Rachel Truitt et al. BTS 2018;3:

Slides:

Advertisements

Similar presentations

Baseline Patient Characteristics Bart A.N. Verhoeven, et al. Stroke 2006;37:

Advertisements

Copyright © 2006 American Medical Association. All rights reserved.

Pathogenesis of Aryl Hydrocarbon Receptor-Mediated Development of Lymphoma Is Associated with Increased Cyclooxygenase-2 Expression Christoph F.A. Vogel,

Amanda M. Nelson, Kathryn L. Gilliland, Zhaoyuan Cong, Diane M

Molecular Therapy - Methods & Clinical Development

Combined treatment with cisplatin and sirolimus to enhance cell death in human mesothelioma Mor-Li Hartman, PhD, John Matthew Esposito, BA, Beow Yong.

Céline Jumeau et al. BTS 2016;j.jacbts

Cell death induced by down-regulation of heat shock protein 70 in lung cancer cell lines is p53-independent and does not require DNA cleavage Steffen.

FL cells are dependent on BCL6 in a NOTCH2-dependent manner.

Sven Y. Surikow et al. BTS 2018;3:

C1ORF106 contributes to intestinal epithelial barrier function.

Michael R. Bristow et al. BTS 2018;3:1-8

Romain Gallet et al. BTS 2016;1:14-28

Everolimus Inhibits SMC Proliferation Through Transcriptional Repression of Telomerase (A) Cell proliferation assay in primary murine vascular smooth muscle.

nab-Paclitaxel targets the tumor epithelial cells.

Rachel Truitt et al. BTS 2018;3:

Nikole J. Byrne et al. BTS 2017;j.jacbts

Effects of neuropeptide treatment on APC stimulation of Ag-specific T cells. Effects of neuropeptide treatment on APC stimulation of Ag-specific T cells.

Michael S. Dodd et al. BTS 2018;3:

AG-221 can reduce intracellular 2HG levels and induce differentiation in primary human IDH2R140Q- or IDH2R172K-mutant AML patient samples treated ex vivo.

Everolimus Silences E2F Target Genes Through TERT-Dependent Epigenetic Histone Modification (A) Western blotting for MCM7 in WT and TERTtg mSMC treated.

Cardiac Fibrosis at 18 Weeks Post TAC (A) Representative images (original magnification ×20) of Picrosirius red-stained cardiac tissue sections from HF +

Bernard et al, Supplementary Figure S1

Adapted viruses replicate in mismatched miR-122-expressing cells.

Hironori Hara et al. BTS 2018;3:

Sven Y. Surikow et al. BTS 2018;3:

Imipramine and promethazine induce the apoptotic cell death of SCLC cells through activation of caspase-3. Imipramine and promethazine induce the apoptotic.

Romain Gallet et al. BTS 2016;1:14-28

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

Hironori Hara et al. BTS 2018;3:

Volume 60, Issue 5, Pages (November 2001)

Hironori Hara et al. BTS 2018;3:

A and B, CO-1686–resistant NCI-H1975 cell clones, COR1-1 and COR10-1 display a reduced dependence on EGFR signaling for survival. A and B, CO-1686–resistant.

Nikole J. Byrne et al. BTS 2017;j.jacbts

Lapatinib reduces IGF-I signaling in trastuzumab-resistant cells.

AhR activation reduces lung DC gene and surface expression of DC-SIGN.

Fig. 3. Effects of Tec on IL-1β-induced apoptosis in chondrocytes.

Induction of apoptosis by NMT siRNAs.

MCM and ACM treatment of acutely isolated MNs results in differential caspase activation and utilization. MCM and ACM treatment of acutely isolated MNs.

Chronic rapamycin treatment impairs β-cell mass and insulin clearance in rats. Chronic rapamycin treatment impairs β-cell mass and insulin clearance in.

BCR–ABL kinase activity rewires GM-CSFR signaling and confers oncogene addiction in TF1 cells. BCR–ABL kinase activity rewires GM-CSFR signaling and confers.

Inhibition of lung cancer cell proliferation and viability by CYT387.

Minocycline treatment inhibited dorsal column transection-induced glial cell death within the distal and proximal AST. A, Percentage of apoptotic microglia/macrophages.

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

Silencing hOGG1 triggers caspase-3 and caspase-7 activation in response to H2O2 in GM00637 cells. Silencing hOGG1 triggers caspase-3 and caspase-7 activation.

G3139 substitutes for heparin, which is required for the biological activity of FGF2. G3139 substitutes for heparin, which is required for the biological.

Céline Jumeau et al. BTS 2016;1:

Mitotic catastrophe symptoms caused by curcumin are followed by apoptosis. Mitotic catastrophe symptoms caused by curcumin are followed by apoptosis. A.

Bcl-2 and caspase inhibition fails to inhibit BAMLET-induced cytotoxicity in MCF-7 cells. Bcl-2 and caspase inhibition fails to inhibit BAMLET-induced.

Biological effects of BRAF silencing: growth curves of A375 (A) and ARO (B) cell lines in the absence or presence of doxycycline. Biological effects of.

