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A case of indolent AML with five-year survival without treatment

Acute myeloid leukemia (AML) is an aggressive hematologic malignancy, and without treatment, patients rarely live more than one year [1–3]. Here, we describe a patient who presented with AML and despite declining treatment remains alive five years after diagnosis. He is a 71-year old man with no history of hematologic illness who was found on a routine checkup in October 2011 to have hemoglobin (Hb) 11.9, neutrophils (ANC) 1400, platelets (Plt) 132,000 (K) and no peripheral blood (PB) blasts. A bone marrow (BM) was normocellular with 23% blasts by morphology and 41% myeloid blasts by flow cytometry; there was no dysplasia or fibrosis. Cytogenetics showed a loss of the Y chromosome. Given the lack of symptoms, he declined treatment. Two years later, he remained asymptomatic and had received no transfusions and developed no infections. His blood count was worse with Hb 10.7, ANC 500 and Plt 77K. A BM in October 2013 showed 44% blasts by morphology and 36% by flow cytometry. The karyotype was 45, X, -Y[5]/46, XY[15]. Observation continued. By February 2015, counts had declined further with Hb 4.6, ANC 200 and Plt 42K, and red blood cell transfusions began. Remaining largely asymptomatic, he continued to decline treatment of AML and was referred to our clinic in August 2016. Circulating blasts (3%) were seen, with ANC 200 and Plt 29K. A BM showed 29% blasts by morphology and 51% by flow cytometry. Now the clone with chromosome Y deletion disappeared and the karyotype was 46, XY [20]. The chromosome genomic array testing (CGAT) was normal as well. There was no evidence of mutations in ASXL1, CBL, CEBPA, CSF3R, DNMT3A, EZH2, FBXW7, FGFR1, FLT3 p.D835, GATA1, GATA2, HRAS, IDH1 p.R132, IDH2, JAK2, KIT, KRAS, MAP2K1, MLL, MPL, MYD88, NOTCH1, NPM1, NRAS, PDGFRA, PHF6, PTEN, RB1, RUNX1, SF3B1, SRSF2, STAG2, STAT3, TET2, TP53, U2AF1, WT1 and ZRSR2. The patient declined treatment again given his very satisfactory quality of life and his survival of five years, albeit with falling counts. We could find only three case reports of patients with AML achieving long survivals without any treatment like our patient [1–3]. The indolent course of his disease must be due to a suppressor pathway either molecular or immune. While its nature must remain speculative, a clinical lesson is that management of AML should reflect a patient’s symptoms as well as the number of blast cells and that observation might be justified in those, particularly older, patients who largely asymptomatic.