Chronic myeloid leukemia (CML) is a myeloproliferative disorder characterized by the presence of an acquired mutation which affects the hematopoietic stem cell, leading to a striking overproduction of immature granulocytes. The first important clue to its pathogenesis the Philadelphia chromosome created by a reciprocal translocation between chromosomes 9 and 22 (t [9; 22] [q34; q11]). The development of the BCR-ABL-targeted imatinib mesylate represents a paradigm shift in the treatment of CML. Imatinib displays inhibitory activity against other kinase(s) that play a role in monocyte/macrophage development. Accordingly many studies revealed the role of cytokines in pathophysiology of myeloid neoplasia including participation of IL-1b in the pathogenesis of CML. This study designed to assess the behavior of IL-1b through newly diagnosed patients, different responders groups (optimal, suboptimal and failure cytogenetic response) and advanced stages (acceleration and crisis groups) of CML Iraqi patients whom receiving Imatinib mesylate (tyrosine kinase inhibitor), trying to elucidate the role of immunity in pathophysiology of CML disease development and treatments. In this study 96 Iraqi CML patients under imatinib mesylate treatment categorized by complete blood picture and fluorescent in situ hybridization analysis into different response groups and stages, then used an enzyme linked immunosorbent assay technique to assess serum level of IL-1b in each response group and advance stage (acceleration and transformed) of CML patients, in comparison to level in 32 healthy control subjects and 32 newly diagnosed CML. Out of 128 patients the mean serum of interleukin 1b level (pg/ ml) for the newly diagnosed, optimal responded, suboptimal responded, failure cytogenetic and advance stage of CML were 6.53 ± 3.81, 18.47 ± 4.29, 18.69 ± 3.03, 5.73 ± 2.44, and 18.10 ± 3.10, respectively. While healthy was 12.17 ± 3.44. The measurement of IL-1b before and during treatment of CML patients may contribute to the early identification of responder and non responder patients, and help in the earlier choice and/or design of alternative therapeutic strategies.

Objective: chronic myeloid leukemia (CML) is a myeloproliferative confusion characterized by the occurrence of an acquired mutation which affect the hematopoietic stem cell, treatment of CML with tyrosine kinase inhibitors (TKI) has resulted in high response rates compared to the interferon alpha and hydroxy urea. However, the long-term consequences of TKI had an effect on calcium (Ca++ ) and phosphate(PO4-2 ) levels which may have adverse events on the cardiac and skeletomuscular contraction. Methods:  in a cross-sectional study, 95 patients with CML receiving different TKI treatment for at least one year duration were randomly divided in to three groups: group (1) who received imatinib myselate (Gleevec) 400mgper oral per day,the second group were patients received gleevec 600mg-800mg/day, while the third group patients were received nilotinib 800mg/day as a second line therapy after failure to imatinib mylselate response . Results: in the present study,serum Ca++  level was a significant lower statistical different with p < 0.05 when compared with serum level of PO4-2inpatients treated with imatinib and nilotinib with lower serumCa++ and PO4-2levelsin imatinibpatientsgroup than patientsused nilotinib group with p-value 0.049 and 0.005 subsequently. Conclusion:  imatinib therapy with the long term use may cause hypocalcemia and hypophospatemia without significant correlation more than treatment with nilotinib where  significant correlation was between serum Ca++ and PO4-2and these changes may give an idea that disturbance of serum Ca++, PO4-2was multifactorial

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Primary Myelofibrosis (PMF) is one of development of the myeloproliferative neoplasms that occurs during change in the DNA of a single hematopoietic stem cell. About 50 % of people with MF have an alteration called V617F JAK2 that initiate in the Janus kinases (JAK2) gene. The gene alteration causes unusual signaling in the JAK pathway, which regulates the production of blood cell. There is many theories suggesting the deregulated irritation and immune genes have a role in patients with myeloproliferative neoplasm (MPN). Aim of this study is to characterize the serum levels of IL-1β and C-reactive protein in PMF patients, also to assess their relationship to the treatments and to the spleen size between different patients of PMF received hydroxyurea and ruxolitinib. The study was conducted between November 2014 up to September 2015, during this period 60 Iraqi patients of primary myelofibrosis receiving hydroxyurea for at least 6 months are taken and 30 samples were also taken from healthy persons as control group. Ultarsongraphy of abdomen to assess the spleen size and peripheral blood indices were taken from patient's records at time of sampling. Screening for interleukin 1β level and C-reactive protein were performed to all patients. Out of these 60 patients, 10 patients with high interleukin 1β level and high C-reactive protein switched to received ruxolitinib therapy to determine its effect in correlation with hydroxurea treated patients and control patients. There was significantly lower IL-1β and CRP in control normal group compared to both patients groups. Patients received ruxolitinib treatment had lower IL-1β and CRP compare to hydroxyurea group but it was not statistically significant. The relationship between CRP and IL 1β in all studied group was significant with non-linear relationship between CRP and IL-1β and only patients on hydroxyurea had significant relationship between CRP and IL-1β. In patients with PMF there ishigh level of IL 1βlevel and C reactive protein which may have a role in the pathogenesis of the disease and new treatment of PMF like ruxolotinib may have ability to reduce their levels through controlling the disease pathogensis, further follow-up and larger sample is needed to assess the cytokine levels on long term follow up.

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