nu-7026 has been researched along with Precursor-Cell-Lymphoblastic-Leukemia-Lymphoma* in 1 studies
1 other study(ies) available for nu-7026 and Precursor-Cell-Lymphoblastic-Leukemia-Lymphoma
| Article | Year |
|---|---|
Determination of the DNA repair pathways utilised by acute lymphoblastic leukaemia cells following daunorubicin treatment.
DNA double strand breaks (DNA-DSBs) are among the most lethal DNA lesions leading to genomic instability and repaired by either homologous recombination (HR) or the non-homologous end joining (NHEJ) mechanisms. The purpose of this study was to assess the importance and the level of activation of non-homologous end joining (NHEJ) and homologous recombination (HR) DNA repair pathways in three cell lines, CCRF-CEM and MOLT-4 derived from T lymphocytes and SUP-B15 derived from B lymphocytes following treatment with chemotherapy agent daunorubicin.. The Gamma histone H2AX (γH2AX) assay was used assess the effects of DNA-PK inhibitor NU7026 and RAD51 inhibitor RI-2 on repair of DNA-DSB following treatment with daunorubicin. In all cell lines, the NHEJ DNA repair pathway appeared more rapid and efficient. MOLT-4 and CCFR-CEM cells utilised both NHEJ and HR pathways for DNA-DSB repair. Whereas, SUP-B15 cells utilised only NHEJ for DSB repair, suggestive of a deficiency in HR repair pathways. Topics: Antibiotics, Antineoplastic; Cell Line, Tumor; Chromones; Daunorubicin; DNA; DNA Breaks, Double-Stranded; DNA End-Joining Repair; DNA Repair; Histones; Homologous Recombination; Humans; Maleimides; Morpholines; Precursor Cell Lymphoblastic Leukemia-Lymphoma; Signal Transduction | 2019 |