Chronic myeloid leukaemia in the South African public health setting: Are we reaching the European LeukemiaNet targets for frontline therapy?

Tshifhiwa B Sikhipha,Claire L Barrett,Gina Joubert,Jacques L.R Malherbe,Christopher D Viljoen,Shivani Dhar

doi:10.4102/sajo.v4i0.158

Tshifhiwa B Sikhipha, Claire L Barrett + Show 4 more

Open Access

https://doi.org/10.4102/sajo.v4i0.158

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Abstract

Background: Successful therapy of chronic myeloid leukaemia (CML) relies on close monitoring of patients’ response to therapy using the standardised real-time quantitative polymerase chain reaction (RQ-PCR) or fluorescent in situ hybridisation (FISH) at 3, 6 and 12 months. The European LeukemiaNet has published recommended therapeutic targets for frontline therapy at specific time points. Imatinib, a tyrosine kinase inhibitor, is used for the frontline treatment of chronic and accelerated phase CML in our setting. Aim: The aim of this study was to evaluate treatment response of patients with CML in chronic or accelerated phase treated with imatinib during the first 2 years of therapy. Setting: Universitas Academic Hospital, South Africa. Methods: In this analytical cohort study, a retrospective file review of all chronic and accelerated phase CML diagnosed between 2009 and 2016, who were initiated on imatinib as front-line therapy, was performed. Clinical and laboratory data were collected for different time intervals as recommended by European LeukemiaNet guidelines. Results: Thirty-seven patients met the inclusion criteria. An optimal response was obtained in 82.6%, 54.2%, 50.0% and 66.7% of patients at 3, 6, 12 and 18 months, respectively. Conclusion: The patient outcomes were comparable with other published studies, with two-thirds of patients achieving an optimal response at 18 months. It is important, however, that factors contributing to suboptimal responses in the remaining third of patients should be explored.

Highlights

Chronic myeloid leukaemia (CML) is a myeloproliferative neoplasm caused by a translocation between chromosome 9 and 22, denoted as t(9;22)(q34;q11.2), involving the fusion of the breakpoint cluster region (BCR) gene on chromosome 22q11.2 and the Abelson gene (ABL1) on chromosome 9q34
Treatment response to Tyrosine kinase inhibitors (TKI) is monitored by fluorescence in situ hybridisation (FISH) or real-time quantitative reverse transcriptase polymerase chain reaction (RQ-PCR), and specific guidelines have been published on the targets of therapy.[5,6]
Successful therapy with a TKI relies on close monitoring of the patient’s response by means of the standardised real-time quantitative polymerase chain reaction (RQ-PCR) or cytogenetic investigations at 3, 6 and 12 months, according to the guidelines proposed by the European LeukemiaNet (ELN).[5]

Summary

Introduction

Chronic myeloid leukaemia (CML) is a myeloproliferative neoplasm caused by a translocation between chromosome 9 and 22, denoted as t(9;22)(q34;q11.2), involving the fusion of the breakpoint cluster region (BCR) gene on chromosome 22q11.2 and the Abelson gene (ABL1) on chromosome 9q34 This translocation is known as the Philadelphia chromosome.[1,2] The resultant fusion oncogene, BCR-ABL1, encodes a tyrosine kinase that drives clonal proliferation of haematopoietic stem cells and mainly affects the granulocytic lineage.[1,2] Tyrosine kinase inhibitors (TKI) target and suppress the BCR-ABL1 tyrosine kinase and have revolutionised the outcome of CML. A tyrosine kinase inhibitor, is used for the frontline treatment of chronic and accelerated phase CML in our setting

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