Abstract
Chronic myeloid leukemia (CML) is a triphasic clonal myeloproliferative disorder characterized by the presence of Philadelphi a chromosome (Ph) in over 95% of cases alongside excessive accumulation of clonal myeloid cells in hematopoietic tissues. This occurs as a result of reciprocal translocation between the long arms of chromosome 9 and 22 t (9;22) (q34; q11) creating the fusion oncogene BCR–ABL1 which exhibits constitutive tyrosine kinase activity. It is one of the commonest haematological malignancies in low economies around the world including Nigeria. The clinical features of CML are often described in 3 phases namely the chronic phase (CP), accelerated phase (AP), and blastic phase (BP) while CP is the most common stage with progression to AP and BP occurring later. Despite that, prognosis of CML is dependent on phase of disease, age, and response to therapy, the only curative approach in use currently is hematopoietic stem cell transplantation with other drugs being used for cytogenetic responses. This study focuses on the aetiopathophysiology, cytogenetics, molecular biology, clinical/laboratory features and treatment options of CML. Rigorous review of literature on the study was retrieved from relevant oncology journals and textbooks abstracted and indexed in PubMed, Google Scholar, ProQuest, CINAHL, and Science Direct. The study discovered that, resistance of CML to imatinib has been reported with research having reached the advanced stage on the use of alternative drugs (e.g., Nilotinib and Desatinib). There are also potentials for these new drugs to become the treatment choice and first line drugs for the treatment of CML.
Highlights
Chronic Myeloid Leukemia (CML) is a form of leukemia characterized by an increased and unregulated growth of predominantly myeloid cells in the bone marrow and the accumulation of these cells in the blood. [1]
CML is characterized by presence of Philadelphia chromosome in different cell lines resulting from reciprocal translocation between chromosomes 9 and 22
In a smaller number of cases, the Philadelphia chromosome cannot be seen under microscopic karyotipic analysis but is visible through Polymerase Chain Reaction (PCR) or Fluorescence in-situ Hybridization (FISH)
Summary
Chronic Myeloid Leukemia (CML) is a form of leukemia characterized by an increased and unregulated growth of predominantly myeloid cells in the bone marrow and the accumulation of these cells in the blood. [1]. CML has an estimated global incidence of one to two new cases per 100,000 population per year with a male to female ratio of 1.8:1 with a slight male predominance [3]. Incidence of CML rises gradually with age to reach a median of around 60 years. A global estimate of 15% of all new cases of leukemia are chronic myeloid leukemia [4]. The median age of CML patients in low-income countries including Nigeria and other African countries is 38 years compared to 67 years in developed countries [6] with a prevalence rate of 30%, Asian (36%). Treatment Options in a Low Resource Economy constituting 2% of all leukaemias seen in childhood, there has been an increased incidence over the last year. This article focuses on the aetiopathophysiology, clinical laboratory features, and treatment of CML
Sign-in/Register to view highlights & summary 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.
