PD and efficacy of AZD4785 in KRAS mutant lung cancer xenograft models

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Inhibition of CR HCT-116 (A and B) or CR HT-29 cells (B) xenografts in EPA and/or FuOx-treated SCID mice. Inhibition of CR HCT-116 (A and B) or CR HT-29.

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Fig. 2. Effects of AZD4785 on proliferation and MAPK pathway signaling in KRAS mutant and wild-type cancer cells in vitro. Effects of AZD4785 on proliferation.

Differentiation of AZD4785 from MAPK pathway inhibitors in vitro

Fig. 1. Potent and selective down-regulation of KRAS mRNA and protein by AZD4785 in vitro and in vivo. Potent and selective down-regulation of KRAS mRNA.

Three different types of transfer functions with a codomain of [0,1].

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Human cells produce type I and III IFNs upon Af stimulation.

Fig. 7 Correlation of NHP and human ISGs.

Differentiation of AZD4785 from MAPK pathway inhibitors in vitro

Fig. 6 In utero injection of inflammatory cytokines or adoptive transfer of activated T cells leads to pregnancy loss. In utero injection of inflammatory.

Fig. 5 Correlation of RNA expression and protein abundance.

BAP1 deficiency results in thymic atrophy and loss of thymocyte populations. BAP1 deficiency results in thymic atrophy and loss of thymocyte populations.

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Antitumor effect of local cancer immunotherapy treatment in various tumor models. Antitumor effect of local cancer immunotherapy treatment in various tumor.

Tumor control by necroptotic cells requires BATF3+cDC1 and CD8+leukocytes. Tumor control by necroptotic cells requires BATF3+cDC1 and CD8+leukocytes. (A)

Fig. 3 ROC curves of mCCNA1 and mVIM assayed in esophageal cytology brushings from control normal-appearing GE junctions versus BE and EAC cases. ROC curves.

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Fig. 4. The effect of combined inhibition of BCL-2 and BCR-ABL on leukemia LT-HSC frequency. The effect of combined inhibition of BCL-2 and BCR-ABL on.

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Fig. 1. Potent and selective down-regulation of KRAS mRNA and protein by AZD4785 in vitro and in vivo. Potent and selective down-regulation of KRAS mRNA.

Fig. 3. Increased expression of exhaustion markers and apoptosis markers on CAR8 cells in the presence of TCR antigen. Increased expression of exhaustion.

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Pharmacological targeting of CDs promotes response to KRASG12C inhibition in vivo. Pharmacological targeting of CDs promotes response to KRASG12C inhibition.

Fig. 5. Vascularization of human liver seed grafts.

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NT157 treatment inhibits LNCaP xenograft growth and delays castration-resistant progression. NT157 treatment inhibits LNCaP xenograft growth and delays.

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Fig. 6 The combined therapeutic efficacy of N-pepABS and low dose of Dox on MDA-MB-231 xenografts. The combined therapeutic efficacy of N-pepABS and low.

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PDL192 and inhibit the growth of xenograft tumors.

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Fig. 7 BEL immune response.

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Fig. 2. Mechanism of PD-L1 down-regulation in NOD HSPCs.

Fig. 5 DDO-5936 dose-dependently impairs the growth of xenografted HCT116 cells in nude mice. DDO-5936 dose-dependently impairs the growth of xenografted.

Fig. 6 TNF-α neutralization prevents ZIKV-induced seizures in mice.

Fig. 8 Immune correlates of protection.

PD and efficacy of AZD4785 in a KRAS wild-type lung cancer PDX model

Fig. 2 Combined transcriptome profiling, ChIP-seq, and ATAC-seq analysis identifies 14 highly plausible direct targets of Runx. Combined transcriptome.

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In response to allergen, T cells and ILCs are equally important sources of IL-13. In response to allergen, T cells and ILCs are equally important sources.

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Fig. 4. PD and efficacy of AZD4785 in KRAS mutant lung cancer xenograft models. PD and efficacy of AZD4785 in KRAS mutant lung cancer xenograft models. (A to C) Mice bearing NCI-H358 tumors were treated with PBS, AZD4785, or CTRL ASO at 50 mpk 5× weekly for 4 weeks. (A) KRAS, DUSP4, and DUSP6 mRNA were measured in NCI-H358 tumors at the end of the study by qRT-PCR. The expression was normalized to 18S ribosomal RNA (rRNA) and expressed relative to PBS. Data are shown as individual tumor data, treatment group geometric mean, and SE. (B) AZD4785 significantly inhibited tumor growth of NCI-H358 tumors compared to PBS (TGI, 72%; P = 0.0047) and CTRL ASO (TGI, 75%; P = 0.001). Data are shown as the geometric mean of the tumor volume and SE. (C) Surrogate endpoint survival graphs for the NCI-H358 study. Data are shown as the percentage of remaining animals with tumors <4× the initial starting volume in each treatment group. (D to F) Mice bearing NCI-H1944 tumors were treated with PBS, AZD4785, or CTRL ASO at 50 mpk 5× weekly for 7 weeks. (D) KRAS, DUSP4, and DUSP6 mRNA were measured in NCI-H1944 tumors at the end of the study by qRT-PCR. The expression was normalized to ACTIN and presented relative to PBS. Data are shown as individual tumor data, treatment group mean, and SE. (E) AZD4785 significantly inhibited tumor growth compared to PBS (TGI, 80%; P = 0.001) and CTRL ASO (TGI, 67%; P < 0.001). Data are shown as the geometric mean of the tumor volume and SE. (F) Surrogate endpoint survival graphs for the NCI-H1944 study. Data are shown as the percentage of remaining animals with tumors <4× the initial starting volume in each treatment group. Sarah J. Ross et al., Sci Transl Med 2017;9:eaal5253 Copyright © 2017 The Authors, some rights reserved; exclusive licensee American Association for the Advancement of Science. No claim to original U.S. Government Works.