Chapter 3 │ Page 86 tested this combination in the most resistant HNSCC-PDO, i.e., HNSCC_001T. Although no significance between mono- and combination therapies was reached, we noted a decrease in organoid survival when NTP was added to both CDDP concentrations, with the biggest e ect in the NTP-CDDP1,04µM combination. A mean normalized organoid survival of 1.83 for CDDP1,04µM vs 1.59 for COMBO1,04µM (p = 0.0911) was observed. Figure 5: NTP-CDDP combination treatment in the HNSCC_001 organoid. Organoids were followed up for 96 hours post treatment with live-cell imaging and processed with the in-house developed Orbits® platform. Data presented as mean ± SEM (n = 9, 3 independent repeats). Statistical significance for all pairwise comparisons was determined via linear mixed model analysis with Tukey’s correction for multiple testing. Reached significance was detected compared to untreated controls (* p ≤ 0.05). Building on our observations that NTP addition could improve the e icacy of CDDP to inhibit tumor kinetics in both the 3D spheroid model and the state-of-the-art HNSCC-PDOs, our next goal was to evaluate the immunogenic capacity of this potent novel strategy. 3.3. The Addition of NTP Improves the Expression of a Diverse Set of DAMPs Following CDDP Treatment CDDP treatment has long been considered to be non-immunogenic, but more recent studies have shown their ability to induce some features of anti-tumor immunity when used at low doses or combined with endoplasmic reticulum stressors/ICD inducers[30, 43, 44]. Interestingly, our lab previously identified NTP-
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