Endah Indriastuti, Arifoel Hajat


Introduction : Chronic myelogeneous leukemia (CML) is a myeloproliferative neoplasm that can progress into various conditions. Transformation of CML into acute lymphoblastic leukemia (ALL) is a rare case.


Case :  A 22-year-old male with history of CML since 2014 and positive BCR-ABL p210 in 2017 came with complaint of weakness. Physical examination showed hepatosplenomegaly. CBC results Hb  7.1 g/dL, WBC 290,620/μL, platelet 434,000/μL. Blood smear evaluation (BSE) suggested CML blastic crisis dd AML-M5. Patient’s condition got worse. CBC result showed  WBC 96,770/μL and  platelet 7,000/μL in 2 weeks later. BSE was dominated by mononuclear cells with scanty blue cytoplasm, no granules, no auer rods, loose chromatine and indistinct nucleoli, suggesting lymphoblasts with a proportion of 60%. Bone marrow aspiration (BMA) and immunophenotyping was done to confirm BSE. The BMA result was dominated by lymphoblast, consistent with ALL. The immunophenotyping result was CD10+, CD34+(0,99%), CD79a+, HLA-DR+, and CD20+.  Molecular examination showed positive RUNX1 and NRAS while negative FLT3, NPM1 and del(5q).


Discussion : BCR-ABL gene can be found both in CML and ALL. CML transformation into ALL had been reported to be related with deletion of a transcription gene. Diagnosis of ALL can be established by BMA and immunophenotyping. CD34+ expression of lymphoblast in ALL can be varied, but in this case was minimal.


Conclusion : Patient with history of CML showed an ALL picture based on BSE, BMA and immunophenotyping suggesting CML transformation into ALL although CD34+ expression was minimal.


Chronic myelogeneous leukemia; acute lymphoblastic leukemia; transformation; BCR-ABL

Full Text:



Salesse S, Verfaillie CM. BCR/ABL: from molecular mechanisms of leukemia induction to treatment of chronic myelogenous leukemia. Oncogene. 2002; 21: 8547-59.

Perotti D, Jamieson C, Goldman J. Chronic myeloid leukemia:mechanisms of blastic transformation. J Clin Invest. 2010; 120(7): 2254-64.

Swerdlow SH, Campo E, Harris E, Haris NL, et al, eds. WHO Classification of tumors of haematolopoietic and lymphoid tissue. 4th ed. Lyon: IARC, 2008. Chapter 2; p.32-37

Melo JV. BCR-ABL gene variants. Baillieres Clin Haematology. 1997;10(29): 203-22.

Roche-Lestienne C, Deluche L, Corm S, Tigaud I, Joha S, et al. RUNX1 DNA-binding mutations and RUNX1-PRDM16 cryptic fusions in BCR-ABL+ leukemias are frequently associated with secondary trisomy 21 and may contribute to clonal evolution and imatinib resistance. Blood. 2008; 111(7): 3735-41.

Mullighan CG, Miller CB, Radtke I, Phillips LA, Dalton J, et al. BCR–ABL1 lymphoblastic leukaemia is characterized by the deletion of Ikaros. Nature. 2008; 453:110-113.

Nakayama H, Ishimaru F, Avitahl N, Sezaki N, Fujiji N, et al. Decreases in Ikaros activity correlate with blast crisis in patients with chronic myelogenous leukemia. Cancer Res. 1999;59(16): 3931-34.



  • There are currently no refbacks.