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.

CD99 could be used to complement current strategy relying on TdT for diagnosis and monitoring of minimal residual disease during the post-therapy follow up of T-ALL patients. Further studies are needed to confirm these findings.

Chronic hepatitis C (CHC) is a worldwide etiology of chronic hepatic insult particularly in Egypt. DNA‐repair systems are responsible for maintaining genomic integrity by countering threats posed by DNA lesions. Deficiency in the repair capacity due to genetic alterations in DNA‐repair genes can lead to genomic instability and increased risk of cancer development. The present work aimed at studying the possible association between XRCC1‐G28152A (rs25487), XRCC3‐C18067T (rs861539), and XRCC7‐G6721T (rs7003908) single nucleotide polymorphisms (SNPs) and the susceptibility to hepatocellular carcinoma (HCC) in Egyptian population. The study was conducted on 100 newly diagnosed HCC patients and 100 age‐ and sex‐matched healthy controls. Laboratory workup revealed that all HCC patients have chronic hepatitis C viral infection. Genotyping of the studied SNPs was performed by real‐time PCR. The heteromutant genotype of XRCC1 (GA) conferred an almost two‐fold increased risk of HCC (OR ,  2.35; 95% CI, 1.33‐4.04). Regarding XRCC7, the heteromutant (TG) genotype conferred a two‐fold increased risk of HCC (OR ,  2.17; 95% CI, 1.23‐3.82). Coinheritance of the polymorphic genotypes of XRCC1 and 7 was significantly higher in HCC cases than controls and was associated with an 11‐fold increased risk of HCC (OR , 11.66; 95% CI,  2.77‐49.13). The frequency of XRCC3 polymorphic genotypes in HCC patients was close to that of the controls.

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.

Non-Hodgkin lymphomas (NHL) entail considerable heterogeneity regarding their morphology, clinical course, etiological factors, or response to therapy. Increased incidence of NHL in immunocompromised individuals and after autoimmune diseases suggests that infections and immune dysregulation could play a role in the susceptibility to NHL. Accordingly, genetic variation in Toll-like receptor (TLR) genes might be considered as molecular risk factors for NHL. The aim of the current study was to investigate the possible association between genetic polymorphism of the TLRs genes and B cell NHL (B-NHL) risk in Egypt. The present study included 100 B-NHL patients and 100 healthy controls. Genotyping of TLR2-1350 T/C and TLR9-1237 T/C were done by polymerase chain reaction restricted fragment length polymorphism (PCR-RFLP) technique. The frequency of TLR2-1350 T/C polymorphic genotypes in B-NHL patients was 18 % for the heteromutant genotype (TC) and 1 % for the homomutant (CC). There was no statistical difference in the distribution of TLR2-1350 T/C genotypes between B-NHL patients and controls. As for TLR9-1237 T/C, the frequency of the heteromutant genotype (TC) was 58 % and the homomutant genotype (CC) was 1 % in B-NHL patients. Calculated risk estimation revealed that TLR9-1237 (TC) heterotype conferred almost fourfold increased risk of B-NHL (odds ratio (OR) = 3.93, 95 % confidence interval (CI) = 2.16-7.14), and the risk was higher in patients with indolent subtypes (OR = 6.64, 95 %CI = 2.31-9.08). In conclusion, the study revealed that TLR9-1237 T/C polymorphism can be considered as molecular risk factor for B-NHL among Egyptians.