Fig. 5: Mal LbL NP efficacy depends on lipid-exchange-driven distribution within tumour nodules.
From: IL-12-releasing nanoparticles for effective immunotherapy of metastatic ovarian cancer
a, Schematic of the proposed mechanism of tumour-targeted IL-12 lipid conjugate dissemination from Mal LbL NPs. b,c, B6C3F1 mice inoculated with 106 HM-1-luc tumour cells on day 0 were administered fluorescently tagged Mal LbL of SAT LbL NPs carrying 20 µg of IL-12 on day 14. One day after dosing, the animals were euthanized, and the omentum containing tumour nodules was frozen in an OCT compound and then frozen, sectioned and stained for confocal microscopy analysis. Representative high-magnification confocal images of omental tumour nodules from Mal LbL (b) and SAT LbL (c). d–f, B6C3F1 mice (two cohorts for n = 7 and 5 animals per group per cohort) inoculated with 106 HM-1-luc tumour cells on day 0 were treated on day 7 with NP vehicle control (unloaded LbL), 20 µg of IL-12 as a free cytokine or conjugated to Mal LbL or SAT LbL. Experimental timeline (d), one representative in vivo IVIS whole-animal i.p. BLI readings from two independent experiments (mean ± s.d., n = 7 animals per group; e) and overall survival (f). Statistics derived using all n from experiment with each animal as a data point. Statistical comparisons between survival curves were performed using a log-rank (Mantel–Cox) test.
