW, Yoon SS, Lee JH, Blotner S, Jukofsky L, Pierceall WE, Zhi J, Simon S, Higgins B, Nichols G, Monnet A, Muehlbauer S, Ott M, Chen LC, Martinelli G
Leuk Res 2021 Jan;100:106489. Epub 2020 Dec 1 doi: 10.1016/j.leukres.2020.106489. PMID: 33302031
Zhou J, Yiying Quah J, Ng Y, Chooi JY, Hui-Min Toh S, Lin B, Zea Tan T, Hosoi H, Osato M, Seet Q, Ooi LAG, Lindmark B, McHale M, Chng WJ
Haematologica 2020 Sep 1;105(9):2286-2297. doi: 10.3324/haematol.2019.230482. [Epub ahead of print] PMID: 33054053Free PMC Article
Mani R, Goswami S, Gopalakrishnan B, Ramaswamy R, Wasmuth R, Tran M, Mo X, Gordon A, Bucci D, Lucas DM, Mims A, Brooks C, Dorrance A, Walker A, Blum W, Byrd JC, Lozanski G, Vasu S, Muthusamy N
Haematologica 2018 Aug;103(8):1288-1297. Epub 2018 May 17 doi: 10.3324/haematol.2018.188193. PMID: 29773600Free PMC Article

Prognosis

Maral S, Albayrak M, Sahin O, Ozturk HBA, Han U, Falay M
J Oncol Pharm Pract 2021 Mar;27(2):464-469. Epub 2020 Jun 17 doi: 10.1177/1078155220932352. PMID: 33620259
Yee K, Papayannidis C, Vey N, Dickinson MJ, Kelly KR, Assouline S, Kasner M, Seiter K, Drummond MW, Yoon SS, Lee JH, Blotner S, Jukofsky L, Pierceall WE, Zhi J, Simon S, Higgins B, Nichols G, Monnet A, Muehlbauer S, Ott M, Chen LC, Martinelli G
Leuk Res 2021 Jan;100:106489. Epub 2020 Dec 1 doi: 10.1016/j.leukres.2020.106489. PMID: 33302031
Winer ES
Hematol Oncol Clin North Am 2020 Apr;34(2):449-463. Epub 2020 Jan 7 doi: 10.1016/j.hoc.2019.11.003. PMID: 32089222
Rea B, Aggarwal N, Yatsenko SA, Bailey N, Liu YC
Mod Pathol 2020 Apr;33(4):566-575. Epub 2019 Nov 4 doi: 10.1038/s41379-019-0396-4. PMID: 31685963
Weinberg OK, Hasserjian RP, Baraban E, Ok CY, Geyer JT, Philip JKSS, Kurzer JH, Rogers HJ, Nardi V, Stone RM, Garcia JS, Hsi ED, Bagg A, Wang SA, Orazi A, Arber DA
Mod Pathol 2019 Sep;32(9):1373-1385. Epub 2019 Apr 18 doi: 10.1038/s41379-019-0263-3. PMID: 31000771

Clinical prediction guides

Heuser M, Smith BD, Fiedler W, Sekeres MA, Montesinos P, Leber B, Merchant A, Papayannidis C, Pérez-Simón JA, Hoang CJ, O'Brien T, Ma WW, Zeremski M, O'Connell A, Chan G, Cortes JE
Ann Hematol 2021 May;100(5):1181-1194. Epub 2021 Mar 19 doi: 10.1007/s00277-021-04465-4. PMID: 33740113Free PMC Article
Molinos-Quintana A, Trujillo-Hacha P, Piruat JI, Bejarano-García JA, García-Guerrero E, Pérez-Simón JA, Muñoz M
Invest New Drugs 2019 Feb;37(1):17-26. Epub 2018 May 2 doi: 10.1007/s10637-018-0607-8. PMID: 29721755
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