Objective To evaluate the effectiveness and safety of chemotherapy regimens represented by pirarubicin (THP) vs. adriamycin hydrochloride (ADM) for non-Hodgkin lymphoma (NHL) in mainland China. Methods The randomized controlled trials (RCTs) about THP vs. ADM for treating NHL were collected in the databases such as CNKI, CBM, VIP and WanFang Data, and the references of the included studies were also retrieved manually, with the retrieval time from January 1989 to September 2012. According to the inclusion and exclusion criteria, two reviewers independently screened articles, extracted data, and assessed the methodological quality of the included studies. Then meta-analysis was performed using RevMan 5.0 software. Results A total of 15 RCTs involving 1 659 patients were included. The results of meta-analysis showed that: a) As for the total effective rate, the CTOP (C: cyclophosphamide, T: pirarubicin, O: vincristine, P: prednison) regimen was superior to the CHOP (C: cyclophosphamide H: adriamycin hydrochloride, O: vincristine, P: prednison) regimen with a significant difference (OR=1.07, 95%CI 1.02 to 1.12, P=0.006); and b) As for the safety, there were significant differences between the two groups in the incidence of cardiac toxicity (OR=0.42, 95%CI 0.30 to 0.57, Plt;0.000 01), gastrointestinal tract response (OR=0.69, 95%CI 0.56 to 0.85, P=0.000 5) and liver damage (OR=0.69, 95%CI 0.48 to 1.00, P=0.05). But no significant differences were found between the two groups in the incidence of mye1osuppression: the decreased hemoglobin (OR=0.83, 95%CI 0.61 to 1.14, P=0.25), leucopenia (OR=0.85, 95%CI 0.68 to 1.07, P=0.17), and thrombocytopenia (OR=0.99, 95%CI 0.70 to 1.39, P=0.95). Conclusion Based on the domestic evidences at current and compared with CHOP regimen represented by ADM, CTOP regimen represented by THP for treating NHL shows a higher total effective rate and less side effects. However, more high quality, large sample and double blind RCTs are required to prove this conclusion for the quality and quantity limitation of the included studies.
【Abstract】ObjectiveTo establish adriamycin (ADM) resistant pancreatic cancer cell line SW1990/ADM and to investigate its drug resistance mechanism.MethodsADM-resistant pancreatic cancer cell line SW1990/ADM was obtained by culture of pancreatic cancer cell line SW1990 in vitro with intermittently increasing the concentration of ADM in the culture medium for ten months. After two months of drug free culture, its biological characteristics, drug sensitivity as well as the expression and function of multidrug resistant gene 1 (mdr1) were detected, respectively. ResultsCompared with the parental cell line, SW1990/ADM showed great changes in biological characteristics and developed a cross resistance to various chemotherapy drugs. The drug resistance indexes of cell line SW1990/ADM to ADM, mitomycin, fluorouracil and gemcitabine were 49.60, 7.25, 3.80 and 1.25, respectively. The level of mdr1 mRNA expression in cell line SW1990/ADM was much higher than that of the parental cell line（P＜0.01). ConclusionWe have established adriamycin resistant pancreatic cancer cell line SW1990/ADM with multidrug resistance phenotype, its multidrug resistance is positively relevant to the expression of mdr1.
Objective To dynamically study the formation of multidrug resistance(MDR) of human hepatocellular carcinoma cell SMMC-7721 induced by Adriamycin (ADM) and the role of multidrug resistance-associated protein(MRP) in its mechanisms.Methods Hepatocellular carcinoma cell SMMC-7721 was cultured in RPMI-1640 medium containing ADM with progressively increased concentration or directly cultured in medium containing different concentrations of ADM. Resistant index of drug-resistant variants of SMMC-7721 cell was determined by drawing cell dosage-reaction curves.Levels of MRP mRNA expression were detected by reverse transcription-polymerase chain reaction(RTPCR). Intracellular rubidomycin(DNR) concentration was examined by flow cytometry(FCM).Results With progressive increasing of ADM concentration in medium resistant index and levels of MRP mRNA expression were correspondingly increased but intracellular DNR concentration was markly reduced. When parental cells were directly cultured in medium containing different concentrations of ADM, the higher the ADM concentration, the higher the level of MRP mRNA expression, but intracellular DNR concentration was kept at the similar high level and most cells died. Conclusion ADM may progressively induce SMMC-7721 cell resistant to multiple chemotherapeutic drugs with reduced intracellular DNR accumulation associated with the overexpression of MRP gene.
