Expression pattern and prognostic implication of SALL4 gene in myeloid leukemias: a case-control study.

SALL4 is a transcription factor that retains stem cells in an undifferentiated state and promotes its self-renewal. In addition, it is implicated in leukemogenesis via its effect on leukemic stem cells. This study aimed to characterize the expression pattern of SALL4 gene in acute myeloid leukemia (AML) and chronic myeloid leukemia (CML) at different progression phases of the leukemic process and to assess its prognostic significance. Real-time PCR was used in 106 patients: 54 AML patients; 43 de novo and 11 in complete remission (CR), 52 CML patients; 31 in chronic phase (CP), 11 in deep molecular response (MR4) and 10 in accelerated/blastic phase (AP/BP); and in 21 nonmalignant bone marrow samples. SALL4 gene expression was elevated in AML, AML-CR and CML-CP (median = 5.180, 4.604 and 14.125 fold changes, respectively). Elevated SALL4 gene expression among AML de novo patient was associated with poor disease-free survival (DFS) rates (p = .022). Among CML patients, the highest percentage of patients with a high SALL4 (p = .033) was among CML-CP. SALL4 has a role in leukemogenesis; high SALL4 expression was associated with poor DFS among AML patients.

The effect of different methods of leucoreduction on plasma coagulation factors.

Removal of leucocytes from blood products, namely leucoreduction, improves the safety of blood transfusion by reducing adverse events associated with the incidental transfusion of leucocytes. Coagulation factors might be compromised during leucoreduction because of exposure of plasma to a variety of filter materials. The aim of the current study was to assess the effect of different methods of prestorage leucofiltration (apheresis and whole blood filters) on prothrombin time, international normalized ratio, partial thromboplastin time and factors V and VIII. There was a significant prolongation of prothrombin time as well as elevation of international normalized ratio in plasma after leucoreduction (14.5 ±â€Š0.7 s vs. 13.9 ±â€Š0.7 s, P = 0.008 and 1.14 ±â€Š0.07 vs. 1.09 ±â€Š0.07, P = 0.005, respectively). Also, there was a statistically significant prolongation of activated partial thromboplastin time in nonleucoreduced plasma (55.6 ±â€Š9.9 s vs. 43.2 ±â€Š12.8 s, P = 0.001). There was no significant filtration effect on factors V and VIII levels. Furthermore, there was no significant difference in factors V and VIII levels between plasma filtered by inline whole blood filters and apheresis machine. Leucodepleted plasma originating from both inline whole blood filter and apheresis machine maintained satisfactory levels of factors V and VIII.

Influence of iron regulating genes mutations on iron status in Egyptian patients with sickle cell disease.

Mutations of the HAMP gene and HFE gene have a role in iron overload. We assessed the frequency of the G71D mutation of the HAMP gene and the H63D mutation of the HFE gene and the correlation between these mutations as well as the correlation between them and the iron overload in sickle cell disease (SCD) patients. Genotyping of G71D of HAMP and of H63D of HFE variants was performed by polymerase chain reaction-restriction fragment length polymorphism on 47 SCD patients and 45 controls. The iron status was assessed by serum ferritin and transferrin saturation. We found 61.7% of the patients had a wild genotype in both genes, 14.9% had a variation in HAMP-G71D, 27.7% had a variation in HFE-H63D, and 4.3% had variations in both. Patients with either HAMP-G71D or HFE-H63D variants did not show significant difference in iron status in comparison to patients with wild type genotypes. Multivariate regression analysis revealed that the number of mutations harbored by the patients tends to affect the serum ferritin level; p=0.07. Thus, The HAMP-G71D and HFE-H63D variants are not uncommon among the Egyptian SCD patients; neither of them alone was found to be a major determinant of iron overload in the studied patients. Nevertheless, the number of harboured mutations may increase the probability of iron overload in these patients.

Comparative characteristics of endothelial-like cells derived from human adipose mesenchymal stem cells and umbilical cord blood-derived endothelial cells.

Adult peripheral blood contains a limited number of endothelial progenitor cells that can be isolated for treatment of ischemic diseases. The adipose tissue became an interesting source of stem cells for regenerative medicine. This study aimed to investigate the phenotype of cells obtained by culturing adipose-derived mesenchymal stem cells (ad-MSCs) in the presence of endothelial growth supplements compared to endothelial cells obtained from umbilical cord blood (UCB). Passage 3 ad-MSCs and mononuclear layer from UCB were cultured in presence of endothelial growth media for 3 weeks followed by their characterization by flow cytometry and polymerase chain reaction. After culture in endothelial inductive media, ad-MSCs expressed endothelial genes and some endothelial marker proteins as CD31 and CD34, respectively. Adipose tissue could be a reliable source for easy obtaining, expanding and differentiating MSCs into endothelial-like cells for autologous cell-based therapy.

The link between genetic polymorphism of glutathione-S-transferases, GSTM1, and GSTT1 and diffuse large B-cell lymphoma in Egypt.

BACKGROUND: Diffuse large B-cell lymphoma (DLBCL) is the most common subtype of non-Hodgkin lymphoma. A number of studies have examined the role of genetic polymorphisms in the risk of DLBCL, and several variants have been identified as potential susceptibility genes, of those glutathione-S-transferases T1 and M1 (GSTT1 and GSTM1). AIM OF THE WORK: The aim of the current study was to investigate the influence of inherited genetic polymorphisms of GSTM1 and GSTT1 genes on the susceptibility to DLBCL in Egypt. METHODS: Genotyping of the candidate genes was performed for 71 Egyptian DLBCL patients and 100 age- and gender-matched healthy controls by multiplex polymerase chain reaction technique. RESULTS: The frequencies of GSTT1 null, GSTM1 null, and dual null genotypes among DLBCL patients were 47.9, 52.1, and 23.9 % respectively. CONCLUSION: GSTT1 null genotype conferred almost fourfold increased risk of DLBCL (OR = 3.9, 95 % CI = 1.97-7.75), and the risk increased when confined to male patients (OR = 4.4, 95 % CI = 1.57-12.63), while GSTM1 null genotype was not associated with DLBCL risk. Further studies on the functional consequences of GSTT1 and GSTM1 genetic polymorphisms would pave the way to declare their role in the pathogenesis of DLBCL or as possible predictors for response to therapy.