Chronic Myloid Leukemic Patients Treated With Tyrosine Kinase Inhibitor
Chronic Myloid Leukemic Patients Treated With Tyrosine Kinase Inhibitor
The aim of the study is to assesse the levels of various biomarkers, specifically interleukin
 (IL)-6, platelet-derived microparticles (PDMPs), 11, 12 soluble vascular cell adhesion
 molecule 1 (sVCAM-1), transforming growth factor (TGF) β1, and sCTLA-4, in TKI-treated
 patients with CML.

 To measure the fluctuations in the levels of sCTLA-4, TGFβ1, and PDMPs, and to clarify the
 clinical significance of these biomarkers during TKI therapy in patients with CML..
Chronic myelogenous leukemia (CML) is a myeloproliferative disorder in which leukemic cells
 display the Philadelphia chromosome generated from a reciprocal t(9:22) (q34:q11)
 translocation.1 The chromosome 9 and chromosome 22 transposal of t (9:22) and (q34:q11)
 causes the cancer gene C-ABL at 9q34 to link with the BCR gene at 22q11, forming the BCR-ABL
 gene on chromosome 22.2 CML is presented by constitutional complaints (fatigue, weight loss,
 and fever), those related to splenomegaly (abdominal fullness, anorexia, abdominal pain, and
 early satiety) and bleeding tendency (easy bruising or bleeding) are most frequent symptoms.
 Splenomegaly (≥ 95%), sternal tenderness, hepatomegaly, purpura, and retinal hemorrhage are
 commonly reported signs at physical exam. To diagnose CML, doctors use a variety of tests to
 analyze the blood and marrow cells.

 *Complete Blood Count (CBC). This test is used to measure the number and types of cells in
 the blood. People with CML often have:

 -  Decreased hemoglobin concentration

 -  Increased white blood cell count, often to very high levels

 -  Possible increase or decrease in the number of platelets depending on the severity

 Blood cells are stained (dyed) and examined with a light microscope. These samples show:

 -  Specific pattern of white blood cells

 -  Small proportion of immature cells (leukemic blast cells and promyelocytes)

 -  Larger proportion of maturing and fully matured white blood cells (myelocytes and
 neutrophils).

 These blast cells, promyelocytes and myelocytes are normally not present in the blood of
 healthy individuals

 -  Bone Marrow Aspiration and Biopsy.

 -  Cytogenetic Analysis.

 -  FISH (Fluorescence In Situ Hybridization).

 -  Polymerase Chain Reaction (PCR).

 The disease is classically staged into chronic phase (CP, most patients at presentation),
 accelerated phase (AP) and blast phase (BP).3 Many definitions have been used for these
 stages, but all the data generated from the tyrosine kinase inhibitor (TKI) studies has used
 the historically standard definition where AP is defined by the presence of one or more of
 the following: ≥15% blasts in the peripheral blood or bone marrow, ≥20% basophils in the
 peripheral blood , platelets <100,000/μL unrelated to treatment or the development of
 cytogenetic evolution. Blast phase is defined by the presence of ≥30% blasts in the
 peripheral blood or bone marrow, the presence of clusters of blasts in marrow or the presence
 of extramedullary disease with immature cells (i.e., a myeloid sarcoma).4 Progression to BP
 occurs at a median of 3-5 years from diagnosis in untreated patients, with or without an
 intervening identifiable AP.5. After initiating therapy for CML, patients should be monitored
 for treatment response assessment. The process of monitoring response to therapy is important
 to determine if an adequate response is being achieved, or if patients should be transitioned
 to a higher dose or different therapy Since therapy is continued indefinitely and relapse
 occurs upon cessation of therapy in most patients, it is critical that the disease is closely
 monitored. Continued monitoring over time is needed, even in the setting of an optimal
 response, in order to detect and treat potential recurrence. Specific response criteria,
 including optimal, suboptimal, and failure have been established to guide appropriate
 increase or change of therapy
Inclusion Criteria:

 1. Newly diagnosed CML patients

 2. Receive TKI treatment (imatinib, nilotinib, dasatinib) selected among those admitted
 to the investigator's hospital.

 3. Ageing group 20yr up to 80 yr.

 Exclusion Criteria:

 1. CML patients who previously treated with TKI.

 2. Age below 20 yrs.