![]() | Only 14 pages are availabe for public view |
Abstract Acute lymphoblastic leukemia (ALL) is the most common malignancy in children characterized by overproduction and accumulation of blast cells in bone marrow and peripheral blood. Notch signaling deregulation is suggested to be a key event in different types of hematological malignancies. Notch signaling appears to be a major oncogenic trigger in T cell acute lymphoblastic leukemia (T-ALL). On the other side, Notch signaling demonstrates a potent tumor suppressor in other forms of leukemia, including B-ALL. The proteolytic release of the Notch-1 intracellular domain (NICD), an essential step in the activation of Notch signaling. So, in this study we identified the γ-secretase activity by measuring its concentration in ALL patient and healthy control. The best-known Notch target genes are two families of basic helix loop helix transcription factors: Hes (Hairy enhance of split) function as transcriptional repressors. Additionally, target genes of the Notch signaling pathways also include c-myc and p21 genes. c-Myc drives cell cycle progression and regulates the expression of key enzymes that control cellular metabolism, and stimulates ribosome biogenesis and protein synthesis through interactions with RNA polymerase III. p21 gene is involved in replicative senescence, terminal differentiation and proliferation in non-hemopoietic and hemopoietic cells. The role of notch target genes in pathogenesis and therapeutic target in ALL is still not clear therefore we tried to study these genes in ALL patients. |