الفهرس 
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Abstract
Chronic myeloid leukemia (CML) is a clonal myeloid stem cell
disorder characterized by excessive accumulation of clonal myeloid
cells in hematopoietic tissues. Clinically CML is divided into three
phases: the chronic phase (CP), the accelerated phase (AP), and the
blast crisis (BC).
CML results from a translocation (9; 22) in the hematopoietic
stem cell resulting in constitutively active BCR-ABL1 oncokinase.
The inhibition of BCR-ABL1 with tyrosine kinase inhibitors (TKIs)
has revolutionized the prognosis of CML.
The first TKI developed for the treatment of CML (imatinib)
has now been in use for more than 15 years. Imatinib works through
competitive inhibition at the adenosine triphosphate binding site of the
BCR-ABL protein. The BCR-ABL inhibition results in apoptosis of
the hematopoietic cells that express BCR-ABL without affecting the
normal cells.
Natural killer (NK) cells, a part of the innate immune system,
possess antitumor cytotoxicity. Cellular death mediated by NK cells
occurs as a result of recognition by the different classes of receptors of
NK cells and by the action of the lytic granules in the NK cells. NK
cells can act on oncoproteins in chronic myeloid leukemia (CML)
patients and so may influence the outcome of CML and patient
response to imatinib.
This study was performed to assess the impact of NK cells
(CD16+56+3-) and NKT cells (CD16+56+3+) on response to therapy in
chronic myeloid leukemia patients and their effects on disease
outcome and prognosis.
Summary
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Our study included 48 CML patients: 21 male (43.8%) and 27
female (56.3%), their ages ranged between 18 and 85 years. The
subjects were stratified into 2 groups: the first group includes 23