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CIK cells and helped to draft the manuscript. JL carried out the establishment of MDR cells, participated in the Observation of cell biological characteristics and helped to draft the manuscript. XH carried out the in vivo pharmacodynamics Y-27632 2HCl and pathomorphology experiments in vitro anti-tumor studies. YL and LF participated in the design of the study and performed the statistical analysis. All authors read and approved the final manuscript.”
“Background Ataxia-telangiectasia (A-T) is an autosomal recessive disorder that affects many parts of the body and leads to increased risk of malignancy, including breast cancer [1–3]. A-T is caused by mutations in the ataxia telangiectasia-mutated (ATM) [4]. ATM, a member of the phosphatidylinositol 3-kinase-like family, plays central roles in the BI 2536 solubility dmso repair of DNA double-strand breaks that was caused by a range of DNA-damaging agents such as ionizing radiation [5].