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Introduction: Autophagy was found to play a major role in the pathogenesis of acute lymphoblastic leukemia (ALL). In this study we investigated the expression of beclin-1, Bad, Bax, Bcl-2, and Bcl-xL in patients with ALL. Material and methods: This was a comparative study conducted on 100 ALL patients (age 8-15) divided into 2 groups. The first group, the ALL group, comprised ALL cases at their initial diagnosis (46 patients), while the second group, the Remission group, comprised in-remission cases (50 patients). mRNA expression levels in patients' blood samples were determined using real-time polymerase chain reaction (PCR). Results: Beclin-1 levels were significantly lower in the ALL group than in the Remission group (0.22 ±0.03 vs. 196.8 ±32.47; p = 0.001). Bad levels were significantly lower in the ALL group (1.0 ±0.18 vs. 163.6 ±36.2; p = 0.001), while Bax levels were significantly higher in the ALL group than in the Remission group (131.52 ±31.4 vs. 4.29 ±0.64; p = 0.001). Bcl-2 levels were significantly higher in the ALL group (2678.91 ±575.5 vs. 7.56 ±2.9; p = 0.001), and Bcl-xL levels were also significantly higher in the ALL group (142.99 ±24.43 vs. 0.99 ±0.2; p = 0.001). There was negative correlation between immunophenotyping with beclin-1 (r =-0.725; p < 0.001), while there was a positive correlation with Bcl-2 (r = 0.533; p < 0.001). Conclusions: Our findings reveal potential prognostic value for these markers in pediatric ALL, with regard to the delicate mutual balance among them.

Introduction: Sickle cell disease (SCD) is a chronic inflammatory disorder characterized by altered levels of several inflammatory cytokines, which may be regulated by genetic polymorphisms and could be associated with diverse clinical presentations. Interleukin 1β (IL-1) and interleukin 6 (IL-6) have a pivotal role in the pathogenesis of many acute and chronic diseases, and their genetic alterations have been considered as molecular contributors to several inflammatory disorders. The current study aimed to define the impact of IL-1β and IL-6 genetic polymorphisms on the clinical course of the disease in a cohort of pediatric SCD patients. Material and methods: Genotyping of IL-1β +3954 C/T and IL-6-174 G/C polymorphisms was performed by the polymerase chain reaction restriction fragment length polymorphism (PCR-RFLP) technique for 84 SCD patients and 100 age-and gender-matched unrelated healthy controls. Results: The polymorphic genotypes of IL-6-174 G/C were associated with patients suffering from repeated, severe attacks of vaso-occlusion (VOC) requiring hospitalization (p = 0.023 and p = 0.03 respectively), while no significant differences were noted between SCD patients harboring the wild or the polymorphic genotypes of IL-1β +3954 C/T and their demographic, clinical or laboratory characteristics. Conclusions: IL-6-174 G/C polymorphism could be considered as a molecular predictor for recurrent, severe attacks of vascular occlusion in Egyptian SCD patients. Considering the important roles of cytokines in SCD pathophysiology, further investigations in larger cohorts are recommended for better characterization of individual variations in immune regulatory genes and identification of novel markers for disease complications and morbidity.

A considerable number of lymphoma patients lacked the expression of either or both isoforms, while all lymphoid leukemia patients expressed both isoforms. The expression pattern differences of p73 isoforms may reflect differences in the biology of these malignancies.

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