1.Minimal Residual Disease Status in Childhood Acute Lymphoblastic Leukaemias by Flow Cytometry and Their Clinical and Haematological Features
Azma RZ ; Zarina AL ; Hamidah A ; Cheong SK ; Jamal R ; Hamidah NH
Medicine and Health 2010;5(1):22-33
Residual disease in patients with acute leukaemia indicates unfavorable prognosis. The evaluation of remission using flow cytometry allows a better estimation of minimal residual disease (MRD) after induction chemotherapy in childhood acute lymphoblastic
leukaemia (ALL) cases. Patients in morphological marrow remission with presence of blast cells of less than 5%, may still have up to 1010 leukaemic cells. However with flow cytometric analysis, lower levels of the residual leukaemic cells (1 in 104 cells) can be detected and it can be used as a tool to predict relapse. This study compared the presenting clinical and haematological features of children with ALL and their residual
disease status determined by flow cytometry. Analysis of their MRD status following remission-induction chemotherapy were done at day-28, week-12 and week-20. The
cases were also followed up to five years, to determine their survival status. Their residual disease status by flow cytometric immunophenotyping was also compared
with their bone marrow findings morphologically. Thirty-eight cases of precursor B-ALL in pediatric patients from UKM Medical Centre (UKMMC) were analyzed. There was no
significant correlation between demographic, clinical and haematological features with MRD status at day-28. However, there was a significant correlation between MRD
status by flow cytometry and by morphological marrow examination at week-12. Three cases showed persistent MRD findings until week-20 where two of the cases relapsed
and died subsequently. Twenty four patients were still alive after five years of follow up.
2.Juvenile myelomonocytic leukaemia: a case series
RZ Azma ; AL Zarina ; A Hamidah ; R Jamal ; NA Sharifah ; O Ainoon ; NH Hamidah
The Malaysian Journal of Pathology 2009;31(2):121-128
Juvenile myelomonocytic leukaemia (JMML), previously known as juvenile chronic myeloid leukaemia
(JCML) is a rare, myelodysplastic – myeloproliferative disease typically presenting in early childhood.
This disorder is diffi cult to distinguish from other myeloproliferative syndrome such as chronic
myeloid leukaemia (CML) because of the similarities in their clinical and bone marrow fi ndings.
However, because of its unique biological characteristics such as absolute monocytosis with dysplasia,
absence of Philadelphia chromosome or BCR-ABL fusion protein, hypergammaglobulinaemia and
raised fetal haemoglobin level, this disorder does not satisfy the criteria for inclusion in the CML
or chronic myelomonocytic leukaemia (CMML) group, as seen in adult patients. We describe a
series of three patients with JMML, who had almost similar clinical and laboratory fi ndings, and
discuss the diffi culty in the classifi cation and treatment of the disease.
3.Real-time quantifi cation for BCR-ABL transcripts in chronic myeloid leukaemia patients in UKMMC, Malaysia
FL Wong ; NH Hamidah ; AA Hawa ; AN Nurul ; CF Leong ; SAW Fadilah ; O Ainoon
The Malaysian Journal of Pathology 2011;33(2):107-112
Molecular pathogenesis of chronic myeloid leukemia (CML) is well established and molecular
monitoring for patients with CML has become an important practice in the management of patients
on imatinib therapy. In the present study, we report the use of RQ-PCR method for detection of
BCR-ABL fusion gene for our CML cases. We performed a two-step RQ-PCR on bone marrow
aspirates or peripheral blood of 37 CML patients. Quantitative expression of BCR-ABL fusion
gene was carried out relative to the expression of a housekeeping gene as endogenous control to
compensate for uneven cell numbers, RNA quality, or variations in reverse transcription effi ciencies.
Twenty-four of these patients were pre-treated with hydroxyurea or alpha interferon prior to the
imatinib therapy. Their BCR-ABL fusion gene levels were monitored for 18 months. All samples
processed were evaluable. The PCR amplifi cation effi ciency of the ABL gene is 90.5% (0.2158)
and the BCR-ABL gene, 93.4% (0.1573).