Acute Myeloid Leukemia with BCR-ABL1 Translocation: A Rare
Entity

Jamal I

doi:10.23880/hij-16000186

Haematology International Journal Research Article 1 min read

Acute Myeloid Leukemia with BCR-ABL1 Translocation: A Rare Entity

Jamal I^*

^* Corresponding author

ISSN: 2578-501X 10.23880/hij-16000186 Received: July 06, 2021 Published: July 20, 2021

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Keywords

Leukemia Hematological Malignancies Translocation

Abstract

Acute myeloid leukemia (AML) with BCR-ABL1 is a provisional entity in WHO classification of hematological malignancies and it is a denovo AML in which patients show no evidence of Chronic myeloid leukemia (CML) [1]. It accounts for &lt;1 % of all AMLs and it primarily occurs in adults with male predominance [2]. Patients present with leucocytosis with blast predominance along with anemia and thrombocytopenia. Compared with CML patients less frequently splenomegaly and lower peripheral blood basophilia [3]. Morphological features include presence of peripheral blood and bone marrow myeloblasts showing minimal differentiation to granulocytic maturation. Average bone marrow cellularity is less than CML and dwarf megakaryocytes are also less common.

Introduction

Acute myeloid leukemia (AML) with BCR-ABL1 is a provisional entity in WHO classification of hematological malignancies and it is a denovo AML in which patients show no evidence of Chronic myeloid leukemia (CML) [1]. It accounts for <1 % of all AMLs and it primarily occurs in adults with male predominance [2]. Patients present with leucocytosis with blast predominance along with anemia and thrombocytopenia. Compared with CML patients less frequently splenomegaly and lower peripheral blood basophilia [3]. Morphological features include presence of peripheral blood and bone marrow myeloblasts showing minimal differentiation to granulocytic maturation. Average bone marrow cellularity is less than CML and dwarf megakaryocytes are also less common [2, 3].

Immunophenotypic studies demonstrate expression of CD34, CD13 and CD33 with aberrant expression of CD7, CD19 and Tdt [4]. Genetic profile demonstrates p210 fusion in most cases with few cases showing p190 transcripts. Loss of chromosome 7, gain of chromosome 8 and other complex karyotypes in addition to (9;22)(q34.1;q11.2) are also seen [5]. AML with BCR-ABL1 appears to be an aggressive disease with poor response to traditional AML therapy or tyrosine kinase inhibitor therapy.

References

Papaemmanuil E, Gerstung M, Bullinger L, GaidzikVI, Paschka P, et al. (2016) Genomic classification and prognosis in acute myeloid leukemia. New Engl J Med 374(23): 2209-2221.
Döhner H, Estey E, Grimwade D, Amadori S, Appelbaum FR, et al. (2017) Diagnosis and management of AML in adults: 2017 ELN recommendations from an international expert panel. Blood 129(4): 424-447.
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Neuendorff NR, Burmeister T, Dorken B, Westermann J (2016) BCR-ABL-positive acute myeloid leukemia: a new entity? Analysis of clinical and molecular features. Ann Hematol 95(8): 1211-1221.
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Acute Myeloid Leukemia with BCR-ABL1 Translocation: A Rare Entity

Introduction

References

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