BackgroundTo compare the efficacy and toxicity of anti-programmed cell death receptor 1 (PD-1) and anti-programmed cell death ligand 1 (PD-L1) versus docetaxel in previously treated patients with advanced non-small cell lung cancer (NSCLC).Materials and methodsPhase III randomised clinical trials (RCTs) were identified after systematic review of databases and conference proceedings. A random-effect model was used to determine the pooled HR for overall survival (OS), progression-free survival (PFS) and duration of response. The pooled OR for overall response and treatment-related side effects were calculated using the inverse-variance method. Heterogeneity was measured using the τ2 and I2 statistics.ResultsAfter the systematic review, we included four phase III RCTs (n=2737) in this meta-analysis. The use of anti-PD-1/anti-PD-L1 agents (atezolizumab, nivolumab and pembrolizumab) was associated with better OS in comparison with docetaxel alone (HR: 0.69; 95% CI 0.63 to 0.75; p<0.00001). Similarly, the PFS and duration of response was significantly longer for patients receiving immunotherapy (HR: 0.85; 95% CI 0.75 to 0.96; p=0.007 and HR:0.32; 95% CI 0.24 to 0.43; p<0.00001, respectively) versus single agent chemotherapy. The overall response rate was also higher for patients who received any anti-PD-1/anti-PD-L1 therapy in comparison with docetaxel (OR: 1.77; 95% CI 1.26 to 2.50; p=0.001). Regarding treatment-related side effects grade 3 or higher, patients who received immunotherapy experienced less events than patients allocated to docetaxel (OR: 0.19; 95% CI 0.12 to 0.30; p<0.00001)ConclusionThe use of anti-PD-1/anti-PD-L1 therapy in patients with progressive advanced NSCLC is significantly better than the use of docetaxel in terms of OS, PFS, duration of response and overall response rate.

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, all patients diagnosed with SCLC and NSCLC treated with chemotherapy at National Institute of Oncology at Asuncion-Paraguay were analyzed retrospectively. Demographic information, treatment modalities, tumor response, were recorded .SPSS 19 was used to analyze the data with p <0.05 as significance. Results: We studied 370 subjects, 28% received chemotherapy, 14,8% chemotherapy plus radiotherapy, 1,1% surgery plus chemotherapy. At IIIA stage NSCLC 18,2% was treated with PTX and CBDCA 1cycle and18,2% with PTX+CBDCA 4cycles (p <0.05). IIIB stage NSCLC 17,6% patients received PTX+CBDCA 4cycles and 22,1% PTX+CBDCA 6 cycles (p<0.05). At IIIA stage NSCLC received PTX + CBDCA 4 cycles.(p<0.05). SCLC has no statistical significance relation between stage and type of chemotherapy. The tumor response to first-line chemotherapy shows 47,5% has no response. 32,4% has response (p<0.05). 17,6% abandoned treatment (p <0.05).Patients who received PTX+CBDCA show a high percentage of abandoned treatment as 20% and patients receiving CDDP +VP-16 had a high abandoned treatment of 80% (p<0.05). 59.8% patients treated with chemotherapy were from countryside places and 40,2% from urban places (p>0.05), 25,6% of patients receiving chemotherapy and 29,6% were receiving chemotherapy and radiotherapy were farmers (p<0.05). 80,4% patients receiving chemotherapy were smokers (p<0.05). 45,1% patients consumed alcohol regularly (p<0.05). Only 12,7% patients had family lung cancer genetic precedence (p<0.05). 43,1% patient under chemotherapy had exposure to toxic environmental agents (p <0.05). 53,5% patient receiving chemotherapy had a stage 2 of ECOG Performance Status (p <0.05). Tumor response to chemotherapy at NSCLC show: 100% patients who received dFdC+CDDP 4cycles; 65,5% with PTX+CBDCA 4 cycles; 42,9% CDDP+VP-16 4 cycles; 65% PTX + CBDCA 6 cycles; 100% of CDDP+ VP16 6 cycles; 100% of dFdC 6 cycles (p <0.05) SCLC has no statistical significance at this analysis. At Second line chemotherapy to NSCLC 23,8% received dFdC+ CDDP 1 cycle and 14,3% PTX+CBDCA 1 cycle. Only 3 patients received third line

reference. CDH1 expression levels were quantified by two step reverse transcription dPCR with GAPDH as an endogenous control. Results: The combined in silico and literature-search based approach gave rise to a list of 14 miRNAs possibly involved in the regulation of CDH1 expression in GC (miR-506, miR-217, miR-199a, miR-153, miR-544a, miR-34c, miR-141, miR-429, miR-101, miR-200a, miR-200b, miR-200c, miR-26b, miR-23a). Tumor and normal paired samples from 17 patients have been analyzed so far. At the end of the qPCR reactions, 8 miRNAs could be successfully quantified (miR-141, miR-429, miR-200a, miR-200b, miR-200c, miR-101, miR-26b and miR-23a); among those miR-101 (p ¼ 0.00236) and miR-26b (p ¼ 0.001623) were found to be significantly lower in tumors compared to normal tissue, while miR-200c showed borderline significance (p ¼ 0.05373). With respect to CDH1, it was similarly found to be significantly less in tumor than normal tissue (p ¼ 0.01). Meanwhile, no significant correlations were found between miRNAs and CDH1 expression levels. Conclusion: Based on our preliminary results both miR-26 and miR-101 seem to contribute to IGC carcinogenesis. To further investigate whether they act by perturbing Ecadherin-mediated signaling and cell-cell adhesion we are planning to analyze a bigger case series.