ARQ 531 is cytotoxic to CLL cells, decreases NF-κB function, and inhibits migration. ARQ 531 is cytotoxic to CLL cells, decreases NF-κB function, and inhibits.

Slides:



Advertisements
Similar presentations
Clancy-Thompson et al., Supplemental Figure 1 A B C Supplemental Figure 1: Mice were given intravenous B16 injection on day 0. A) After bearing tumors.
Advertisements

Glioma-derived soluble factor(s) enhance IL-10 signaling.
KG-501 suppresses NSCLC/IL-1β CM–induced migration of HUVECs by regulating IL-1β–induced CXC chemokine gene expression in NSCLC cells. KG-501 suppresses.
Human Immunodeficiency Virus Type 1 Protease Inhibitor Modulates Activation of Peripheral Blood CD4+ T Cells and Decreases Their Susceptibility to Apoptosis.
IL-1β stimulates CXCL5 and CXCL8 gene expression and protein secretion in A549 cells in a time- and dose-dependent manner. IL-1β stimulates CXCL5 and CXCL8.
Metalloproteinases Are Involved in Lipopolysaccharide– and Tumor Necrosis Factor-–Mediated Regulation of CXCR1 and CXCR2 Chemokine Receptor Expression.
Prostaglandin E2 is a key factor for CCR7 surface expression and migration of monocyte-derived dendritic cells by Elke Scandella, Ying Men, Silke Gillessen,
Inhibition of glycogen synthase kinase-3 activity leads to epigenetic silencing of nuclear factor κB target genes and induction of apoptosis in chronic.
Glenn Cruse, PhD, Shailendra R. Singh, PhD, S
Supplementary Fig. 1 Co-treatment inhibited Ki67 expression.
Selinexor is effective in acquired resistance to ibrutinib and synergizes with ibrutinib in chronic lymphocytic leukemia by Zachary A. Hing, Rose Mantel,
DNAPKcs is required for DNA repair in the presence of androgen.
Cetuximab treatment increases IFNγ receptor 1 expression.
Suppressive effect of CD39+CD73+ melanoma cells on T-cell proliferation, and reversion of this effect via treatment with the CD39-blocking antibody, CD39.
FIP200 deficiency alters mitochondria activation and ROS production in T cells. FIP200 deficiency alters mitochondria activation and ROS production in.
Increased chemokine content and leukocyte infiltrate in D6-negative tumors. Increased chemokine content and leukocyte infiltrate in D6-negative tumors.
by Kamira Maharaj, John J
Response of monocytes to hY4 delivery and cytokine levels in CLL serum
FLC treatment results in an increase in ploidy in a significant fraction of cells. FLC treatment results in an increase in ploidy in a significant fraction.
Volume 20, Issue 2, Pages (February 2012)
Microenvironmental agonists generate de novo phenotypic resistance to combined ibrutinib plus venetoclax in CLL and MCL by Kallesh D. Jayappa, Craig A.
Targeting ubiquitin-activating enzyme induces ER stress–mediated apoptosis in B-cell lymphoma cells by Scott Best, Taylor Hashiguchi, Adam Kittai, Nur.
Confirmation of synergy and cytotoxicity of genotype-selective drug pairs. Confirmation of synergy and cytotoxicity of genotype-selective drug pairs. A,
AML cells display differential sensitivity to inhibition of IKBKE and TBK1. AML cells display differential sensitivity to inhibition of IKBKE and TBK1.
Senescence-associated defective HLA-DR upregulation does not modulate immunosuppressive properties of MSCs. (A) Fit and senescent MSCs were subjected to.
Apoptosis induced by ssHHT in HL60 and its derivative, the HL60/MRP, cells. Apoptosis induced by ssHHT in HL60 and its derivative, the HL60/MRP, cells.
Exosome-mediated inhibition of T cells is reversible.
BEZ235 induces MAPK signaling in a FOXO3A-dependent manner.
CD151 effects on mammary cell morphology and adhesion.
Cytotoxic activity of HER2-lytic hybrid peptide.
A, chemical structures of PRIMA-1 and PRIMA-1Met.
