Tumor immunotherapy is highlighted in tumor studies and has a remarkable curative effect on tumors. Programmed cell death-1 (PD-1), which is mainly expressed in activated T and B cells, is an important immune inhibitory molecule. Its ligand PD-L1 could be highly expressed in cancer cells, and the PD-1 pathway shows sustained activation in a tumor micro-environment. PD-1/PD-L1 inhibitors can block the combination of PD-1 and PD-L1, inhibit negative to regulatory signals, and restore the activity of T cells, thereby enhancing immune response. Recent studies showed that PD-1 and PD-L1 inhibitors have been effective in many tumor types. This review summarizes PD-1/PD-L1 inhibitors and their clinical effects on different tumor types.

Background and purpose:Quinonoids can change the cell cycle distribution of tumor cells, and effect the radiosensitizing. This study aimed to investigate the radiosensitization effects, cell cycle and apoptosis of cryptotanshinone on H22 hepatoma-bearing mice. Methods:The mouse hepatoma H22 model was established, then divided into blank control group, irradiation alone group, high dose of cryptotanshinone group, cryptotanshinone (low, medium and high)+IR groups. After irradiated, observed the growth of tumor’s conditions, record epigenetic tumor irradiation time, calculated the delay time of tumor growth and enhancement factor (EF). After 22 days, mice were killed, stripped tumor, and calculated the inhibition rate. The cell cycle distribution and apoptosis were measured by lfow cytometry. Results:Cryptotanshinone (low, medium and high) groups inhibited the tumor growth better than the blank group, and had the signiifcant radiosensitizing effect. The enhancement factor was 1.22, 1.43,2.19, respectively. Cells were treated with cryptotanshinone which had significant effects on cell cycle, and induced apoptosis, which indicated signiifcant G2/M phase arrest and a decrease in S phase. Conclusion:Cryptotanshinone inhibited the tumor growth and had the radiosensitizing effects on H22 hepatoma-bearing mice. One of the mechanism may be that it might make significant G2/M phase arrest and S phase decreased, and induced apoptosis. So cells were more sensitive to radiation.

OBJECTIVE:To study the inhibitory effect of dihydrotanshinone(DTS)on human lung cancer GLC-82 cell and its mechanism. METHODS:After treated with 0(blank control),5,10,20,40,80 and 100 μg/ml DTS for 24 and 48 h,MTT as-say was used to measure the inhibition rates and IC50 of cells;cell apoptosis was detected by flow cytometry after treated with 17.85 μg/ml DTS for 12,24 and 48 h to calculate apoptotic rate;Western blot was used to detect the protein expressions of Bcl-2, Bax and Caspase-3. RESULTS:Compared with blank control group,different concentrations of DTS inhibited the proliferation of cells;24 and 48 h maximal inhibition rate were 54.48% and 64.95%,respectively;IC50 were 62.36 and 33.94 μg/ml. DTS could induce cell apoptosis in positive time dependent manner,and the range of inhibition rate was 5.6%-29.6%;Western blot showed DTS could down-regulate the expression of Bcl-2 protein and up-regulate the expression of Caspase-3 protein (P<0.01 or P<0.05). CONCLUSIONS:DTS have significant inhibitory effect on GLC-82 cells and also induce cell apoptosis,by a possible mech-anism of down-regulating the expression of Bcl-2 protein and up-regulating the expression of Caspase-3 protein.

'Social beings' model of standardized training program for residents in Shanghai is one of the important measures in the health care reform. According to the requirements of the standardized training of residents in thoracic surgery, the article preliminarily explored the standardized training model for residents from four aspects such as individualized treatment of different professional backgrounds, focus-ing on the training needs of residents with different starting point of social beings, developing training programs for different training time and combining the master's degree graduate education. And based on the characteristics of thoracic surgery, it also summed up the past experience and explored the clinical practice teaching.

OBJECTIVETo investigate the proliferation effects and apoptosis induction of cryptotanshinone on Hela cell line of cervical cancer.

METHODThe MTT assay was used to detect the growth inhibition rates of Hela cells at 24, 48, 72 h which cultured with cryptotanshinone in different concentrations. The cell cycle distribution and apoptosis were measured by flow cytometry. The protein expressions of E6, p53 and p21 were studied by Western blot.

RESULTThe different concentrations (0.5-16 mg x L(-1)) of cryptotanshinone had cytotoxicity on Hela cells, which were clearly dose and time-dependent. The IC50 of 24, 48, 72 h were 17.8, 8.17, 6.55 mg x L(-1), respectively. Cells were treated with cryptotanshinone which had significant effects on cell cycle of Hela cell, and induced apoptosis. Western blot showed cryptotanshinone decreased expressions of HPV E6 and increased expressions of p53 and p21 proteins.

CONCLUSIONCryptotanshinone had significant cytotoic and radiosensitization effects on cervical cancer Hela cells. One of the mechanism may be that it might make significant G0/G1 phase arrest and induced apoptosis, a decrease in S phase, and restore the function of p53 to induce apoptosis in Hela cells to kill the tumor cell.

Apoptosis ; drug effects ; Blotting, Western ; Cell Cycle ; drug effects ; Cell Proliferation ; drug effects ; Drugs, Chinese Herbal ; therapeutic use ; Female ; Flow Cytometry ; HeLa Cells ; Humans ; Oncogene Proteins, Viral ; metabolism ; Phenanthrenes ; therapeutic use ; Repressor Proteins ; metabolism ; Tumor Suppressor Protein p53 ; metabolism ; Uterine Cervical Neoplasms ; drug therapy

Objective To investigate the effect of L-carnitine (LCNT) combined with epirubicin (EPI) on cell proliferation and apoptosis of two lung adenocarcinoma cell lines (GLC-82 and A549). Methods GLC-82 and A549 cells were divided into control group, EPI group, LCNT group and EPI+LCNT group, respectively. The cell proliferation rate was examined by MTT assay 24 h after the treatment, and the cell cycle and cell early apoptosis were analyzed by flow cytometry. The expression of P53 and Bcl-2 proteins were detected by Western Blot. Results Compared with the control group, the proliferation rate of GLC-82 and A549 cells was 37.56％(P<0.01) and 6.32％(P>0.05) after 24 hours of 20.00μg/ml LCNT treatment indicating LCNT could promote the proliferation of GLC-82 cells. Compared with the EPI group, EPI+LCNT had smaller inhibitory effect on the proliferation of GLC-82 cells, and the inhibition rate of the EPI+LCNT group was 12.14％lower than that of EPI group (P<0.05). Compared with the EPI group, EPI+LCNT could significantly increase the G0/G1 phase ratio of GLC-82 cells (50.42％±1.21％vs. 25.94％± 0.66％, P<0.01) and A549 cells (54.92％±1.71％vs. 38.63％±0.69％, P<0.01), decrease the S phase ratio of GLC-82 cells (34.21％±0.96％vs. 59.68％±1.25％, P<0.05), and prevent the early apoptosis of GLC-82 cells without affecting apoptosis of A549 cells. Moreover, in the EPI+LCNT group, the expression of P53 protein in GLC-82 and A549 cells was down-regulated (P<0.05), and the expression of Bcl-2 protein in GLC-82 cells was up-regulated (P<0.01) and no significant change in A549 cells (P>0.05). Conclusions Comparing with the EPI, the combination of LCNT and EPI has less proliferation inhibition and apoptosis induction on GLC-82 cells, and without significant effect on A549 cells. LCNT can promote the proliferation of GLC-82 cells and block the cell cycle at G0/G1 phase. This mechanism may be related to down-regulation of P53 protein and up-regulation of Bcl-2 protein expression.