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BackgroundAcute myeloid leukemia (AML) is the most common acute leukemia occurring in adults. It is an aggressive myeloid neoplasm with maturation arrest of myelopoiesis, leading to an accumulation of myeloblasts in the bone marrow and peripheral blood.ObjectiveTo evaluate alterations in myeloid-derived suppressor cells level and MUC1 gene expression in patients with de novo acute myeloid leukemia concerning disease characteristics and response to induction chemotherapy.Patients and methodsThe study was performed on 50 AML patients and 50 healthy controls. Detection of myeloid-derived suppressor cells (MDSCs) in peripheral blood was performed by mononuclear separation and flow cytometry. MUC1 gene expression was performed by RNA extraction, reverse transcription, and real-time PCR at Hematology Department Medical Research Institute, Alexandria University.ResultsWe have demonstrated that AML patients had both increased presence of MDSCs in peripheral blood as well as MUC1 overexpression in comparison to normal controls. MDSCs showed a significant correlation regarding response to induction chemotherapy on day 28. While MDSCs and not MUC1 are associated with inferior response to induction chemotherapy on day 28.ConclusionThe current data suggested that AML patients exhibit an increased presence of MDSCs as well as MUC1 gene overexpression in comparison with normal controls. While MDSCs showed a significant correlation regarding response to induction chemotherapy on day 28, MDSCs and not MUC1 are associated with inferior response to induction chemotherapy on the same day.

In view of the improved care of thalassemic patients which resulted in doubling of life expectancy, additional previously undescribed complications are now being recognized.In particular, a chronic hypercoagulable state has been observed in these patients, yet the actual mechanism of its production has not been fully elucidated. To our knowledge, the tissue factor pathway and its inhibitor have not been studied in thalassemics. The aim of the present work was to estimate tissue factor pathway inhibitor (TFPI) relation to oxidative stress assessed by thiobarbituric acid reactive substances (TBARS). Twenty patients with thalassemia major and ten healthy controls were enrolled in the study. Complete blood picture, serum ferritin, screening tests for coagulation, prothrombin and partial thromboplastin times(PT,PTT) and prothrombin activity (P activity %) have been estimated. The mean TFPI was higher in patients than controls but did not reach statistical significance, TBARS and serum ferritin were significantly higher in patients than controls(p=0.000)reflecting the presence of oxidative stress. No relation was found between TFPI and chelating agent (desferrioxamine) intake, splenectomy or TBARS. In conclusion, tissue factor pathway (TFP) as reflected by increased TFPI could be, at least in part incriminated in the thalassemia-induced hypercoagulable state.