Introduction exposure to radiation, such as victims of

Introduction

Chronic
myeloid leukaemia (CML) is a haematopoietic stem cell disorder categorised as
an uncontrolled neoplastic growth of myeloid cells in bone marrow with
increased number of these cells present in peripheral blood (Pasic and Lipton,
2017). It is classified as myeloproliferative disorder along with polycythemia
Vera, essential thrombocythemia and myelofibrosis. CML is considered a rare disorder compared with
other leukaemia. In UK 8600 leukaemia cases are diagnosed per year and 750 of
these cases are CML (Cancer research, 2018). The worldwide incidences are 1-2
cases per 100000 individuals each year. The incidences are high in population
with high exposure to radiation, such as victims of atomic bomb. Patients also
treated with radiotherapy for other leukaemia have increased risk of developing
CML (Apperley, 2018).

CML
is well-studied disorder which is caused by a specific genetic mutation, in which part of chromosome 9 attach to
chromosomes 22 to form Philadelphia
(Ph) chromosomes ((Vaidya et al., 2011). The Ph chromosomes dysregaulate
the activity of tyrosine kinase protein (TKP). TKP is an essential protein
which regulates metabolic pathways and acts as a mediator for cell
proliferation and apoptosis. Dysregulation of
TKP leads to increased granulocytic stimulating factors (G-CSF) which in turn
results in over production of myeloid cells in marrow (McKenzie and Williams, 2010). The disease progress in three phases, which include chronic
phase (CP), accelerated phase (AP) and blastic phase (BP) with different
clinical and laboratory presentations. Thompson et al., 2015 states that more
than 85% of cases are diagnosed at chronic phase. In chronic phase patients are
mostly asymptomatic and If not treated appropriately the disease can progress
to more advanced accelerated or blastic phase. The diagnosis of CML is
initially suspected in full blood counts and peripheral blood smear which is later
confirmed by further laboratory tests including bone marrow biopsy,
cytogenetic, polymerase chain reaction (PCR)  and FISH (Fluorescent in situ
hybridization) (Baccarani et al., 2012).

The
treatment for CML patients have revolutionised over a period of time, starting
with arsenic therapy which had limited benefits to modern treatment with
tyrosine kinase inhibitors which have almost eradicated disease. Patients
respond well to treatment at chronic phase and maintain normal health for
several years. However; as disease progress to advance stage the prognosis
decreases with a reduce survival rate of 6 month or less (Thompson et al.,
2015).