ObjectiveTo explore the clinical features and factors inlfuencing the prognosis of childhood non-Hodgkin's lymphoma (NHL).MethodsPathologically diagnosed 78 pediatric patients with NHL and treated in the Afifliated Hospital of Qingdao University from January 2004 to August 2013 were collected and analyzed. Patients were grouped according to age, sex, tumor size, immunologic classiifcation, B-symptoms, LDH, hemoglobin and clinical staging. The 5-years event-free survival rate (EFS) were calculated and analyzed by Kaplan-Meier method, and the difference of the survival rate between groups were com-pared. Using Cox proportional hazards model, we analyzed the possible factors that might inlfuence 5-years event-free survival rate EFS , such as age and clinical staging. TheOR value and the 95%CI were calculated.ResultsAmong the 78 cases, median age of onset is 7 years old, male to female ratio is 2.90:1, there are 25 cases of T-cell type and 53 cases of B-cell type. According to pathological types,Burkitt lymphoma is the most common (34.6%), followed by T-lymphoblastic lymphoma (20.5%), diffuse large B-cell lymphoma (11.5%). According to the St. Jude malignant lymphoma staging system, there are 2 cases in stage I, 9 in stageⅡ, 35 in stageⅢ and 32 in stageⅣ. Swelling of periphery lymph node (80.7%) was observed as initial symptom in 26 cases of lymphoblastic lymphoma. Among 45 cases of mature B-cell tumor, the main clinical feature including abdominal cavity and gingival were observed in 27 cases of Burkitt lymphoma. Among the 73 cases received treatments, 66 cases (90.5%) attained CR (complete remission) and 4 cases (5.5%) attained PR (partial remission) by cytology and radiographic assessment after two course of combined chemotherapy, 2 cases (2.7%) rapidly relapsed after the remisson of one course treatment, 1 case (1.3%) appeared the central nervous system inifltration in the chemotherapy. With median follow-up time of 42 months, the 5-year EFS of the 73 cases was (67.0+5.5)%. Single factor analysis showed that B-symptom, LDH, and clinical staging were signiifcantly correlated with prognosis (P<0.05), while age, sex, tumor size, hemoglobin and immune classiifcation was independent of prog-nosis (P>0.05). Multiple factor analysis showed that LDH and clinical staging inlfuenced the prognosis (OR=3.34,95%CI 2.275?10.683,P<0.01;OR=4.354,95%CI 1.519?12.475,P<0.01) .Conclusionclinical features of childhood NHL are variable. LDH and clinical staging at primary diagnosis are important factors affecting the prognosis.

Objective To study the effect of axitinib on the proliferation and apoptosis of human lung adenocarcinoma PC9 cells and its mechanism. Methods PC90 cells were treated with different concentrations (0, 0.125, 0.25, 0.5, 1, 2, 4, 8, 16, 32, and 64 μmol/L) of axitinib for 72 h, and half-inhibitory concentration (IC50) was calculated. The cell proliferation ability was detected by CCK-8 method. Plate cloning experiments were performed to observe the effect of axitinib on the formation of PC9 cell clones. The mitochondrial membrane potential and apoptosis of PC9 cells were detected by flow cytometry. The expression of cleaved-Caspase-3 protein in PC9 cells was detected by Western blot. Results Asitinib inhibited the proliferation of PC9 cells in a concentration-dependent manner. The IC50 at 72 h was 10.18μmol/L. The clone formation rates of PC9 cells were (100.0±3.2)％, (58.6±2.7)％, (29.3±3.3)％, and (10.9±3.0)％10 d after treatment with 0, 1, 2 and 4 μmol/L axitinib, and the difference was statistically significant (F= 316.922, P< 0.01). The apoptotic rate of PC9 cells at early and late stages increased after treatment with different concentrations of axitinib for 48 h, and the differences were statistically significant (both P< 0.01). After treatment with 0, 4, 8 and 16 μmol/L axitinib for 24 h, the percentage of PC9 cells with low mitochondrial membrane potential was (11.9±1.9)％, (38.5±2.3)％, (56.3±2.7)％, and (76.9±3.1)％, and the difference was statistically significant (F=234.320, P<0.01). The expression level of cleaved-Caspase-3 protein in PC9 cells increased, and the relative expression levels were 1.00±0.04, 1.26±0.09, 1.78±0.12, and 2.10±0.11, respectively, and the difference was statistically significant (F=55.670, P<0.01). Conclusions Axitinib could inhibit the proliferation of human lung adenocarcinoma PC9 cells. Axitinib induces the apoptosis of PC9 cells possibly through decreasing the mitochondrial membrane potential of PC9 cells.