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AML to DCMA CME Committee Acute Myeloid Leukemia with t(8;21) Translocation and Rare Myelodysplastic Features By Richard Chiu, D.O.,1,2 Rudolf Estess, D.O.,2 Hadi Yaziji, M.D.,1,3 and Farhad Askarian, M.D.1,3 1Department of Pathology, Larkin Community Hospital, Miami, FL 33012 2Department of Family Medicine, Larkin Community Hospital, Miami, FL 33012 3Vitro Molecular Laboratories, Miami, FL 33174 Address correspondence to: Richard Chiu, D.O. Larkin Community Hospital Palm Springs Campus Department of Pathology 1475 W. 49th Place, Hialeah, FL 33012 Phone: (626) 493-3540 Email: [email protected] Abstract Acute myeloid leukemia (AML) is a diverse group of hematologic malignancies characterized by uncontrolled proliferation of early myeloid progenitors, a process which impairs bone marrow hematopoiesis. The disease is driven by multiple cytogenetic abnormalities and mutations which affect its clinical course and prognosis, and the disease may arise from a pre-existing background of myelodysplastic syndrome (MDS). In this report, the authors describe a 74-year-old Hispanic man presenting with fatigue and weakness, and labs showing leukocytosis (WBC 29.8), macrocytic anemia, and thrombocytopenia. His blood smear revealed myeloblasts with Auer rods, and his bone marrow cellularity on both core biopsy and flow cytometry, consisted of 22-23% myeloblasts positive for CD34 and CD117. His cytogenetic profile was positive for t(8;21)(q22;q22) translocation and Y chromosome loss. Despite lacking MDS-related cytogenetic findings, myelodysplastic features of pseudo-Pelger-Huet neutrophils, erythroblasts with nuclear budding and megaloblastoid form, ringed sideroblasts, and macrocytic red cells were observed in his bone marrow and blood smear. His molecular profile was negative for mutations in FLT3 and IDH, precluding him for targeted therapy against those mutations. The patient was diagnosed with AML and started on CPX-351 (Vyxeos) involving a combination of cytarabine and daunorubicin for induction chemotherapy. This is a noteworthy AML case given the co-occurrence of the conventional t(8;21) translocation portending favorable prognosis, with myelodysplastic changes portending a poorer prognosis. Keywords: acute myeloid (myelogenous) leukemia, t(8;21) translocation, myelodysplastic syndrome, myeloblasts, cytarabine, daunorubicin, CPX-351 (Vyxeos) Introduction Acute myeloid leukemia is a heterogeneous group of malignancies characterized by clonal proliferation of early myeloid progenitors with impaired ability to differentiate.1 The leukemic myeloid progenitors accumulate in the bone marrow and impede production of normal blood cells, causing anemia and thrombocytopenia, and recurrent infection from dysfunctional granulocytes.2 The disease may arise as a primary, de novo cancer, or as a cancer secondary to prior chemotherapy or underlying pre-leukemic disease, such as myelodysplastic syndrome (MDS).3 AML has multiple subtypes defined by their cytogenetic and molecular profiles, which dictate their prognosis and treatment.3 The World Health Organization (WHO) chiefly classifies AML into four groups: AML with recurrent genetic abnormalities, AML with myelodysplasia- related changes, AML secondary to therapy, and AML not otherwise specified (based on the older FAB system).4 Diagnosis of AML is made by demonstrating í 20% myeloblasts in bone marrow or peripheral blood, or by demonstrating Auer rods or one of the three AML-defining translocations: t(8;21), t(15;17), and inv(16).2 AML arising from a pre-leukemic background of myelodysplastic syndrome harbors a different set of cytogenetic abnormalities associated with poorer outcomes than primary, de novo AML.1,3 The prognosis of AML is influenced by their cytogenetic and mutational profiles.1,5 Good prognosis is conferred by translocations t(8;21), t(15;17), and inv(16),1,6 while poor prognosis is conferred by translocations inv(3), t(6;9), and t(9;22), deletions/monosomies of chromosomes 5 and 7, and complex karyotypes.3,5 Prognosis is also affected by multiple mutations, such as those involving fms-like tyrosine kinase 3 (FLT3) and isocitrate dehydrogenase (IDH), which currently serve as new targets of therapy. Table 1 lists the most commonly found cytogenetic changes and mutations in AML, with their associated functions and prognoses. The standard treatment for AML consists of a regimen of cytarabine and daunorubicin,1 which more recently have been given as a liposomal formulation (CPX-351/Vyxeos) to patients with AML secondary to prior chemotherapy or hematologic malignancy like MDS.3,7 Targeted therapy against CD33 (gemtuzumab/ozogamicin), mutated FLT3 (e.g., midostaurin, sorafenib), or mutated IDH (e.g., ivosidenib, enasidenib) can also be added to the regimen if the patient tests