ABSTRACT
Objective To identify the rate of hepatitis B virus (HBV) reactivation and potential risk factors in hepatitis B surface antigen negative/hepatitis B core antibody positive patients with lung cancer receiving adjuvant chemotherapy without concomitant antiviral prophylaxis.Methods The records of 3280 patients with lung cancer who received adjuvant chemotherapy were retrospectively reviewed from January 2003 to December 2011.Among these patients,367 hepatitis B surface antigen negative/hepatitis B core antibody positive patients were analyzed for the HBV reactivation in this study.The HBV serology marker and biochemical tests of the 367 patients were performed.The data were analyzed by chi square test.Results Among 367 hepatitis B surface antigen negative/hepatitis B core antibody positive patients with lung cancer,14 patients suffered HBV reactivation.Univariate analysis showed that age≥70 years(x2 =13.003,P=0.019),abnormal liver computed tomography findings (x2 =11.225,P =0.026) and the amount of corticost eroids≥ 150 mg(x2 =7.008,P =0.033)were associated with HBV reactivation.However,gender and adjuvant chemotherapy regimens were not related with HBV reactivation.Conclusion HBV reactivation occurs in a proportion of hepatitis B surface antigen negative/hepatitis B core antibody positive patients with lung cancer during adjuvant chemotherapy.
ABSTRACT
OBJECTIVE@#To assess the effect of celecoxib in combination with adriamycin(ADM) on cell proliferation and apoptosis.@*METHODS@#Cell lines were treated with celecoxib,and cell proliferation was examined by the method of 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide(MTT) at different time. The cellular apoptotic rate was analyzed by flow cytometry. RT-PCR was applied to distinguish the level of caspase-9 mRNA expression. Immunohistochemistry was used to detect the caspase-9 protein expression in Raji cells.@*RESULTS@#Celecoxib inhibited the proliferation and increased the apoptosis of Raji cell lines in a dose-dependent and time-dependent manner within 20-100 μmol/L. Compared with the celecoxib alone, the proliferation of Raji cell lines incubated with celecoxib and adriamycin was decreased. Caspase-9 mRNA and protein expression in Raji cells were significantly enhanced after the treatment of celecoxib (P<0.05).@*CONCLUSION@#Celecoxib can inhibit the proliferation of Raji cells in a dose-dependent and time-dependent manner. Celecoxib may lead to the apoptosis of Raji cells by up-regulating activities of caspase-9. Adriamycin could intensify the effect.
Subject(s)
Humans , Apoptosis , Burkitt Lymphoma , Pathology , Caspase 9 , Genetics , Metabolism , Celecoxib , Cell Line, Tumor , Cell Proliferation , Dose-Response Relationship, Drug , Doxorubicin , Pharmacology , Drug Synergism , Pyrazoles , Pharmacology , RNA, Messenger , Genetics , Metabolism , Sulfonamides , PharmacologyABSTRACT
OBJECTIVE@#To determine the effect of arsenic trioxide combined with adriamycin(ADM) on the proliferation and apoptosis of human lymphoma cells.@*METHODS@#Raji cells were divided into an experimental group and a control group, and the experimental group was further divided into 1 micromol/L As(2)O(3) group,2 micromol/L As(2)O(3) group, ADM group,1 micromol/L As(2)O(3) and ADM group,2 micromol/L As(2)O(3) and ADM group. Human lymphoma cells Raji were treated with As(2)O(3) combined with ADM. Wright-Giemsa dying assay was used to observe the apoptosis morphology of lymphoma cells. The proliferation of the cells treated with As(2)O(3) and adriamycin was detected by the method of 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide(MTT). Flow cytometry(FCM) was used to detect the apoptosis rate of lymphoma and the fluorescene density in the lymphocytes. Effect of arsenic trioxide and adriamycin on the mutant p53 expression in Raji cells was detected by semi-quantitive RT-PCR.@*RESULTS@#Evident apoptotic morphological changes of Raji cells were observed 24 hours after treatment with As(2)O(3) or ADM. Compared with As(2)O(3) or ADM alone, As(2)O(3) combined with ADM could increase the inhibition ratio significantly (P0.05).@*CONCLUSION@#As(2)O(3) and ADM alone or combined can inhibit the proliferation, induce cell apoptosis, and downregulate the expression of mutant p53 in vitro. As(2)O(3) combined with ADM has synergistic anti-lymphoma cell effect in vitro. As(2)O(3) has no significant effect on the concentration of ADM on the Raji cells, but can enhance the chemosensitivity of Raji cells, and its mechanism may be that it can downregulate the expression of mutant p53.