AIM: To explore the differences of efficacy and side-effects in advanced stage non-small cell lung cancer (NSCLC) patients treated with gemcitabine plus cisplatin or vinorelbine plus cisplatin. METHODS: Eligible patients were randomly assigned to GP (gemcitabine+cisplatin) group or NP (vinorelbine plus cisplatin) group. In GP group, 36 evaluable patients were treated with gemcitabine 1000 mg?m~ -2 IV on day 1 and 8 and cisplatin 75 mg?m~ -2 IV which was divided into 1-3 days dosing, in a 21 days per cycle manner. In NP group, 30 evaluable patients were treated with vinorelbine 25 mg?m~ -2 IV on day 1 and 8 and cisplatin 80 mg?m~ -2 IV which was divided into 1-3 days dosing, 21 days per cycle. All the patients at least received two cycles therapy. The response rate, median survival time (MST), l year survival, and side-effects were observed. RESULTS: The response rates were 41.6 % vs 36.7 %; MST were 10.3 months vs 9.6 months; 1 year survival rate were 44.4 % vs 40.0 %(P= 0.33 ) in GP group and NP group, respectively. III-IV grade thrombocytopenia toxicity incurred significantly higher in GP group than in NP group, with the occurrence rate being 47.2 % vs 6.6 % (P

0.05). The adverse reaction rates of the two regimen were no statistical difference. CONCLUSION: The 2-week regimen and the 3-week regimen of L-OHP combined with 5-FU/CF have the same efficacy in MCC patients.

Multidrug resistance (MDR) is the phenomenon observed in tumor cells that describes the simultaneous emergence of cellular resistance to the cytotoxic attack by structurally and mechanism unrelated chemotherapeutic drugs. The mdr 1 gene was sufficient to confer the MDR phenotype, including the expression of the P Glycoprotein (P Gp). P Gp appears to play an important role in tumor cells by acting as an energy dependent efflux pump to remove various drugs from the cell before they have a chance to exert their cytotoxic effects. It is generally accepted that reversal or inhibition of P Gp function in tumor cells is an important way for modulating MDR. It has been demonstrated in the laboratory that MDR mediated by the P Gp may be modulated by a wide variety of compounds. These compounds , which include verapamil and cyclosporin, generally have little or no effect by themselves on the tumor cells, but when used in conjunction with antineoplastic agents, they decrease, and in some instances eliminate, MDR. This paper will introduce some new reversal agents and discuss their physical and chemical characteration and others.

0.05 ); the positive percentage of IGFBP-2 was statistically higher in breast cancer with metastasis in lymph node than those without metastasis in lymph node (P 0.05 ,r_s= 0.271 ). CONCLUSION: The expression of IGFBP-2 may play an important role in the progression, invasion and metastasis of breast cancer, and there is a positive correlation between the expression of IGFBP-2 and ER in breast cancer. It demonstrates that over expression of IGFBP-2 may be a reference to evaluate unfavourable prognosis of breast cancer.

Objective To investigate the enhancing effect of Celecoxib on the anti-proliferative effect of cisplatin (DDP) against human cervical carcinoma HeLa cells and to explore the possible mechanism. Methods After treatment of HeLa cells with Celecoxib or/and DDP, the growth suppression of HeLa cells was measured by MTT assay. Cell cycle and apoptosis were examined by flow cylometry. Results The inhibition of Celecoxib on HeLa cells was dose -dependent and time -dependent.The inhibitory effect was remarkable enhanced in asynergistic or additive pattern after treatment with the combination of Celecoxib and DDP (P =0.000) . Celecoxib (50 μmol/L) and DDP (16 μmol/L) could respectively induce the apoptosis of HeLa cells and this effect of apoptosis induction was increased when combinated Celecoxib with DDP. They could change cell cycle of HeLa cells lines with G_0/G_1 phase cells increasing and S phase cells decreasing. Conclusion Celecoxib combined with DDP shows synergistic anti-tumor effects.

AIM:To observe autophagic apoptosis induced by docetaxel in cervical cancer HeLa cells in vitro,and explore its potential molecular mechanism. METHODS:Cervical cancer HeLa cells in vitro were treated with docetaxel of different concentrations (1,5,10,20,40 ?g/mL) and different time (6,12,24,48,72 h). The growth inhibiting of HeLa cells was observed by methyl thiazolyl tetrazolium(MTT) assay. Inverted microscope and electron microscopy were used to observe cell morphological changes. The apoptosis ratio and cell cycle were determined by flow cytometry(FCM). The expression of autophagy gene Beclin 1 was examined by reverse transcriptase polymerase chain reaction(RT-PCR) technique. RESULTS:Docetaxel inhibited the proliferation of cervical cancer HeLa cells in a dose-dependent and time-dependent manner(P