Results: The median age of presentation was 57 years, and 47% (n ¼ 57) patients were aged 40-60 years. There were with 55 % males (n ¼ 67), 86 % (n ¼ 104) of all patients were non smokers. PDL1 was positive in 38.8 % (n ¼ 47) patients, with 12.4 % (n ¼ 15) patients having PDL1 ! 50%. PDL1 positivity was not significantly different among gender, smoking status or age or various EGFR mutations. Of all the patients, 15 patients did not take therapy. So survival analysis was possible only for 106 patients. Progression free survival (PFS) for PDL1 negative patients was 11 months (95% C.I. 8.6-13.6 months), while for PDL1 positive patients was 13 months (95% C.I. 6.3-19.6 months) p ¼ 0.986 (not significant). The analysis also showed that PFS in patients with PDL1 positive with DEL 19 mutation was 15 months v/s7 months in L858R mutation(p ¼ 0.09). In PDL1 negative patients, PFS was 12 months v/s 10 monthsin Del 19 v/s L858R mutation. Conclusions: The present study showed a higher PDL1 positivity rate in EGFR mutant patients than what is previously reported. Also, the median PFS was not stastically different in PDL1 negative vs PDL1 positive patients. This is in contradiction to data previously presented. However, it could also be due to the fact that most of our patients were non smokers and could also represnt a geographic variation in PDL1 expression. Further studies are warranted to clarify this data.
investigated the potential use of COX-2 inhibitors in cancer proliferation and apoptosis. Methods: Celecoxib, rofecoxib, etoricoxib, meloxicam, ibufrofen and indomethacin are the COX-2 inhibitors included in this study. Docetaxel and Cisplatin are the chemotherapeutic agents that we combined with COX-2 inhibitors. Lung cancer cell lines (NCI-H1048-Small cell lung cancer, A549-Non-small cell lung cancer) were purchased from ATCC LGC Standards. At indicated timepoint, following 24h and 48h incubation, cell viability and apoptosis were measured with Annexin V staining by flow cytometry. Statistical analysis was performed by GraphPad Prism (version 6). Results: In Small cell lung cancer cells, following 24h incubation, combinations of docetaxel and meloxicam, docetaxel and ibuprofen, docetaxel and indomethacin, showed increased apoptosis when compared to docetaxel alone (p<0.0001). In Non-small cell lung cancer cells, the 24h incubation was not enough to induce satisfactory apoptosis, but following 48h incubation, docetaxel plus indomethacin showed more cytotoxicity when compared to docetaxel alone (p<0.0001). In addition, the combination of cisplatin plus indomethacin was the only combination to be found with higher cytotoxicity when compared to cisplatin alone after 48h treatment (p<0.0001). Conclusion: Depending on the drug, the synergistic effect of COX-2 inhibitors plus chemotherapeutic agents has been demonstrated in lung cancer. Our suggestion is that COX-2 inhibitors could be used as additive and maintenance treatment in combination to antineoplastic agents in lung cancer patients.
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