Purpose Leukemia accounts for a significant mortality across the globe every year. The main objective of the present research work was directed towards studying the anticancer effects of scutellarin-a plant flavone, against K562 human leukemia cells, along with examining its effects on cellular apoptosis, cell cycle, cell migration and cell invasion as well as Raf/MEK/ERK signalling pathway. Methods Cell viability of K562 leukemia cells was evaluated by WTS-1 assay, while apoptotic effects induced by scutellarin in K562 cells were examined by fluorescence microscopy, flow cytometry, and western blot methods. Effects on cell cycle were measured by flow cytometry. Transwell Matrigel assay was performed to evaluate whether scutellarin induces inhibition of cell migration and cell invasion effects in K562 cells. Results Scutellarin was shown to suppress the viability of the K562 cells dose-dependently with an IC50 of 6 μM. Further, scutellarin was shown to induce apoptosis which was initially exhibited by DAPI and annexin-V/propidium iodide (PI) staining and then confirmed by western blot in which it was shown to trigger regulation of Bax and downregulation of Bcl-2 in K562 human leukemia cells. Scutellarin also induced G0/G1 cell cycle arrest which was accompanied by suppression of cell migration and invasion. Scutellarin also led to the decline of the expression of p-Raf, p-MEK1/2 and p-ERK1/2 in a concentration-dependent manner. Conclusion In conclusion, scutellarin could inhibit the growth of K562 human leukemia cells by inducing apoptosis, cell cycle arrest, inhibition of cell migration and invasion and downregulating the expressions of p-Raf, p-MEK1/2 and p-ERK1/2.Purpose To compare the efficacy and impact of GEMOX and GDP in the treatment of patients with non-Hodgkin's lymphoma (NHL). Methods A total of 68 patients with NHL admitted to the hospitals of the authors from February 2013 to April 2016 were equally distributed into the GEMOX Group (treated with Gemcitabine and Oxaliplatin) and the GDP Group (treated with Gemcitabine, Cisplatin, and Dexamethasone), with cycle repetition every 3 weeks. The efficacy was analyzed every two weeks. The side effects were analyzed once a week. Comparison of survival was performed using Kaplan-Meier method and log-rank test and Cox univariate and multivariate regression analyses. Results Efficacy in the two groups was not statistically different (p>0.05). The incidence of III-IV grade of nausea and vomiting in the GDP Group was higher than in the GEMOX Group (p less then 0.05). The overall incidence decreased hemoglobin, nausea and vomiting, and renal dysfunction of the GDP Group was also higher than in the GEMOX Group (p less then 0.05). Analysis by multivariate Cox model found that the clinical classification and the grade of malignancy were independent prognostic factors (p less then 0.05). The odds ratio (OR) values of the clinical classification in the GEMOX Group and the GDP Group were 2.874 and 24.074, respectively. The OR values of the grade of malignancy in the GEMOX Group and the GDP Group were 14.034 and 6.873, respectively. Conclusion Both the GEMOX regimen and the GDP regimen had good short-term efficacy on NHL patients, but the GEMOX regimen is to be preferred since as it had fewer side effects than the GDP regimen.Purpose This meta-analysis evaluated the potential influence of environmental radon exposure on childhood leukemia. Methods We searched comprehensive electronic databases from PubMed, EMBASE, and Cochrane Library to identify studies evaluating the association between radon and leukemia. Results Ten eligible studies published from 1995 to 2014 were enrolled. Of these 10 studies, 8 were case-control studies (involving 10803 cases and 16202 controls) and 2 were cohort studies (involving 1,428 cases). Overall results as odds ratio (OR) with the corresponding 95% confidence intervals (95%CI) for case-control studies and fully adjusted hazard ratio (HR) with corresponding 95%CI for cohort studies were identified. A positive but weak association was found between radon exposure and childhood leukemia in case-control studies (summary OR 1.22, 95%CI 1.01-1.42) rather than cohort studies (summary HR 0.97, 95%CI 0.81-1.15). Heterogeneity or publication bias was not observed. Moreover, overall ORs were not changed by removing any single study, suggesting the stability and reliability of conclusions. Conclusions Future prospective studies with well-controlled confounders are needed to verify the conclusion.Purpose Osteosarcoma causes extensive human mortality and there is urgent need to develop novel therapies or to identify efficient therapeutic targets for its management. Herein the role and therapeutic potential of miR-17 was explored in osteosarcoma. Methods The normal hFOB.19 cell line and the osteosarcoma cell lines SAOS-2, HOS, 143B, T1-73 and mG63 were used in the present study. The expression analysis of miR-17 was carried out by quantitative Real-Time polymerase chain reaction (qRT-PCR). https://www.selleckchem.com/products/Trichostatin-A.html Lipofectamine 2000 reagent (Invitrogen, Carlsbad, CA, USA) was used for transfection. WST-1 assay was used for determination of cell proliferation and autophagy was detected by transmission electron microscopy (TEM). Wound healing and transwell assays were used for the determination of cell migration and invasion. Protein expression was determined by western blot analysis. Results The expression of miR-17 was significantly elevated in all the osteosarcoma cells. Suppression of miR-17 resulted in decrease of the viability and colony formation of the SAOS-2 osteosarcoma cells. The inhibition of SAOS-2 cell proliferation upon miR-17 suppression was found to be due to induction of autophagy which was accompanied with enhancement in the expression of LC3B II and Beclin-1. Suppression of miR-17 was also accompanied by inhibition of the SAOS-2 cell migration and invasion. The in silico analysis showed that miR-187 targets PTEN in the SAOS-2 cells. The expression of PTEN was found to be downregulated in all the osteosarcoma cells and suppression of miR-17 expression caused enhancement in the expression of PTEN. Overexpression of miR-17 caused inhibition of the proliferation and colony formation of the SAOS-2 cells. Additionally, silencing of miR-17 could abolish the effects of miR-17 inhibition in the SAOS-2 cells. Conclusion MiR-17 may be proven a therapeutic target in the management of osteosarcoma.