Monitoring M-BCR-ABL expression level in CML patients by RQ-PCR: experience of a single Center

Department of Pathology, Faculty of General Medicine, University of Medicine and Pharmacy of Targu Mures, Romania
Romanian journal of morphology and embryology = Revue roumaine de morphologie et embryologie (Impact Factor: 0.66). 03/2013; 54(1):37-42.
Source: PubMed


Chronic myelogenous leukemia (CML) is characterized by the Philadelphia chromosome and the BCR-ABL fusion gene that encodes an abnormal tyrosine kinase. Development of specific tyrosine kinase inhibitors completely changed the management of these patients.

Materials and methods:
Between April 2008 and July 2012, at the Molecular Biology Laboratory, University of Medicine and Pharmacy of Targu Mures, Romania, we monitored the M-BCR-ABL transcript level by real time quantitative PCR in case of 15 CML patients diagnosed at the Hematology and Transplant Center of Targu Mures.

Modification of M-BCR-ABL expression level shows statistically significant correlation (p=0.013) with the clinical course of these patients.

Molecular biology techniques have an important role in monitoring CML patients and regular analysis is recommended.

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    ABSTRACT: The Philadelphia chromosome and the resulting BCR-ABL fusion gene represent the hallmark event in chronic myeloid leukemia (CML) and their discoveries radically changed the management of these patients. Currently Wilms tumor 1 gene (WT1) is intensively investigated as high WT1 expression levels have been demonstrated in case of multiple solid tumors and malignant hematological syndromes (acute myeloid and lymphoid leukemia, myelodysplastic syndromes and chronic myeloid leukemia). The aim of our study was to investigate the WT1 expression in CML patients and its possible contribution to disease evolution. Patients and Methods: In the Laboratory of Molecular Biology, University of Medicine and Pharmacy of Tirgu Mures, Romania, we regularly determined the M-BCR-ABL and WT1 expression levels by RQ-PCR (real-time quantitative polymerase chain reaction) testing in case of 19 CML patients: six patients monitorized from the diagnosis and 13 patients first tested during therapy. Results: Eight CML (four advanced stage and four CP) patients showed high WT1 expression level, and in case of 11 patients the WT1 expression levels were undetectable or lower than 0.02%. The only significant difference between the high and low WT1 expression groups was represented by the clinical stage. In the majority of pretreated patients (10 out of 13 patients), the WT1 expression levels were low or undetectable. Conclusions: High WT1 expression in CML patients is detected especially in the advanced stages of the disease. Efficient Imatinib therapy may contribute to low WT1 levels in CP patients.