Objective To investigate the growth of tumors and the natural life length of the rats after the adriamycinethylcellulose microspheres(ADM-EC mc) were injected in the rats bearing transplantable liver cancer through their hepatic arteries.Methods ADM-EC mc were infused into the proper hepatic arteries of the Wistar rats (W256). All of the rats were divided randomly into five groups, group 1: control, group 2: normal saline, group 3: conventional ADM, group 4: placebo ethylcellulose microspheres, and group 5: ADM-EC mc. Results As compared with other four groups, the ADM-EC mc (group 5) showed the best inhibition of the growth of tumors and the longest mean life length of the rats. Conclusion Hepatic arterial infusion of ADM-EC mc can inhibit the growth of the tumor, aggravate the necrosis, and improve the effects of the chemotherapy of liver cancer.
OBJECTIVE To manufacture adriamycin-porous tricalcium phosphate (A-PTCP) ceramic drug delivery system (DDS) as a possible method for bone defect treatment after bone tumor operation. METHODS A-PTCP DDS was made from putting adriamycin into PTCP. Thirty rabbits were divided randomly into group A(24 rabbits) and group B(6 rabbits). A-PTCP was implanted in the greater trochanter of the right femur in group A. Adriamycin were injected into veins in group B. Muscle around A-PTCP and plasma were taken out at different period. Adriamycin concentrations in muscle and plasma were measured by high performance liquid chromatography (HPLC). RESULTS A-PTCP could gradually release adriamycin over 10 weeks. Adriamycin concentrations in the muscle were higher than that in plasma. CONCLUSION A-PTCP may be a new method for repairing bone defects after bone tumor operation.
Objective To determine whether intravesically administered Adriamycin can prevent superficial bladder tumor to recur through assessing the efficacy of with intravesical Adriamycin and without intravesical Adriamycin after TURB-t. Method The search strategy was made according to the demand of Cochrane Collaboration. Medline, Embase，CBMdisc and the Cochrane Library were searched for RCTs. Data were extracted by two reviewers using the designed extraction form. RevMan were used for data management and analysis. Results Thirty three relevant trials were searched, of which eighteen trials were included and fifteen trials were excluded. Meta-analysis showed intravesically administered Pirarnbicin (THP), Epirubicin (EPI) and Adriamycin (ADM) can reduce the recurrence rate of superficial bladder cancer after operation during one or two years. Conclusions Intravesically administered THP, EPI and ADM can reduce the recurrence rate of superficial bladder cancer after TUPB-t’s operation during one or two years. In addition, the factors affecting the prognosis should be performed, such as the dosage of irrigation of bladder, reserving time and the course.
