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Previous studies on the association between alcohol intake and the risk of myelodysplastic syndromes (MDS) have been inconclusive. We conducted a meta-analysis to evaluate alcohol intake as a risk factor for MDS. We performed a systematic literature search of articles published before March, 2014 using Web of Science, PubMed and the Cochrane Library. Two evaluators independently selected and reviewed studies based on predetermined selection criteria. The fixed- or random-effects models were used to summarize the estimates of odds ratios (ORs) with 95% confidence intervals (CIs). A total of 9 studies (8 case-control and 1 cohort) met the inclusion criteria of this meta-analysis. No significant association was observed between alcohol consumption and MDS when comparing drinkers to non-drinkers (OR=1.16, 95% CI: 0.88-1.53) or between subgroups stratified by alcohol history, gender, ethnicity, study design, source of patients or MDS subtypes. However, the data indicated a stronger association of alcohol with MDS in individuals who consumed ≥10 g/day (OR=1.55, 95% CI: 1.08-2.21) vs. those who consumed <10 g/day (OR=1.09, 95% CI: 0.78-1.53). This meta-analysis suggests that alcohol intake may increase the risk of MDS in a dose-dependent manner. However, additional well-designed, prospective cohort studies are required to verify these findings and identify other risk factors associated with MDS. [ABSTRACT FROM AUTHOR]

Adult T-cell acute lymphoblastic leukemia (T-ALL) has a poor prognosis. Although it has been found that activation of Notch1 signaling occurs in >50% T-ALL patients, γ-secretase inhibitors that target Notch1 signaling are of limited efficacy. However, c-Myc is an important direct target of Notch1 and, thus, c-Myc is another potential therapeutic target for T-ALL. Valproic acid (VPA), a histone deacetylase inhibitor, has been reported to treat various hematological malignancies. In the present study, we showed that c-Myc expression, at a transcriptional level, was dose-dependently downregulated in VPA-induced growth inhibition in T-ALL cell lines, Jurkat and CCRF-CEM cells. 10058-F4, a small molecule c-Myc inhibitor, could increase the downregulation of c-Myc and markedly increase the growth inhibition and cell death induced by VPA in Jurkat and CCRF-CEM cells, which was accompanied by obvious cleavage of capase-3. Z-VAD-FMK, a caspase inhibitor, partially prevented the anti-leukemic effect. The results of the present study suggest that c-Myc inhibitors increase cell death induced by VPA in a caspase-dependent and -independent manner, and their combination could be a potent therapeutic strategy for adult T-ALL patients. [ABSTRACT FROM AUTHOR]