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ATCC
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ATCC
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BioWare Corporation
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Image Search Results
Journal: Oncotarget
Article Title: The inhibition of malignant melanoma cell invasion of bone by the TLR7 agonist R848 is dependent upon pro-inflammatory cytokines produced by bone marrow macrophages
doi: 10.18632/oncotarget.25711
Figure Lengend Snippet: MTS assays of cultures of B16F10 cells, the mammary tumor cell line MMT060562 (MMT), and the lung carcinoma cell line Ex-3LL (3LL) treated with the indicated doses of IL-6, IL-12, and IFN-γ for one day. The data are representative of more than three independent experiments. * p <0.01.
Article Snippet: The mouse spontaneous mammary tumor (MMT) cell line MMT060562 and the
Techniques:
Journal: Clinical Cancer Research
Article Title: RG7212 Anti-TWEAK mAb Inhibits Tumor Growth through Inhibition of Tumor Cell Proliferation and Survival Signaling and by Enhancing the Host Antitumor Immune Response
doi: 10.1158/1078-0432.ccr-13-0405
Figure Lengend Snippet: Figure 2. RG7212 inhibits tumor growth in tumors with high-level Fn14 expression. A, RG7212 antitumor efficacy in ACHN xenografts. TGI is dose-related and statistically significant (P 0.004) with 3.75 mg/kg biweekly dosing. B, immunoblot and IHC show high levels of Fn14 protein in tumor cell lines that respond to RG7212, when grown as xenografts in mice. C, TWEAK concentrations in conditioned media from tumor cell lines measured by ELISA. D, RG7212 is inactive in Fn14-nonexpressing 22Rv1 prostate cancer model. Statistical analysis of xenograft data was determined by the rank-sum test and one-way ANOVA and a post hoc Bonferroni t test (10 mice per group). P values are comparisons of RG7212 to vehicle-treated mice. See also Supplementary Fig. S1 and Supplementary Table S2.
Article Snippet: Human U2OS, HCT116, ACHN, AsPC1,Calu-3, Caki-1, AsPC-1, Panc-1, SJSA, SK-MES-1, MDA-MB-231, KPL4, U118MG,MDA-MB-436, HEC1A,
Techniques: Expressing, Western Blot, Enzyme-linked Immunosorbent Assay
Journal: Clinical Cancer Research
Article Title: RG7212 Anti-TWEAK mAb Inhibits Tumor Growth through Inhibition of Tumor Cell Proliferation and Survival Signaling and by Enhancing the Host Antitumor Immune Response
doi: 10.1158/1078-0432.ccr-13-0405
Figure Lengend Snippet: Figure 3. TWEAK induces proliferation, survival, and immune signaling and gene expression. A, RG7212 blocks TWEAK-induced signaling. B, most highly TWEAK-induced genes across 4 Affymetrix gene arrays promote survival, TNFAIP3, VCAM1, BIRC3, TNFRSF9; regulate NF-kB activation: NFKB2, TRAF1, TNFAIP3, BIRC3, NFKBIE; leukocyte recruitment: CSF2, IL8, CCL2; proliferation: HBEGF. Data shown for models with in vivo efficacy data, ACHN, MDA-MB-436, and Pan02 and for U2OS that proliferates in response to TWEAK in vitro. Expression changes with 8-hour TWEAK stimulation shown; changes at 1, 4, 8, and 24 hours in Supplementary Table S1. , BIRC3 mRNA 97-fold increase with TWEAK stimulation in U2OS cells was not plotted to maintain scale. C, heatmap representation of TWEAK-induced cytokines by qPCR in Fn14-expressing cells. Values shown represent highest fold change with 4-, 8-, or 24-hour TWEAK stimulation. All changes are significant by P < 0.05. Uncolored squares represent no statistical increase. No changes in any genes in nonexpressing Fn14 line 22Rv1 by qPCR or in B16BL6 by Affymetrix gene array with TWEAK stimulation (data not shown). Five-fold increase in CXCL3 in ACHN not quite significant P ¼ 0.06. Not included: Panc-1 only increases: <1.5-fold in CSF1 and IL8 and H322M only increase: 2.5-fold in CCL5 (all changes P < 0.05). D, TRAF1 and c-IAP-2 proteins initially degraded then increased in TWEAK-stimulated cells. Immunoblots: Caki-1 and ACHN cell lysates from TWEAK (100 ng/mL)-stimulated cells. TWEAK increases NIK and pIKBa; pretreatmentwith MG132 (25mmol/L) for 1hour at 37C leads to accumulation of both but does not lead to increases in TRAF1 or c-IAP-2. See also Supplementary Fig. S3C, S3J, S3B, and Table S3.
Article Snippet: Human U2OS, HCT116, ACHN, AsPC1,Calu-3, Caki-1, AsPC-1, Panc-1, SJSA, SK-MES-1, MDA-MB-231, KPL4, U118MG,MDA-MB-436, HEC1A,
Techniques: Gene Expression, Activation Assay, In Vivo, In Vitro, Expressing, Western Blot