Acute lymphoblastic leukemia (ALL) accounts for 30% of all pediatric cancers. Currently available treatments exhibit toxicity and certain patients may develop resistance. Thus, less toxic and chemoresistance‑reversal agents are required. In the present study, the potential effect of curcumin, a component of Curcuma longa, as a pharmacological co‑adjuvant of several chemotherapeutic agents against ALL, including prednisone, 6‑mercaptopurine, dexamethasone, cyclophosphamide, l‑asparaginase, vincristine, daunorubicin, doxorubicin, methotrexate and cytarabine, was investigated in the REH ALL cell line cultures treated in combination with chemotherapeutic agents and curcumin. The results of cell viability, gene expression and activation of NF-κB and caspase 3 indicated that curcumin potentiates the anticancer effects of the aforementioned chemotherapeutic agents in the REH ALL cell line. Following treatment with the above chemotherapeutic agents, curcumin enhanced caspase‑3 activation and downregulated nuclear factor‑kappa B (NF‑κB) activation. Curcumin also downregulated the oxidative stress induced by certain chemotherapies. Notably, curcumin did not affect the gene expression of cell survival proteins such as B‑cell lymphoma (Bcl)‑2, Bcl‑extra large, survivin, c‑Myc and cyclin D1, which are regulated by the NF‑κB transcription factor. In conclusion, curcumin has the potential to improve the effect of chemotherapeutic agents against ALL.

A maternally transmitted Xp+ chromosome was associated with an abnormal phenotype, including developmental delay and short stature, in two male cousins and their 12 year old aunt. The respective mothers were not mentally impaired but had short stature. The G banding pattern identified the extra chromosome segment as a repeat of Xq26.3-->qter attached to an apparently intact Xp22.3 sub-band, so the Xp+ chromosome may be described as rea(X)(Xqter-->p22.3::Xq26.3-->Xqter). The rearranged chromosome was late replicating in 97 to 100% of the metaphases in the mothers but it was early replicating in 43% of the lymphocytes in the mentally defective female (n = 100 cells/subject). Fluorescence in situ hybridisation using X and Y chromosome paints, as well as cosmids A and 1A1 specific for loci within Xq28, confirmed both the identity of the extra segment and the entirety of the Xp pseudoautosomal region. Therefore, the phenotypic consequences in this family can be related to the Xq26.3-->qter functional disomy allowing for the effects of X inactivation in the female carriers.