Synergistic cytotoxicity of 17AAG and TNF treatment in human lung cancer cell lines. Synergistic cytotoxicity of 17AAG and TNF treatment in human lung.

Confocal microscopy analysis of SK-BR-3 and HC cells treated with CF488A-labeled HER2-lytic hybrid peptide. Confocal microscopy analysis of SK-BR-3 and.

Five-day exposure to decitabine (DAC) sensitizes cells to doxorubicin (Doxo). Five-day exposure to decitabine (DAC) sensitizes cells to doxorubicin (Doxo).

Initial testing and characterization of cAMPr in ES cells.

SY-1425 induces maturation in RARA-high AML

WP1066 inhibits the progression of OCIM2 cells through the cell cycle.

Expression of the cell death markers activated caspase-3 and LC3 I/II in TUBO cells. Expression of the cell death markers activated caspase-3 and LC3 I/II.

Untargeted LC/MS metabolite profiling of DFMO-treated HT-29 colorectal cancer cells. Untargeted LC/MS metabolite profiling of DFMO-treated HT-29 colorectal.

MAPK/ERK signaling regulates TLR4 gene expression in response to BRAFV600E. MAPK/ERK signaling regulates TLR4 gene expression in response to BRAFV600E.

KRASG12D- and BRAFV600E-induced survival in PDECs requires IGF1R signaling. KRASG12D- and BRAFV600E-induced survival in PDECs requires IGF1R signaling.

AS1411 alters subcellular distribution of PRMT5 in a time-dependent, dose-dependent, and nucleolin-dependent manner. AS1411 alters subcellular distribution.

Protection is associated with trogocytosis but not phagocytosis of human cells. Protection is associated with trogocytosis but not phagocytosis of human.

BEZ235 induces accelerated senescence after radiation (IR) in vitro.

Blockade of cell cycle at G2-M phase in Bel-7402 cells treated with IG-105. Blockade of cell cycle at G2-M phase in Bel-7402 cells treated with IG-105.

Mechanism by which flavopiridol induces cell cycle arrest and apoptosis in rhabdoid tumor cells. Mechanism by which flavopiridol induces cell cycle arrest.

Resistance to entrectinib in xenopatient and colorectal cancer cell models carrying NTRK1 translocations. Resistance to entrectinib in xenopatient and.

Quercetin induces autophagy, blocks cell cycle and activation of ERK and JNK signaling pathways participates in the G1 arrest in P39 cells. Quercetin induces.

Curcumin decreases viability and proliferation of Bcr-Abl-expressing cells. Curcumin decreases viability and proliferation of Bcr-Abl-expressing cells.

WEE1 inhibition followed by TRAIL treatment results in apoptotic cell death in MB231 cells. WEE1 inhibition followed by TRAIL treatment results in apoptotic.

Günaj Rakipovski et al. BTS 2018;3:

Presentation transcript:

Rachel Truitt et al. BTS 2018;3:265-276 Detecting Changes in Cell Viability With Sunitinib Treatment Using a Rat CMT Model (A) Activated caspase 3/7 levels in response to treatment with 0.1% dimethyl sulfoxide (vehicle), 1 μmol/l sunitinib, or 1 μmol/l staurosporine for 8 h (dimethyl sulfoxide and sunitinib) or 6 h (staurosporine). ****p < 0.0001 relative to vehicle (n = 3 experiments); ***p < 0.001 1 μmol/l sunitinib versus staurosporine (n = 3 experiments). (B) Time-dependent changes in caspase 3/7 activation. Fold changes (relative to vehicle) in caspase levels for cardiac microtissues (CMT) treated with 1 μmol/l or 10 μmol/l sunitinib for 4 h, 8 h, or 12 h. **p < 0.01 1 μmol/l sunitinib 4 h versus 8 h; *p < 0.05 1 μmol/l sunitinib 4-h versus 12-h time points (n = 2 experiments for all time points); ‡‡p < 0.01 10 μmol/l sunitinib 4 h versus 8 h; ‡p < 0.05 10 μmol/l sunitinib 4-h versus 12-h time points (n = 2 experiments for all time points). (C) Dose-dependent changes in caspase activation in CMT treated with 50 nmol/l, 200 nmol/l, 1 μmol/l, 10 μmol/l sunitinib for 8 h. *p < 0.05 50 nmol/l versus 200 nmol/l sunitinib (n = 2 experiments); *p < 0.05 200 nmol/l versus 1 μmol/l sunitinib (n = 2 experiments for 200 nmol/l; n = 4 experiments for 1 μmol/l); **p < 0.01 1 μmol/l versus10 μmol/l sunitinib (n = 4 experiments for 1 μmol/l; n = 2 experiments for 10 μmol/l). (D) Detecting necrotic/late apoptotic cells. Percentages of cells stained with trypan blue were manually measured and normalized to vehicle levels to express as a fold change. **p < 0.01 10 μmol/l sunitinib versus 1 μmol/l staurosporine (n = 2 experiments); ***p < 0.001 vehicle versus 10 μmol/l sunitinib (n = 2 experiments for sunitinib; n = 3 experiments for vehicle). RLU = relative light units. Rachel Truitt et al. BTS 2018;3:265-276 2018 The Authors