Presentation is loading. Please wait.

Presentation is loading. Please wait.

FGF19 amplification in liver cancer cell lines is associated with response to NVP-BGJ398. FGF19 amplification in liver cancer cell lines is associated.

Published byViktor Thorstensen Modified over 5 years ago

Similar presentations

Presentation on theme: "FGF19 amplification in liver cancer cell lines is associated with response to NVP-BGJ398. FGF19 amplification in liver cancer cell lines is associated."— Presentation transcript:

1 FGF19 amplification in liver cancer cell lines is associated with response to NVP-BGJ398.
FGF19 amplification in liver cancer cell lines is associated with response to NVP-BGJ398. A, scatter plot showing the correlation between FGF19 copy number and transcript expression of FGF19, FGFR4, and β-Klotho (KLB) in liver cancer cell lines. B, effect of NVP-BGJ398 on FGFR downstream signaling as measured by FRS2 Tyr-phosphorylation and Erk1/2 activation by Western blot analysis after 40 minutes of FGFR inhibitor treatment. Expression of α-actinin indicates equal loading. C, effect of 3 different shRNAs targeting FGFR4 in JHH7 cells upon induction with doxycycline (Dox), compared with a nontargeting shRNA. FGFR4 expression and FRS2 Tyr-phosphorylation are shown in doxycycline-induced and noninduced cell lines. Western blot analysis shows α-actin as a loading control. D, effect of FGFR4 downregulation on monolayer cell proliferation assays at day 7 after cell seeding. Vito Guagnano et al. Cancer Discovery 2012;2: ©2012 by American Association for Cancer Research

Download ppt "FGF19 amplification in liver cancer cell lines is associated with response to NVP-BGJ398. FGF19 amplification in liver cancer cell lines is associated."

Similar presentations

The expression and signaling of FGFR3 in WM cells.

The expression and signaling of FGFR3 in WM cells.
Inducible EGFR T790M-Mediated Gefitinib Resistance in Non-small Cell Lung Cancer Cells Does Not Modulate Sensitivity to PI103 Provoked Autophagy  Flavia.

Inducible EGFR T790M-Mediated Gefitinib Resistance in Non-small Cell Lung Cancer Cells Does Not Modulate Sensitivity to PI103 Provoked Autophagy  Flavia.
From: IGF-1 Regulates the Extracellular Level of Active MMP-2 and Promotes Müller Glial Cell Motility Invest. Ophthalmol. Vis. Sci.. 2015;56(11):6948-6960.

From: IGF-1 Regulates the Extracellular Level of Active MMP-2 and Promotes Müller Glial Cell Motility Invest. Ophthalmol. Vis. Sci ;56(11):
Effects of MAX reconstitution and of BRG1 depletion in lung cancer cells. Effects of MAX reconstitution and of BRG1 depletion in lung cancer cells. A,

Effects of MAX reconstitution and of BRG1 depletion in lung cancer cells. Effects of MAX reconstitution and of BRG1 depletion in lung cancer cells. A,
EMT correlates with PERK but not IRE1 signaling in primary human tumors. EMT correlates with PERK but not IRE1 signaling in primary human tumors. A, two.

EMT correlates with PERK but not IRE1 signaling in primary human tumors. EMT correlates with PERK but not IRE1 signaling in primary human tumors. A, two.
MAPK pathway inhibitors.

MAPK pathway inhibitors.
PI3K isoform–selective inhibitors and PTEN induction decrease ERK phosphorylation. PI3K isoform–selective inhibitors and PTEN induction decrease ERK phosphorylation.

PI3K isoform–selective inhibitors and PTEN induction decrease ERK phosphorylation. PI3K isoform–selective inhibitors and PTEN induction decrease ERK phosphorylation.
Luminex phosphorylation measurements are reproducible and have broad dynamic range Individual difference in insulin‐induced phosphorylation of ERK measured.

Luminex phosphorylation measurements are reproducible and have broad dynamic range Individual difference in insulin‐induced phosphorylation of ERK measured.
Reduction of Sca-1 increases PPARγ expression.

Reduction of Sca-1 increases PPARγ expression.
Inducible EGFR T790M-Mediated Gefitinib Resistance in Non-small Cell Lung Cancer Cells Does Not Modulate Sensitivity to PI103 Provoked Autophagy  Flavia.

Inducible EGFR T790M-Mediated Gefitinib Resistance in Non-small Cell Lung Cancer Cells Does Not Modulate Sensitivity to PI103 Provoked Autophagy  Flavia.
NRP2 represses IGF-IR expression and signaling.

NRP2 represses IGF-IR expression and signaling.
Inhibition of FGFR signaling and tumor growth in SNU-16 xenograft model by administration of E7090. Inhibition of FGFR signaling and tumor growth in SNU-16.

Inhibition of FGFR signaling and tumor growth in SNU-16 xenograft model by administration of E7090. Inhibition of FGFR signaling and tumor growth in SNU-16.
CHK1 downregulation upon ERG overexpression.

CHK1 downregulation upon ERG overexpression.
Treatment with BLU9931 leads to tumor regression in the FGF19-amplified Hep 3B liver cancer model. Treatment with BLU9931 leads to tumor regression in.

Treatment with BLU9931 leads to tumor regression in the FGF19-amplified Hep 3B liver cancer model. Treatment with BLU9931 leads to tumor regression in.
NF1 downregulation activates MAPK pathway signaling.

NF1 downregulation activates MAPK pathway signaling.
MITF upregulation leads to Hsp90i resistance

MITF upregulation leads to Hsp90i resistance
Downregulation of SPRY4 expression is associated with FGFR1–FRS2 activation. Downregulation of SPRY4 expression is associated with FGFR1–FRS2 activation.

Downregulation of SPRY4 expression is associated with FGFR1–FRS2 activation. Downregulation of SPRY4 expression is associated with FGFR1–FRS2 activation.
EGFR is intrinsically active in FGFR3-activated cell lines with combination efficacy from targeting both EGFR and FGFR3. EGFR is intrinsically active in.

EGFR is intrinsically active in FGFR3-activated cell lines with combination efficacy from targeting both EGFR and FGFR3. EGFR is intrinsically active in.
The role of SRC-C3G-RAP1 signaling in transformation induced by CRKL

The role of SRC-C3G-RAP1 signaling in transformation induced by CRKL
Daple is required for activation of Gαi3, Rac1, and AKT signals and in the antagonistic inhibition of β-catenin–dependent Wnt signals downstream of EGF/EGFR.

Daple is required for activation of Gαi3, Rac1, and AKT signals and in the antagonistic inhibition of β-catenin–dependent Wnt signals downstream of EGF/EGFR.

Similar presentations

Ads by Google