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Rethink the potential of your secondary AML (sAML) patients

Diagnosed secondary AML patient who is ready to beat their disease

sAML has been historically associated with poor outcomes.1 It is important to properly identify sAML and consider a treatment plan with curative intent for appropriate patients. Treating these patients with chemotherapy plus HSCT is an opportunity to improve outcomes2,3

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With the rising incidence of sAML, it is important to be able to properly identify 2 different subtypes4-6:

  • AML with myelodysplasia‑related changes (AML‑MRC)
    • Antecedent MDS or MDS/MPN
    • MDS-related cytogenetic abnormalities
    • Multilineage dysplasiaa
  • Therapy‑related AML (t‑AML)
1/3 of sAML patients

sAML subtypes AML‑MRC and t‑AML make up approximately 1/3 of AML cases7,8

Double Helix DNA

While some sAML patients can be diagnosed by obtaining a thorough medical history, a majority of AML‑MRC patients have genetic alterations that require identification through additional testing.9 This may include cytogenetic analysis (karyotype) as well as molecular genetic and/or FISH testing10

Chemotherapy can provide the opportunity for appropriate sAML patients to receive HSCT—a treatment approach with curative intent2,3

  1. Dysplasia present in ≥50% of cells in at least 2 cell lines, unless an NPM1 mutation or biallelic mutation of CEBPA is present.5,6

AML=acute myeloid leukemia; FISH=fluorescent in situ hybridization; HSCT=hematopoietic stem cell transplant; MDS=myelodysplastic syndromes; MPN=myeloproliferative neoplasms.

References: 1. Granfeldt Østgård LS, Medeiros BC, Sengeløv H, et al. Epidemiology and clinical significance of secondary and therapy-related acute myeloid leukemia: a national population-based cohort study. J Clin Oncol. 2015;33(31):3641-3649. 2. Wang ES. Treating acute myeloid leukemia in older adults. Hematology Am Soc Hematol Educ Program. 2014;2014(1):14-20. 3. Lipof JJ, Loh KP, O’Dwyer K, et al. Allogeneic hematopoietic cell transplantation for older adults with acute myeloid leukemia. Cancers (Basel). 2018;10(6):179. 4. Ossenkoppele G, Montesinos P. Challenges in the diagnosis and treatment of secondary acute myeloid leukemia. Crit Rev Oncol Hematol. 2019;138:6-13. 5. Arber DA, Orazi A, Hasserjian R, et al. The 2016 revision to the World Health Organization classification of myeloid neoplasms and acute leukemia. Blood. 2016;127(20):2391-2405. 6. Vardiman JW, Thiele J, Arber DA, et al. The 2008 revision of the World Health Organization (WHO) classification of myeloid neoplasms and acute leukemia: rationale and important changes. Blood. 2009;114(5):937-951. 7. Nagel G, Weber D, Fromm E, et al; German Austrian AML Study Group (AMLSG). Epidemiological, genetic, and clinical characterization by age of newly diagnosed acute myeloid leukemia based on an academic population-based registry study (AMLSG BiO). Ann Hematol. 2017;96(12):1993-2003. 8. Leone G, Mele L, Pulsoni A, et al. The incidence of secondary leukemias. Haematologica. 1999;84(10):937-945. 9. Miesner M, Haferlach C, Bacher U, et al. Multilineage dysplasia (MLD) in acute myeloid leukemia (AML) correlates with MDS‑related cytogenetic abnormalities and a prior history of MDS or MDS/MPN but has no independent prognostic relevance: a comparison of 408 cases classified as “AML not otherwise specified” (AML-NOS) or “AML with myelodysplasia-related changes” (AML-MRC). Blood. 2010;116(15):2742-2751. 10. Arber DA, Borowitz MJ, Cessna M, et al. Initial diagnostic workup of acute leukemia: guideline from the College of American Pathologists and the American Society of Hematology. Arch Pathol Lab Med. 2017;141(10):1342-1393.