Abstract

Objective: Quantification of the BCR-ABL transcript is recommended to follow-up CML patients that treated by Imatinib mesylate (IM) as a tyrosine kinase inhibitor. BCR-ABL transcripts have been recognized as a molecular marker for response to therapy in CML patients (pts). Monitoring of this marker to be more effective for identifying optimal responses and can help to inform the decision to switch to alternative therapies. Quantitative reverse transcriptase PCR (Q-PCR) of BCR-ABL1 RNA is a critical laboratory technique for accurate and sensitive monitoring of the efficiency of tyrosine kinase inhibitor therapy. The aim of our study was to analyze the molecular response (MR) in Kurdish CML patients who are treated with Imatinib.Materials and Methods: We studied 60 blood samples from CML patients in chronic phase (CP), 36 females and 24 males, under IM treatment and monitored by Q-PCR on 12 months. The median duration of CML was 5 years (range: 1-15). The median duration of IM treatment was 4 years (range: 1-10). Results: 40% (24 pts), 28.33% (17 pts) and 15% (9 pts) and respectively had reached early molecular response (EMR) at 1.0-2.0 log, major molecular response (MMR) at 3.0 log and deep molecular response (DMR) at 4.0-5.0 log and also undetectable BCR‑ABL1 levels (CMR) were achieved in 16.67% (10 pts) at 12 months.Conclusion: We highlighted the possibility to use of Q-PCR as a warning at diagnosis, and may use to identify patients who could benefit from a more scrupulous follow-up.

Highlights

  • Chronic myeloid leukemia (CML) is a hematologic stem cells disorder that determined by increased of myeloid cells in the bone marrow, spleen and peripheral blood [1,2]

  • For the purpose of targeted therapy for patients with chronic myeloid leukemia (CML), monitoring is vital for optimizing treatment and affordable results

  • Since 2001 the Imatinib treatment has been used as a front-line therapy in CML patients [7]

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Summary

Introduction

Chronic myeloid leukemia (CML) is a hematologic stem cells disorder that determined by increased of myeloid cells in the bone marrow, spleen and peripheral blood [1,2]. Ph is found in more than 90% of CML patients and typically leads to p210 kDa BCR-ABL as a chimeric fusion protein [5,6]. This fusion protein is an active tyrosine kinase that is the cause of CML disorder [1,2,3,4,5,6]. Since the advent of BCR-ABL1 tyrosine kinase inhibitors (TKIs), patients with CML have significantly improved overall survival (OS) and lower rates of disease progressions compared with conventional therapies [7,8,9].

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