Real-World Evidence of Patient Outcome Following Treatment of Advanced Gastrointestinal Stromal Tumor (GIST) with Imatinib, Sunitinib, and Sorafenib in Publicly Funded Health Care in Poland.

BACKGROUND This study aimed to undertake an analysis of ten years of real-world evidence (RWE) on overall survival (OS) following treatment of advanced gastrointestinal stromal tumor (GIST) with imatinib, sunitinib, and sorafenib using data from the Polish National Health Fund. MATERIAL AND METHODS Data from the Polish National Health Fund, the sole Polish public payer, identified 1,641 patients with advanced GIST who were treated with imatinib (n=1047), sunitinib (n=457), and sorafenib (n=137). The differences in overall survival (OS) were analyzed. RESULTS For patients with advanced GIST, the median follow-up time for patients treated with imatinib was 71 months (95% CI, 64.8-79.2), the median OS was 56.9 months (95% CI, 50.4-61.2), with survival at 12 months (89.5%), 24 months (77.9%), 36 months (66.9%), and 60 months (48.4%). The median follow-up time for patients treated with sunitinib was 41.4 months (95% CI, 34.6-49.3), the median OS was 22.8 months (95% CI, 19.2-26.8), with survival at 12 months (68.2%), 24 months (47.1%), and 36 months (31%). The median follow-up time for patients treated with sorafenib was 17.4 months (95% CI, 14.6-22.9), the median OS was 16.9 months (95% CI, 13.7-24.3), with survival at 12 months (61.9%), at 24 months (36.2%), and at 36 months (16.8%). CONCLUSIONS Real-world data collected in a ten-year period confirmed the effectiveness of the use of imatinib, sunitinib, or sorafenib for the treatment of advanced GIST and was comparable with the findings from clinical trials.

Natural killer cell-dendritic cell crosstalk in the initiation of immune responses.

Dendritic cells (DCs) and natural killer (NK) cells play a critical role in early defences against cancer and infections. They specialise in complementary functions, including IL-12 or IFN-alpha/beta secretion and antigen presentation for the former, and IFN-gamma secretion and killing of infected or tumour cells for the latter. Both DCs and NK cells are also sensors of the immune system that have developed different, but partially overlapping, systems to identify pathology associated danger signals. Evidence of NK-DC interaction has accumulated recently. This interaction may lead to NK cell activation, DC activation, or apoptosis depending on the activation status of both cell types. Thus, the outcome of NK-DC crosstalk is likely to influence both innate and adaptive immune responses. This review addresses the molecular mechanisms under-lying the different NK-DC interactions, and their in vivo significance in anti-tumour or antimicrobial immunity. Finally, we discuss the potential clinical implications of this new field.