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Objective: To detect the expression of microRNA-210(miR-210) in childhood acute lymphoblastic leukemia(ALL), and to evaluate the role of the joint detection of miR-210 and MRD in the prognosis and clinical treatment of pediatric ALL., Methods: Eighty-eight children diagnosed with ALL were included in the study. miR-210 was quantitatively detected by real-time quantitative polymerase chain reaction(RQ-PCR) in 88 ALL patients. The average Ct value of samples obtained from 5 pediatric ALL patients with long-term complete continuous remission (CCR>5 years) was used as a calibrator. The expression levels of miR-210 in newly diagnosed patients was calculated by the 2 -ΔΔCt method and presented as multiple changes compared with that of the 5 CCR patients., Results: The expression of miR-210 in the favorable prognosis group was significantly higher than that in the unfavorable prognosis group (10.64±1.5 vs 3.27±0.68)(P<0.05). Compared with the miR-210 high-expression group, poorer relapse-free survival(RFS), event-free survival(EFS) and overall survival(OS) (P all <0.001) were found in the low-expression group. Based on the expression of miR-210 and MRD, the 88 cases were divided into 3 groups. The relapse rate of miR-210-MRD high-risk group (70%) was significantly higher than that of the miR-210-MRD middle-risk group(6.25%) and miR-210-MRD low-risk group (2.1%). Kaplan-Meier survival analysis demonstrated that the miR-210-MRD high-risk group had poorer RFS, EFS and OS than those in other 2 groups (P all <0.01)., Conclusion: The expression level of miR-210 is an independent prognostic factor for pediatric ALL, and the miR-210 is a good useful indicator for predicting the relapse and induction failure of childhood ALL. Joint detection of miR-210 and MRD can help predict outcomes more precisely, thus may be used as an effective mean of determining prognosis, monitoring recurrence, and guiding treatment.

Objective: To investigate the clinical features and outcomes of neuroblastoma (NB) children aged above 5 years, and to provide a theoretical basis for improving prognosis., Methods: A retrospective analysis was performed for the clinical data of 54 previously untreated NB children, and their clinical features and outcome were analyzed. The Kaplan-Meier method was used for survival analysis., Results: Among the 54 children, there were 36 boys and 18 girls, and all of them had stage 3 or 4 NB. Of all the children, 41 (41/54, 76%) had retroperitoneal space-occupying lesions, 10 (10/54, 18%) had mediastinal space-occupying lesions, 2 (2/54, 4%) had intraspinal space-occupying lesions, and 1 (1/54, 2%) had pelvic space-occupying lesions. At the end of the follow-up, 30 children (30/54, 56%) survived, among whom 23 (77%) achieved disease-free survival (9 achieved complete remission after chemotherapy for recurrence), 6 (20%) achieved partial remission of tumor (all of them received chemotherapy again due to recurrence), and 1 (3%) experienced progression (with progression after chemotherapy again due to recurrence); 24 children (44%) died, among whom 22 died after chemotherapy again due to recurrence and 2 died of multiple organ failure during the first treatment. According to the Kaplan-Meier survival analysis, the mean survival time was 53.8 months, and the children with stage 3 NB had a significantly higher overall survival rate than those with stage 4 NB (80% vs 53%; p<0.01). The children with recurrence had a significantly lower mean survival time than those without recurrence (51.68 months vs 62.57 months; p<0.01)., Conclusions: Older children often have late-stage NB, but standard treatment can improve their outcomes.

