ir-AEs ir-AEs[38][39]ir-AEsICIsir-AEsir-AEs ir-AEs6-12[40]ICIs2-4(1)ir-AEs ir-AEsTNF-[39]TNF-MMFTNF-; [41]ICIsir-AEs 3

ir-AEs ir-AEs[38][39]ir-AEsICIsir-AEsir-AEs ir-AEs6-12[40]ICIs2-4(1)ir-AEs ir-AEsTNF-[39]TNF-MMFTNF-; [41]ICIsir-AEs 3.5. another screen 2.2.3. ICIsir-AEs 12 13ir-AEs em meta /em ir-AEsir-AEs13.3%(95%CI: 9.8%-16.7%)ir-AEs1.2%(95%CI: 0.8%-1.6%)CTLA-4(31.6%, 95%CI: 20.6%-42.6%)(34.0%, 95%CI: 30.2%-37.9%)PD-1/PD-L13ir-AEs4.6%(95%CI: 3.2%-5.9%)31.6%(95%CI: 1.1%-2.2%)PD-15.6%(95%CI: 4.6%-6.5%)2%;8.3%(95%CI: 6.1%-10.6%)33.3%(95%CI: 1.8%-4.8%)ir-AEsICIsCTLA-4(29.1%95%CI: 25.2%-32.9%)PD-1CTLA-4(18.2%, 95%CI: 15.1%-21.4%)PD-L1(0.5%, 95%CI: 0%-0.9%)(0.3%, 95%CI: SB-408124 HCl 0%-0.6%)ir-AEs(10%)ir-AEs; PD-1CTLA-4(15.8%, 95%CI: 12.8%-18.8%)3ir-AEs(7.3%, 95%CI:

B

B. growth of non-malignant cells. Thomas-EMF also inhibited B16-BL6 cell proliferation studies showed that exposure of malignant cells to Thomas-EMF for 15 min advertised Ca2+ influx which could become clogged by inhibitors of voltage-gated T-type Ca2+ channels. Blocking Ca2+ uptake