There were two discordant cases seen in which individuals were categorized as ALK positive by FISH but were negative by our analysis. The exact same people showed no clinical response to crizotinib, indicating FISH false positive results. Considering the inherent interobserver variability and subjective character in FISH and IHC review, GS-1101 cost this may be a possible reason for the discordance. In summary, an alternative method has been developed by us for screening ALK fusions in NSCLC using direct, digital log profiling with NanoStrings nCounter technology. This would be beneficial in labs already equipped with a NanoString device, in which, additionally to standard gene expression and DNA copy number studies, ALK mix diagnosis can be involved as an application. The assay is easy to perform, quantitative, reproducible, very painful and sensitive, automatable, and costeffective. We believe that the ALK fusion transcript analysis may be a more practical approach for screening patients with NSCLC and should be thought about as a prescreening solution before FISH in the recognition of unusual ALK fusion cancers for ALK targeted therapies. Recently, considerable interest has been centered on the possible great things about tumor necrosis factor related apoptosis inducing ligand for cancer treatment because so many tumor cell types have been shown to be sensitive and painful to TRAIL induced apoptosis. On the other hand, untransformed cells are generally TRAIL Cellular differentiation resistant. The design of TRAIL is related to other members of the tumor necrosis family of cytokines, and its gene is found on chromosome 3 at position 3q26. WALK is capable of inducing apoptosis by way of a caspase dependent process that is activated via the professional apoptotic TRAIL receptors, TRAIL R1 and TRAIL R2, which incorporate cytoplasmic death domains. Some studies have established that the mix of angiogenesis drugs recombinant TRAIL and chemotherapy or radiotherapy enhances TRAIL induced apoptotic effects. General, the vast majority of TRAIL associated reports have examined the therapeutic factors and general side effects of TRAIL and the apoptotic signaling pathways of TRAIL receptors. But, it’s become clear that TRAIL also causes several non apoptotic signaling pathways. In pancreatic ductal adenocarcinoma cells this contributes to metastasis, invasion and irritation, as shown within an orthotopic pancreatic cyst type in SCID mice. Overexpression of TRAF2 and Bcl xL in pancreatic cyst cells has previously been reported. Consequently, the goal of this study was to analyze the functions of these proteins in TRAIL induced expression of uPA and IL 8. We also analyzed the involvement of TRAIL R1 and TRAIL R2 in these effects.