positive for these mutations.3,5,8 If complete remission is achieved with induction chemotherapy, hematopoietic stem cell transplantation can be administered to qualifying patients with the intent to cure.7 Case Presentation The patient is a 74-year-old Hispanic man referred to Larkin Palm Springs Hospital by his primary physician after his lab work showed leukocytosis (WBC 29.8), macrocytic anemia (Hgb 6.7, Hct 20, MCV 109), and thrombocytopenia (Plt 44). He reported experiencing fatigue and weakness but denied fever, chills, night sweats, weight loss, bruising or bleeding, skin rashes, or body pain. Physical exam revealed some pallor, but no cachexia or lymphadenopathy. He denied smoking, prior chemotherapy, and family history of cancers or blood disorders. The patient had concurrent type 2 non-ST segment elevation myocardial infarction (NSTEMI) due to cardiac ischemia from his anemia, with elevated troponins (2.20) but no ST changes on EKG or concurrent chest pain. Chest x-ray and abdominal CT scan were unremarkable. Table 2 presents the patient’s laboratory results from his hospital stay. The patient’s CBC showed elevated monocytes (45.5%, 13.58 x 103/uL), immature granulocytes (13.8%, 4.13 x 103/uL), and nucleated RBCs (0.06 x 103/uL), with low neutrophil percent (17%). Given these findings, a diagnosis of chronic myelomonocytic leukemia was initially favored, but a manual differential count of the peripheral blood smear instead revealed a significant presence of blasts (>50% of white count) and normal monocyte percentage (5%). Several blasts on blood smear showed Auer rods (Figure 1), characteristic of acute myeloid leukemia. Red cells and platelets were morphologically normal. The monocytosis initially shown by CBC, was caused by the automated hematology analyzer misinterpreting the blasts as monocytes (Table 2). Bone marrow core biopsy showed hypercellular marrow (95%) for the patient’s age, and its 500-cell differential count showed excess myeloblasts positive for CD34 and CD117 comprising 22% of bone marrow cellularity (Figure 2A-C). The differential cell count also revealed left-shifted myeloid spectrum with 14% promyelocytes, 19% myelocytes, and 15% mature granulocytes; in contrast, monocytes consisted of only 1% of the marrow cell population. Flow cytometry performed on the bone marrow aspirate showed a similar cell distribution as the manual differential count, with myeloblasts (Figure 3A) positive for CD34, CD117, and HLA- DR comprising 23% of bone marrow cellularity. A few neutrophils in the bone marrow showed pseudo-Pelger-Huet anomaly (Figure 3B), but no hypersegmentation or toxic granulation was observed. The bone marrow core yielded a high myeloid-erythroid ratio of 5:1, with erythroid precursors accounting for 15% of its cellularity. The erythroid precursors exhibited normal maturation, but rare cells with nuclear budding, megaloblastoid forms, karyorrhexis, and bi- lobed nuclei (Figure 3C-F) were also seen, as were sideroblasts and iron-laden erythroid progenitors (Figure 2D) on Prussian blue stain. Red cells showed anisocytosis with elevated RDW-SD (70.2), but no poikilocytosis was seen on blood smear, and reticulocyte count and percentage were within normal range. Reticulin stain of bone marrow did not reveal increased marrow fibrosis. Megakaryocytes were present in normal numbers and morphology. Cytogenetic analysis revealed the presence of the t(8;21)(q22;q22) translocation, a commonly seen chromosomal rearrangement in AML that carries relatively favorable prognosis, and loss of Y chromosome (45X,-Y) in all 20 karyotyped cells. To determine if the myeloblasts developed from a prior background of myelodysplastic syndrome (MDS), fluorescence in situ hybridization was conducted on some of the most commonly seen cytogenetic abnormalities in MDS – inv(3), del(5q), del(7q), monosomy 5 and 7, trisomy 8, del(17p), del(20q), and 11q23 – which returned negative. In addition, no mutations were detected in isocitrate dehydrogenase (IDH1 and IDH2 isoforms) and FMS-like tyrosine kinase 3 (FLT3-ITD, FLT3-TKD) genes which carry prognostic significance in AML. To assess for monoclonal gammopathy, serum protein electrophoresis with immunofixation was performed on the patient’s serum, which revealed normal quantities of albumin, globulin, kappa and lambda light chains, normal albumin/globulin and kappa/lambda ratios, and absence of M-spike. To rule out iron, folate, or vitamin B12 deficiency, or fecal occult bleeding as causes of the patient’s anemia, additional lab tests were performed which revealed normal levels of iron, transferrin, transferrin saturation, vitamin B12, and folate. Fecal occult blood test was negative. Due to risk of tumor lysis syndrome, disseminated intravascular coagulation, and hyperviscosity
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