Fig. 5. Pharmacological JAK2 inhibition in vivo abrogates tumor-initiating potential after chemotherapy. Pharmacological JAK2 inhibition in vivo abrogates.

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Treatment with BLU9931 leads to tumor regression in the FGF19-overexpressing PDX-derived xenograft LIXC012. Treatment with BLU9931 leads to tumor regression.
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Fig. 6. AZD6738 induces DNA damage and apoptosis and exhibits antitumor efficacy in xenograft models of high-risk medulloblastoma and neuroblastoma. AZD6738.
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. 6. Combinatorial VCPI and OV M1 treatment is efficacious in vivo and ex vivo. Combinatorial VCPI and OV M1 treatment is efficacious in vivo and ex.
Fig. 8. In vivo suppression of MM by CMLD
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Fig. 6. Increased efficacy of immunotherapy in lymphangiogenic B16 melanomas depends on CCR7 signaling before therapy and local activation and expansion.
Fig. 8. mRIPO elicits neutrophil influx followed by DC and T cell infiltration into tumors. mRIPO elicits neutrophil influx followed by DC and T cell infiltration.
Fig. 1 ZIKV-related flaviviruses cause fetal demise in mice that can be prevented by mAb treatment. ZIKV-related flaviviruses cause fetal demise in mice.
Fig. 5 A competent Fc is required for the antitumor immune response.
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Fig. 7 Gel scaffold for inhibition of postsurgical recurrence of B16F10 tumors. Gel scaffold for inhibition of postsurgical recurrence of B16F10 tumors.
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Fig. 3 In situ vaccination with CpG and anti-OX40 is therapeutic in a spontaneous tumor model. In situ vaccination with CpG and anti-OX40 is therapeutic.
Fig. 4. BET inhibition sensitizes HR-proficient tumors to PARPi treatment in vivo. BET inhibition sensitizes HR-proficient tumors to PARPi treatment in.
Fig. 4 DMF enhances VSVΔ51 therapeutic efficacy in syngeneic and xenograft tumor models. DMF enhances VSVΔ51 therapeutic efficacy in syngeneic and xenograft.
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Inhibition of JNK signaling sensitizes mammary tumors and metastases to chemotherapy Inhibition of JNK signaling sensitizes mammary tumors and metastases.
Role of immune and inflammatory cells in lung cancer–associated PH
Fig. 8 Combining M7824 with radiation or chemotherapy enhances antitumor efficacy. Combining M7824 with radiation or chemotherapy enhances antitumor efficacy.
Fig. 5 Local gel scaffold for T cell memory response.
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Fig. 4. Improved tumor response to docetaxel in TNBC and trastuzumab in HER2-amplified PDX models with the addition of S Improved tumor response.
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Antitumor effects of FF and gemcitabine on two pancreatic PDX models.
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Fig. 1. β-APP overexpression or exposure to inflammatory mediators induces sIBM-like pathology in cultured rat myocytes that is abrogated by arimoclomol.
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JAK2 knockdown abrogates tumorsphere expansion after chemotherapy
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CD8+ T cells were immunomodulated and required for the efficacy of anti–4-1BB/anti–PD-1 combination treatment. CD8+ T cells were immunomodulated and required.
Fig. 2. BET inhibition enhances PARPi-induced DNA damage.
Effect of MI-773 dosing on long-term efficacy.
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Fig. 3 M7824 inhibits tumor growth and metastasis and provides long-term antitumor immunity. M7824 inhibits tumor growth and metastasis and provides long-term.
IL-6 signaling affects response to erlotinib in head and neck (HNSCC) cells. IL-6 signaling affects response to erlotinib in head and neck (HNSCC) cells.
Fig. 8 Combining M7824 with radiation or chemotherapy enhances antitumor efficacy. Combining M7824 with radiation or chemotherapy enhances antitumor efficacy.
Metformin and rapamycin decreased tumor weights in obese prediabetic mice. Metformin and rapamycin decreased tumor weights in obese prediabetic mice. A:
CO-1686 does not inhibit WT EGFR signaling in vivo and is active in EGFR-mutant transgenic mouse lung cancer models. CO-1686 does not inhibit WT EGFR signaling.
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E-cadherin synthetic lethal effects operate in vivo in E-cadherin–defective breast tumors. E-cadherin synthetic lethal effects operate in vivo in E-cadherin–defective.
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AV3 potentiates the effect of gemcitabine in the PDX model in mice
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Fig. 6. Combinatorial VCPI and OV M1 treatment is efficacious in vivo and ex vivo. Combinatorial VCPI and OV M1 treatment is efficacious in vivo and ex.
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Fig. 5. Pharmacological JAK2 inhibition in vivo abrogates tumor-initiating potential after chemotherapy. Pharmacological JAK2 inhibition in vivo abrogates tumor-initiating potential after chemotherapy. (A and B) Female athymic mice were injected with MDA-436 or HCC-38 cells in the no. 4 mammary fat pad. Mice bearing tumors ≥150 mm3 were randomized to treatment with vehicle, paclitaxel [20 mg/kg per day × 4 doses intraperitoneally (i.p.)], or paclitaxel (20 mg/kg per day × 4 doses i.p.) + BSK805 [100 mg/kg per day orally (p.o.)]. Paclitaxel doses are represented by arrows. Tumor volumes were measured twice weekly. Two complete responses to dual therapy were achieved in mice bearing HCC-38 tumors. Bars represent means ± SEM. Differences were analyzed by one-way analysis of variance (ANOVA) with Tukey’s contrasts. (C) Representative images of mammospheres from treated tumors in (A) and (B). Scale bars, 200 μm. (D) Quantification of mammospheres from tumors harvested at the end of treatment. Bars represent means + SEM for n = 9 measurements. (E) Severe combined immunodeficient (SCID)/beige mice implanted with PDX model PDX4013 were randomized to treatment with vehicle (intraperitoneal saline and oral gavage with oral suspension agent), paclitaxel (20 mg/kg per day × 4 doses i.p.), BSK805 (80 mg/kg per day p.o.), or paclitaxel (20 mg/kg per day × 4 doses i.p.) + BSK805 (80 mg/kg per day p.o.). Tumor volumes were measured twice weekly. (F) Image of JAK2-FISH in the PDX4013 model demonstrating gene amplification. Scale bar, 20 μm. Justin M. Balko et al., Sci Transl Med 2016;8:334ra53 Published by AAAS