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

Published byHenryka Krzemińska Modified over 4 years ago

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Presentation on theme: "PD and efficacy of AZD4785 in a KRAS wild-type lung cancer PDX model"— Presentation transcript:

1 Fig. 6. PD and efficacy of AZD4785 in a KRAS wild-type lung cancer PDX model.
PD and efficacy of AZD4785 in a KRAS wild-type lung cancer PDX model. Mice bearing LXFA 526 tumors were treated with PBS, AZD4785, or CTRL ASO at 50 mpk 5× weekly. (A) KRAS and DUSP6 expression measured by qRT-PCR in the LXFA 526 tumors after 4 weeks of dosing. The expression is normalized to 18S rRNA and expressed relative to PBS. (B and C) KRAS protein expression measured by IHC in LXFA 526 tumors after 4 weeks of dosing. (B) Representative images are shown (scale bars, 100 μm) and (C) quantitation of KRAS (H score) determined by Image analysis platform. Data are the mean H score and SE. (D) AZD4785 showed modest inhibition of tumor growth versus PBS (51%; P = 0.001); however, there was no significant TGI compared to the CTRL ASO. Data shown are treatment group geometric mean and SE. (E) Surrogate endpoint survival graphs for the LXFA 526 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.

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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.

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

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.

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. 4. Antitumor efficacy of ERY974 against various cancer types.

Fig. 4. Antitumor efficacy of ERY974 against various cancer types.
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Group data during free walking between sessions 1 and 16.
Fig. 7 Correlation of NHP and human ISGs.

Fig. 7 Correlation of NHP and human ISGs.
Differentiation of AZD4785 from MAPK pathway inhibitors in vitro

Differentiation of AZD4785 from MAPK pathway inhibitors in vitro
NCMs regulate T cell survival in TLOs via PD-L1.

NCMs regulate T cell survival in TLOs via PD-L1.
Fig. 5 Hypoxic tumors from obese mice associate with increased production of IL-6 by adipocytes and myeloid cells. Hypoxic tumors from obese mice associate.

Fig. 5 Hypoxic tumors from obese mice associate with increased production of IL-6 by adipocytes and myeloid cells. Hypoxic tumors from obese mice associate.
Fig. 5 Quantitative assessment of the efficacy of the tissue-engineered implant to heal the TMJ disc defect. Quantitative assessment of the efficacy of.

Fig. 5 Quantitative assessment of the efficacy of the tissue-engineered implant to heal the TMJ disc defect. Quantitative assessment of the efficacy of.
Antitumor effect of local cancer immunotherapy treatment in various tumor models. Antitumor effect of local cancer immunotherapy treatment in various tumor.

Antitumor effect of local cancer immunotherapy treatment in various tumor models. Antitumor effect of local cancer immunotherapy treatment in various tumor.
Fig. 1. MSCs undergo in vivo apoptosis after infusion without affecting immunosuppression. MSCs undergo in vivo apoptosis after infusion without affecting.

Fig. 1. MSCs undergo in vivo apoptosis after infusion without affecting immunosuppression. MSCs undergo in vivo apoptosis after infusion without affecting.
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.

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.
Fig. 3 M7824 inhibits tumor growth and metastasis and provides long-term antitumor immunity. M7824 inhibits tumor growth and metastasis and provides long-term.

Fig. 3 M7824 inhibits tumor growth and metastasis and provides long-term antitumor immunity. M7824 inhibits tumor growth and metastasis and provides long-term.
Fig. 2 Preserved long-term functionality of the TEHVs over 1-year follow-up as assessed by ICE and cardiac MRI flow measurements. Preserved long-term functionality.

Fig. 2 Preserved long-term functionality of the TEHVs over 1-year follow-up as assessed by ICE and cardiac MRI flow measurements. Preserved long-term functionality.
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Fig. 6. Nontaxane chemotherapies induce TMEM-dependent prometastatic changes in the breast cancer microenvironment. Nontaxane chemotherapies induce TMEM-dependent.
Fig. 4 High P-eIF2α expression in human prostate tumors with loss of PTEN function is associated with increased risk of metastasis or death after surgery.

Fig. 4 High P-eIF2α expression in human prostate tumors with loss of PTEN function is associated with increased risk of metastasis or death after surgery.
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Fig. 8 Combining M7824 with radiation or chemotherapy enhances antitumor efficacy. Combining M7824 with radiation or chemotherapy enhances antitumor efficacy.

Fig. 8 Combining M7824 with radiation or chemotherapy enhances antitumor efficacy. Combining M7824 with radiation or chemotherapy enhances antitumor efficacy.
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