Objective: To evaluate the efficacy of BCH-03 and CCLG-08 protocols in treating E2A-PBX1 pediatric acute lymphoblastic leukemia (ALL)., Method: From January 2003 to January 2011, 59 ALL patients identified as E2A-PBX1 were analyzed in a retrospective study. There were 37 and 22 patients treated with Protocol BCH-03 and CCLG-08, respectively. The clinical characteristics at diagnosis, response to early treatment, the time of relapse, relapse-free survival (RFS) and event-free survival (EFS) in the two groups were analyzed., Result: There were no significant differences in gender, age, initial white blood cell count, the central nervous system involvement, immunophenotype, prednisone response, the rate of complete remission, and the time of relapse between the two groups (P > 0.05). The only difference in induction therapy of the two protocols existed in the glucocorticoids used, that is, BCH-03 used 60 mg/m(2) prednisolone and CCLG-08 used 6 mg/m(2) dexamethasone. The doses of vincristine, daunorubicin and L-asparaginase were the same in the two groups. At the end of induction therapy, the MRD negativity rate in BCH-03 group was significantly higher than that in CCLG-08 group (84.2% vs. 47.1%, P = 0.018). The incidences of severe infection of the two groups during induction of remission were similar (P = 0.135). The EFS of BCH-03 group was significantly superior to that of CCLG-08 group (94.5% vs. 71.5%, P = 0.010), and the RFS of BCH-03 group tended to be better than that of CCLG-08 group (94.5% vs. 78.6%, P = 0.059)., Conclusion: Compared to Protocol CCLG-08, Protocol BCH-03 was more effective for pediatric E2A-PBX1 ALL, and 60 mg/m(2) prednisolone was more suitable for the induction therapy of this subtype of pediatric ALL.

The aim of this study was to investigate the effect of suppression of nicotinamide phosphoribosyltransferase (NAMPT) expression on imatinib-sensitivity in chronic myelogenous leukemia (CML) cell line K562 and its mechanisms, NAMPT siRNA was synthesized and transfected into K562 cells. PI/Calcein staining technique was used to determine survival rate of transfected K562 cells at 48th hour after exposure to 1 µmol/L imatinib. MTS method was used to determine the proliferation changes of transfected K562 cell at 48th hour after exposure to different doses of imatinib, then half inhibitory concentration (IC(50)) was calculated. Expression of NAMPT at 3rd-48th hour after exposure to 1 µmol/L imatinib was determined by Western blot. To explore the effect of NAMPT-siRNA and imatinib on the expression of apoptosis-related genes, the microarray data from NCBI GEO Data-Sets was analyzed, then the results were confirmed by Western blot. The luciferase reporter assay was used to determine the effect of NAMPT and imatinib on transcriptional activity of NF-κB transcription factors. The results showed that after exposure to 1 µmol/L imatinib for 3 - 48 h, there was no significant change of NAMPT expression in K562 cells. The expression of NAMPT could be effectively inhibited by the NAMPT-siRNA. After exposure to 1 µmol/L of imatinib for 48 h, the survival rate of NAMPT-siRNA interference group was lower than that of negative control group (P < 0.05), indicating that suppression of NAMPT expression can increase the sensitivity of K562 cells to imatinib and enhance the killing effect of imatinib on K562 cells. The IC(50) of imatinib in NAMPT-siRNA interference group was the lowest compared with that of control group (P < 0.05) after exposure to different concentrations of imatinib for 48 h, the fitted survival curves showed that the slope of NAMPT-siRNA interference group was the largest ranging between 0.01 - 0.1 µmol/L of imatinib. Data mining of expression profiling indicated that the anti-apoptotic factor Bcl-2 decreased in K562 cells treated with either NAMPT-siRNA or imatinib, which was confirmed by Western blot. The inhibitory effect was much more significant when both NAMPT-siRNA and imatinib were used. The results of luciferase reporter assay showed that either NAMPT-siRNA or imatinib decreased transcriptional activity of NF-κB. The decreased effect was much more significant when both NAMPT-siRNA and imatinib were used. It is concluded that survival of K562 cells affected by imatinib may not be due to regulation of expression of NAMPT. When expression of NAMPT decreases, the K562 cells are more sensitive to imatinib, this may be related with the decreased transcriptional activity of NF-κB and its downstream effector Bcl-2.