Fig. 3. TKI sensitivity assessed by the MANO method.

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Fig. 1 CSF1 is increased in blood of melanoma patients and correlates with disease progression. CSF1 is increased in blood of melanoma patients and correlates.

Fig. 4. Primary human metastatic melanomas contain CCL21-expressing LECs, and expression of VEGFC positively correlates with hallmarks of tumor inflammation.

Lymphoma cells with BCL2/PMAIP1 coamplification are highly sensitive to BCL-2 inhibitor. Lymphoma cells with BCL2/PMAIP1 coamplification are highly sensitive.

Fig. 1. IL-6 is associated with resistance to EGFR TKIs and is induced by stress hormones. IL-6 is associated with resistance to EGFR TKIs and is induced.

Fig. 6. AZD6738 induces DNA damage and apoptosis and exhibits antitumor efficacy in xenograft models of high-risk medulloblastoma and neuroblastoma. AZD6738.

Fig. 5. Correlation between CD34+CD45RA−CD90+ cell dose, engraftment success, and onset of neutrophil/platelet recovery in nonhuman primates. Correlation.

18F-FDG uptake is a noninvasive biomarker of combined MEK–mTORC1 inhibition. 18F-FDG uptake is a noninvasive biomarker of combined MEK–mTORC1 inhibition.

BET inhibition and depletion repress the expression of BRCA1 and RAD51

Fig. 2. Pharmacologic inhibition of ALK impairs STING activation.

Fig. 5. Correlation of tail and long bone growth velocities with Cxm serum concentrations in mice. Correlation of tail and long bone growth velocities.

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. 4. Functional annotation of VUS in EGFR.

Fig. 1. Schematic representation of the MANO method.

Fig. 2. Mutant KRAS mediates resistance to PARPi and sensitivity to PARPi and MEKi Mutant KRAS mediates resistance to PARPi and sensitivity to PARPi and.

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

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 DMF promotes viral infection.

Fig. 4 Topical application of SAAP-148 ointment eradicates acute and established infections of MRSA and A. baumannii from the skin. Topical application.

Fig. 3 BX795 blocks the synthesis of HSV-1 virions.

Fig. 2. GPC3 expression in normal and tumor tissues.

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

Fig. 3. Paclitaxel promotes TMEM-dependent vascular permeability, cancer cell dissemination, and metastasis in breast cancer. Paclitaxel promotes TMEM-dependent.

Fig. 1. Paclitaxel delays tumor growth and promotes infiltration of TIE2hi/VEGFhi macrophages and TMEM assembly. Paclitaxel delays tumor growth and promotes.

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Increased ADMA in pregnancy is associated with SGA birth outcomes

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

Fig. 3. Wisper controls CF behavior and survival.

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. 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. 3. Applying the rapid test to analyze human patient sera.

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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. 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.

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Representative CT and PET/CT images of three patients with NSCLCs

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Fig. 1. Drug combination screen identifies BETi as acting synergistically with PARPi. Drug combination screen identifies BETi as acting synergistically.

Fig. 5 Local gel scaffold for T cell memory response.

Fig. 1 BX795 suppresses HSV-1 infection.

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. 4. Improved tumor response to docetaxel in TNBC and trastuzumab in HER2-amplified PDX models with the addition of S Improved tumor response.

Jamie A. Saxon, PhD, Lynette M. Sholl, MD, Pasi A. Jänne, MD, PhD

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Pearson correlation of gene expression identifies distinct groups of male- and female-enriched genes. Pearson correlation of gene expression identifies.

Fig. 7. Treatment with DLK inhibitors reduces p-c-Jun and protects against neuronal and synaptic loss in vitro and in ALS mouse models. Treatment with.

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

Fig. 4. The effect of single-dose rozanolixizumab on the concentration of IgG subtypes in healthy subjects. The effect of single-dose rozanolixizumab on.

Fig. 2 In vitro and preclinical study with 18F-MPG.

Fig. 4 Surgery initiates a systemic inflammatory response that triggers the outgrowth of distant immunogenic tumors and can be inhibited by perioperative.

Bexarotene is neuroprotective in mouse and human HD neurons in vitro

Fig. 6. CXM correlates with age and growth velocity.

Fig. 6 Innate and adaptive immunity, but not ADCC, contributes to M7824 antitumor activity. Innate and adaptive immunity, but not ADCC, contributes to.

Fig. 3 CSF1 is expressed in human melanoma.

miR‐205 modulates tumor cell sensitivity to MET‐TKIs

Growth of TKI‐resistant EGFR delE746‐A750 PC‐9 NSCLC cells is associated with elevated cellular free fatty acid and expression of FASN, and is suppressed.

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CSF1 secretion by melanoma cells is induced by CTL-derived cytokines

Correlation of reovirus RNA/protein with proliferating tumor cells

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Fig. 2. CD treatment facilitates regression of murine atherosclerosis.

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.

GR cells are dependent upon sustained CDC25C signaling as pharmacologic or genetic inhibition of CDC25C induce synthetic lethality. GR cells are dependent.

Fig. 4. Paclitaxel promotes the expression of invasive isoforms of MENA in the primary breast cancer microenvironment. Paclitaxel promotes the expression.

Greater induction of apoptosis following EGFR TKI treatment correlates with higher basal BIM expression across a panel of EGFR-mutant lung cancers. Greater.

MYC expression is correlated with dasatinib sensitivity in cancer cell lines and in vivo. MYC expression is correlated with dasatinib sensitivity in cancer.

Fig. 2 BX795 is nontoxic to HCE cells at therapeutic concentration.

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. 3. TKI sensitivity assessed by the MANO method. TKI sensitivity assessed by the MANO method. (A) Ba/F3 cells expressing each of the 16 genes shown on the right were mixed and cultured in the presence of different concentrations of gefitinib, erlotinib, afatinib, osimertinib, rociletinib, crizotinib, alectinib, or puromycin. Bar code read numbers of the compound-treated cells were normalized to those of the dimethyl sulfoxide (DMSO)–treated mixture, and the relative viability (%) of each cell clone on day 5 is color-coded according to the indicated scheme. (B) Comparison of cell viability measured with alamarBlue cell viability assay and the MANO method for Ba/F3 cells with 10 EGFR mutants in (A). Each data point was normalized to vehicle-treated cells. Pearson’s correlation coefficient (r) was calculated as 0.89 (P < 0.0001). The low ratio area is magnified in the right panel. (C) Changes in the relative cell populations in the tumors of mice treated with TKIs. The MANO method was used to quantify the bar code read numbers of tumors in 10 erlotinib-treated and 10 vehicle-treated mice. The bar code number for each cell line was normalized to the total bar code numbers of the tumor on day 18, and the calculated number was subsequently used to determine the percentage contribution of each cell line to the tumors. The mean relative cell population (%) within the tumors is shown for mice treated with either vehicle (green circle) or erlotinib (orange circle). The blue and pink arrows represent decrease and increase in the relative cell populations, respectively, in the tumors treated with erlotinib compared to those treated with vehicle. Error bars denote SD. Shinji Kohsaka et al., Sci Transl Med 2017;9:eaan6566 Published by AAAS