Abstract
Introduction: The hallmark of chronic myeloid leukemia (CML) is the development of the fusion gene, BCR-ABL which has unopposed tyrosine kinase activity. The first tyrosine kinase inhibitor (TKI) imatinib is claimed to have superior efficacy and side effect profile as compared to traditional treatment options. This study was conducted to see our patients’ molecular response to imatinib treatment. The objective of this study was to determine the frequency of complete molecular response in patients after six months of imatinib therapy.Methods: A descriptive case series was designed and conducted in Oncology department, Jinnah hospital Lahore (May-November 2016). Newly diagnosed patients of CML aged between 20 and 65 years were enrolled. They were prescribed 400 mg imatinib daily and complete molecular response was assessed after six months of treatment.Results: Mean age was 39.76 ± 9.072 years. Some 66 of them were males while 69 were females. Some 40 patients (29.6%) were found to be in complete molecular response after six months of imatinib therapy.Conclusion: Imatinib at a dose of 400 mg/day is optimal as the primary therapy for CML.
Highlights
The hallmark of chronic myeloid leukemia (CML) is the development of the fusion gene, BCRABL which has unopposed tyrosine kinase activity
The objective of this study was to determine the frequency of complete molecular response in patients after six months of imatinib therapy
Chronic myeloid leukemia (CML) is a myeloproliferative neoplasm in which translocation between chromosome 9 and 22 leads to the development of a hybrid chromosome 22 called as Philadelphia chromosome
Summary
The hallmark of chronic myeloid leukemia (CML) is the development of the fusion gene, BCRABL which has unopposed tyrosine kinase activity. This study was conducted to see our patients’ molecular response to imatinib treatment. The objective of this study was to determine the frequency of complete molecular response in patients after six months of imatinib therapy. The underlying molecular defect is a fusion gene called BCR-ABL which encodes the oncoprotein BCR-ABL1 ( referred to as p210, p190, p230) with a constitutive active tyrosine kinase activity [1,2]. Tyrosine kinase inhibitor (TKI) therapy has promising response rates in CML [5]. Imatinib mesylate was the prototype drug approved by FDA in 2001 This has revolutionized the treatment of CML from control towards cure [6]. This study was conducted to document response rates in our patients to standard dose of imatinib
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
