This study was aimed to investigate effect of aconite alkaloids on proliferation and apoptosis of hu-man gastric cancer cell line SGC-7901 . Effects of different concentrations of aconite alkaloids on proliferation of human gastric cancer cell line SGC-7901 were investigated with MTT assay; induced apoptosis and cell cy-cle blocking were detected with flow cytometer ( FCM ) . The results showed that the IC50 of aconite alkaloids on human gastric cancer cell line SGC-7901 was 0 . 2318 ± 0 . 0022 , 0 . 1601 ± 0 . 0227 , 0 . 1031 ± 0 . 0231 mg/ml at 24 h , 48 h and 72 h , respectively , compared to the control group with significant difference ( P <0.01). When the aconite alkaloids concentration was 0.8 mg/ml, it appeared with obvious apoptosis. The apop-tosis rate was ( 59 . 38 ± 5 . 05 )%. The FCM detection showed that compared with control group , the percentage of S-phase cells increased in the treatment group . And a typical sub-diploid peak appeared before G0 / G1 phase . It was concluded that aconite alkaloids can inhibit the proliferation of human gastric cancer cell line SGC-7901 in vitro, induce the apoptosis of cells and make SGC-7901 cells remain in S phase.

Objective:To investigate the effect of gemcitabine on myeloid derived suppressor cells (MDSC) in the spleen of B lymphoma cell-bearing mice, and the therapeutic effect of gemcitabine combined with intratumoral injection of dendritic cells (DCs) in treatment of large B lymphoma. Methods: BALB/c mice were inoculated subcutaneously with B lymphoma A20 cells; large tumors were formed 30 d after inoculation. Gr-1~+ CD11b~+ MDSC proportion in the spleen was analyzed by flow cytometry before and after gemcitabine treatment. Splenic MDSC sorted by immunomagnetic beads was further treated with gemcitabine, and then the apoptosis of MDSC was examined by Annexin-V/PI staining. Tumor growth and survival time of A20 tumor-bearing mice were observed after treatment with gemcitabine and intratumoral injection of DCs. Results: Splenic Gr-1~+ CD11b~+ MDSC ratio in A20 cell-bearing mice was 10 times higher than that in the normal mice. Gemcitabine induced apoptosis and necrosis of purified MDSC in vitro in a time-dependent manner. The percentage of MDSC in the spleen of A20 tumor-bearing mice was decreased after injection of a single dose of gemcitabine. Gemcit-abine or intratumoral injection of DCs alone inhibited growth of tumor to a certain degree, with the mean survival periods of mice in the gemcitabine, DCs, and untreated groups being (48.8±3.6) d, (47.2±7.4) d, and (38.8±2.2) d, respectively. Gemcitabine chemotherapy combined with intratumoral DC injection resulted in continuous shrink of the tumors, and 60% of the mice survived for more than 90 d. Conclusion: Gemcitabine can effectively eliminate splenic MDSC in tumor-bearing mice. Gemcitabine chemotherapy and DCs immunotherapy can work synergistically in the treat-ment of huge lymphoma. These results provide an experimental basis for the comprehensive chemotherapy and immunotber-apy of relapsed or refractory lymphoma.

Objective To assess the efficacy of mecobalamin and glutathione in preventing the neurotoxicity induced by oxaliplatin (L-OHP).Methods A randomized,placebo and control study was made ,in which 9 6 patients with colorectal cancer received L-OHP and 5-Fluorouracil (5-FU)was randomly divided into control group treated with normal saline,mecobalamin group with mecobalamin and glutathione group with glutathione,respectively,32 cases for each.Rate of neurotoxicity and severity was observed by L-OHP-specific neurotoxicity grading and neurological symptom score (NSS).Results Rates of neurotoxicity in control group,mecobalamin group and glutathione group were 90.3%(28 /32),46.7%(14 /32)and 59.4%(19 /32)respectively.After 3-cycle and 6-cycle chemotherapy,the rate of neurotoxicity in degree Ⅱ~Ⅲ was lower in mecobal-amin group than in other groups,but the differences were not significant (P >0.05),whereas NSS score was obviously lower in mecobalamin group than in other groups (P <0.05,P <0.01),but the difference between control group and glutathione group was not significant (P >0.05).Conclu-sion Mecobalamin can prevent the rate and severity of oxaliplatin-induced neurotoxicity.

Objective To assess the efficacy of mecobalamin and glutathione in preventing the neurotoxicity induced by oxaliplatin (L-OHP).Methods A randomized,placebo and control study was made ,in which 9 6 patients with colorectal cancer received L-OHP and 5-Fluorouracil (5-FU)was randomly divided into control group treated with normal saline,mecobalamin group with mecobalamin and glutathione group with glutathione,respectively,32 cases for each.Rate of neurotoxicity and severity was observed by L-OHP-specific neurotoxicity grading and neurological symptom score (NSS).Results Rates of neurotoxicity in control group,mecobalamin group and glutathione group were 90.3%(28 /32),46.7%(14 /32)and 59.4%(19 /32)respectively.After 3-cycle and 6-cycle chemotherapy,the rate of neurotoxicity in degree Ⅱ~Ⅲ was lower in mecobal-amin group than in other groups,but the differences were not significant (P >0.05),whereas NSS score was obviously lower in mecobalamin group than in other groups (P <0.05,P <0.01),but the difference between control group and glutathione group was not significant (P >0.05).Conclu-sion Mecobalamin can prevent the rate and severity of oxaliplatin-induced neurotoxicity.

Patient-derived tumor xenograft(PDTX)models are based on the transfer of primary tumor tissue directly from the patient into immunodeficient mice.PDTX models retain many of the key characteristics of the original cancers,including heterogeneity,histo-logical characteristics,molecular diversities,and host microenvironments.These models do not only serve as platforms for co-clinical trials to determine precisely targeted therapies,but can also be applied to the development of biomarkers and action targets for drug responsiveness and personalized drug selection.PDTX models combined with clinical,genomic,and pharmacodynamic data and ap-plied to the individualized treatment of cancer patients could increase the specificity of drug use,improve clinical treatment success, and promote the development of individualized treatment and precise medical regimes.This review summarizes the historical back-ground,influential modeling factors,clinical applications,and limitations of PDTX mouse models.