Fig. 7 BRD0705 impairs colony formation in AML cell lines and patient cells and shows in vivo efficacy in multiple AML mouse models. BRD0705 impairs colony.

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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.

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In vivo prophylactic and therapeutic efficacy of C12G6 in mice

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.

In vivo responses of AMLMLL to ATRi.

Fig. 6. Treatment with a DLK inhibitor is neuroprotective and reverses stress-induced gene expression changes. Treatment with a DLK inhibitor is neuroprotective.

Fig. 2 TLR8 is aberrantly expressed on pDCs from SSc patients.

Fig. 8. In vivo suppression of MM by CMLD

Fig. 2 Maraba treatment results in complete responses in the window of opportunity setting. Maraba treatment results in complete responses in the window.

Fig. 3. A circadian rhythm in fibroblast wound-healing response.

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. 4 Infection-induced CLV dysfunction is associated with decreased LMC coverage. Infection-induced CLV dysfunction is associated with decreased LMC.

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Maraba treatment sensitizes 4T1 tumors to immune checkpoint blockade

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Fig. 5. Antitumor efficacy of ERY974 in immunocompetent human CD3 transgenic mice. Antitumor efficacy of ERY974 in immunocompetent human CD3 transgenic.

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Fig. 6. Effects of CD31-NP targeting in perfused human kidneys.

Fig. 5 A competent Fc is required for the antitumor immune response.

Fig. 1 Chemical inactivation of BPL kills Mtb and prevents growth in mouse macrophages. Chemical inactivation of BPL kills Mtb and prevents growth in mouse.

Fig. 4. In vivo analysis of slpA mutant in the Syrian Golden hamster.

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

Fig. 7 Gel scaffold for inhibition of postsurgical recurrence of B16F10 tumors. Gel scaffold for inhibition of postsurgical recurrence of B16F10 tumors.

Fig. 2. Effects of SFN in mouse hepatocytes and in rat models of diet-induced glucose intolerance. Effects of SFN in mouse hepatocytes and in rat models.

Fig. 5 Combination intravenous reovirus and checkpoint inhibition in an orthotopic syngeneic brain tumor model. Combination intravenous reovirus and checkpoint.

Fig. 4. MATE1 transcription in RCC.

Fig. 6. Apoptotic MSCs exert in vivo immunosuppression in a TH2-type inflammation model in the absence of cytotoxic cells. Apoptotic MSCs exert in vivo.

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. Actin polymerization rhythms are required for circadian regulation of adhesion and wound-healing efficacy by fibroblasts. Actin polymerization.

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Fig. 7. KIF11 informs patient prognosis, and targeting improves survival in a preclinical model. KIF11 informs patient prognosis, and targeting improves.

Fig. 2 Paralog-selective inhibitors of GSK3α and GSK3β were designed and characterized. Paralog-selective inhibitors of GSK3α and GSK3β were designed and.

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. 7. mRIPO therapy restricts tumor growth and produces antigen-specific antitumor immunity. mRIPO therapy restricts tumor growth and produces antigen-specific.

Fig. 4. Efficacy of C12G6 compared with and in combination with oseltamivir in mice. Efficacy of C12G6 compared with and in combination with oseltamivir.

Fig. 2. Exposure of both TCR and CAR antigens diminishes efficacy of CAR8 but not CAR4 cells. Exposure of both TCR and CAR antigens diminishes efficacy.

CD facilitates RCT in vivo and promotes urinary cholesterol excretion

Fig. 3 Agonists of innate immunity are effective only when released locally from the hydrogel. Agonists of innate immunity are effective only when released.

Fig. 1. In vivo fates of patient-derived AML cells defined by mutational profile. In vivo fates of patient-derived AML cells defined by mutational profile.

Fig. 5. Prophylactic and therapeutic efficacy of C12G6 in ferrets.

Fig. 3 CSF1 is expressed in human melanoma.

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Fig. 5 BRD0705 induces differentiation in AML cell lines and primary patient samples through GSK3α-selective inhibition. BRD0705 induces differentiation.

Fig. 5 ALRN-6924 shows robust antileukemic activity in primary AML cells and in vivo. ALRN-6924 shows robust antileukemic activity in primary AML cells.

Fig. 6. Eradication of FLT3-ITD+ AML cells in vivo through combined inhibition of kinase and antiapoptotic pathways. Eradication of FLT3-ITD+ AML cells.

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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.

Effect of HDC on the ROS production in mouse lungs after melanoma cell inoculation. Effect of HDC on the ROS production in mouse lungs after melanoma cell.

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Fig. 7 BRD0705 impairs colony formation in AML cell lines and patient cells and shows in vivo efficacy in multiple AML mouse models. BRD0705 impairs colony formation in AML cell lines and patient cells and shows in vivo efficacy in multiple AML mouse models. (A to C) Colony formation assay of the indicated AML cell lines (A), five primary AML samples (B), and human CD34 cells (C) after BRD0705 treatment. Data are represented as means ± SEM of three replicates. (D) MLL-AF9 cells (250,000) injected into secondary recipient mice after 24 hours of pretreatment with DMSO, BRD0705, BRD3731, or BRD0320. Kaplan-Meier curves are shown (n = 5 per group). (E) MLL-AF9 cells injected into secondary recipient mice in a serially diluted manner (500,000, 250,000, 100,000, or 50,000 cells). Frequency of LICs calculated using ELDA software. (F) MLL-AF9 AML cells injected into secondary recipient mice 3 days before treatment with vehicle (black) or BRD0705 at 30 mg/kg (red). Kaplan-Meier curves for each group of mice (n = 5 per group). (G) HL-60–Luc cells injected into recipient mice and treated with vehicle (black) or BRD0705 at 15 mg/kg (red) or 30 mg/kg (blue). Bioluminescence was quantified. (H) Kaplan-Meier curves for each group of mice treated as in (G) (n = 5 per group). (I) MV4-11–Luc cells injected into recipient mice and treated with vehicle (black), BRD0705 (red), BRD3731 (blue), or BRD0320 (dashed blue). Bioluminescence was quantified. Data are means ± SEM. *P value calculated for the latest time point. (J) Kaplan-Meier curves for each group of mice (n = 10 per group). P < 0.05 determined by log-rank (Mantel-Cox) test in comparison with vehicle. Florence F. Wagner et al., Sci Transl Med 2018;10:eaam8460 Published by AAAS