【Abstract】ObjectiveTo compare the effects of newcastle disease virus (NDV) and adriamycin (ADM) on surface structure and actin of hepatocellular carcinoma cell lines SMMC-7721. Methods SMMC-7721 carcinoma cell lines were divided into 2 groups. NDV was added into one group, while ADM was added into the other group. The cells were then cultured at 5 time phases (8, 16, 24, 36 and 48 h). Intracellular actin and Ca2+ were examined by using immunofluorescence method. CD44 and intercellular adhesion molecule-1 (ICAM-1) were detected by using immunochemical method and flow cytometry, respectively. The change of cellular surface structure was observed by scan electron microscope. Results Cells gradually contracted and turned round over time. It was observed that actin was segmented and cells alignment became disordered. The mean fluorescence intensity of actin decreased in both groups, but it was obvious in NDV group. There were significant differences of fluorescence intensity between 2 groups at the phases of 16 h (P＜0.05), 24 h (P＜0.05), 36 h (P＜0.01) and 48 h (P＜0.05), except the one after 8 h. Intracellular Ca2+ concentration increased gradually in both groups, and the amplifications in NDV group were significantly higher at the phases of 24 h, 36 h and 48 h than those in ADM group (P＜0.01， P＜0.05 and P＜0.01, respectively). There were also differences at 8 and 16 h, but there were no statistical significance. The expression of CD44 in cells decreased. The mean fluorescence intensity of ICAM-1 raised gradually, and then came to peaking at 36 h, but there was no significant difference between two groups. All the above indices between different phases in the same group showed significant differences (P＜0.05). Conclusion Both NDV and ADM could make tumor cells degenerate and rupture, but the effect of NDV is more intensive. It could increase the fragility of cells and hasten the process of cell rupture. Disintegrated cancer cell and changes of adhesion molecule could lead cancer cells be identified, encapsulated, and killed by immune cells under static condition.
Objective To investigate the effects of adenovirus-mediated melanoma differentiation-associated gene-7 (mda-7)/IL-24 and/or adriamycin (ADM) on transplanted human hepatoma in nude mice and to explore a new way for hepatoma gene therapy combined with chemotherapy. Methods The recombinant adenovirus vector carrying Ad.mda-7 was constructed; Ad.mda-7 and/or ADM were injected into the tumor-bearing mice. Their effects on the growth of the tumor and the survival time of the mice were observed. The expressions of VEGF and TGF-β1 were detected by an immunohistochemistry method. Results Ad.mda-7 was constructed and expressed in vivo successfully. Compared with other three groups 〔control group (43.4±1.67) d, ADM group (64.2±4.14) d, Ad.mda-7 group (61.4±1.67) d〕, the mice treated with Ad.mda-7 combined with ADM had longer average survival time 〔(83.8±4.82) d, P＜0.01〕; the average size of tumor treated with Ad.mda-7 combined with ADM diminished significantly compared with that treated with ADM or Ad.mda-7 separately (P＜0.01). VEGF and TGF-β1 expressions of Ad.mda-7 group were (56.2±7.7)%, (35.2±4.5)%, respectively, and were lower than those in ADM group (VEGF: P＜0.05; TGF-β1: P＜0.01). VEGF expression of Ad.mda-7+ADM group was (37.3±5.0)%, and was significantly lower than that in other three groups (P＜0.01). TGF-β1 expression of Ad.mda-7+ADM group was (31.2±3.1)% and significantly lower than that in control group and ADM group (P＜0.01), however, there was no significant difference compared with Ad.mda-7 group (Pgt;0.05). Conclusion Ad.mda-7 combined with ADM has b antitumor potency and synergistic effects and suppresses the growth of human HCC xenograft in nude mice, possibly by inducing the apoptosis of hepatoma cell lines and suppressing tumor angiogenesis.
Objective To investigate the effect of the drug-resistance characteristic of neoplasm cell on the expression of Fas during the chemical medi-cure.Methods The adriamycin-resistance hepatic carcinoma cells (HepG2 cell lines) were estabilished by cell biology. Changes of expression of the HepG2 cell lines was determined by immunohistochemistry. Results When the HepG2 cell lines were not induced by adriamycin, the expression of Fas of them was weak and Fas mainly existed in cell membrane. When induced by adriamycin, the expression was enhanced and Fas mainly existed in cytochylema. Simultaneously, the death rate of the cell lines changed. The death rate of the drug-resistance cell lines in 0.1 μg/ml ADM was almost as same as that of non-drug-resistance cell lines without ADM (Ｐ＞0.05) and was significantly different from that of non-drug-resistance cell lines in 0.1 μg/ml ADM (Ｐ＜0.05). Conclusion Changes of the expression of Fas may be one of the drug-resistance mechanisms of carcinoma cell.