Tumor MMP-1 functionally regulates the permeability of endothelial cell barriers and contributes to HEp3-hi/diss transendothelial migration. Tumor MMP-1.
Mcl-1 knockdown promotes cleavage of caspase-3 in nonadherent melanoma cells. Mcl-1 knockdown promotes cleavage of caspase-3 in nonadherent melanoma cells.
Β-Cryptoxanthin at a concentration of 10 μmol/L decreases proliferation in HCT116 cells after 6 and 8 days of treatment. β-Cryptoxanthin at a concentration.
LY induces cytotoxicity in hMECs via inhibition of Akt/p70S6K kinase activities. LY induces cytotoxicity in hMECs via inhibition of Akt/p70S6K.
Tipifarnib combined with bortezomib induces cell death in diverse multiple myeloma and AML cell lines. Tipifarnib combined with bortezomib induces cell.
ALT-803 stimulates proliferation and activation of human NK cells and T cells in vitro. ALT-803 stimulates proliferation and activation of human NK cells.
Cells lacking CDK6 kinase function are required to mutate p53.
IL1R8 is downmodulated in human lymphoma cell lines.
Cytotoxic effect of BET inhibition in malignant B-cell lines and CLL patient-derived B cells is independent of survival signals. Cytotoxic effect of BET.
Effect of coapplication of dexrazoxane and doxorubicin on DSB formation, TOP2A protein level, and apoptosis. Effect of coapplication of dexrazoxane and.
Per1 inhibits growth and induces apoptosis in prostate cancer cell lines. Per1 inhibits growth and induces apoptosis in prostate cancer cell lines. LNCaP,
Platinum-based chemotherapy increased TXNIP expression, and overexpression of TXNIP enhanced the effectiveness of this therapy. Platinum-based chemotherapy.
EGFR signaling regulates transcription of PDGFRβ gene.
Combined inhibition of coamplified RTKs is required for response.
Trametinib and combination promote moDC maturation and decrease moDC viability. Trametinib and combination promote moDC maturation and decrease moDC viability.
Induction of apoptosis by statins in NB4 cells and NB4 variant cell lines. Induction of apoptosis by statins in NB4 cells and NB4 variant cell lines. A,
CpG oligodeoxynucleotide (CpG ODN)–induced activation of different types of primary malignant B cells. CpG oligodeoxynucleotide (CpG ODN)–induced activation.
Constitutive expression of JAK3M511I and HOXA9 leads to development of both AML and T-ALL in vivo. Constitutive expression of JAK3M511I and HOXA9 leads.
Ibrutinib decreases ofatumumab-mediated complement-dependent cytotoxicity. Ibrutinib decreases ofatumumab-mediated complement-dependent cytotoxicity. A,
MYC expression is correlated with dasatinib sensitivity in cancer cell lines and in vivo. MYC expression is correlated with dasatinib sensitivity in cancer.
Validation of MYC-driven drug responses.
Expression of chemokine receptors in A-498 cell line.
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.
The effect of βAR signaling on the generation of a cytotoxic CD8+ T-cell response in vivo. The effect of βAR signaling on the generation of a cytotoxic.
THZ1 in combination with targeted therapy enhances cell death and hinders the establishment of drug-resistant colonies in diverse oncogene-addicted cellular.
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.
Recruitment of CD8+, CD4+, and Foxp3+ cells into oral lesions in response to anti–PD-1 treatment. Recruitment of CD8+, CD4+, and Foxp3+ cells into oral.
B-cell development in young Pax5+/− mice.
ARQ 531 improves survival in the Eμ-TCL1 engraftment model compared with ibrutinib. ARQ 531 improves survival in the Eμ-TCL1 engraftment model compared.
AMG 176 exhibits robust single-agent activity in vivo.
Low initial levels of CD4+ Tregs, proliferating CD8+, and Granzyme B+ CD8+ T cells and high posttreatment tumor MHC class II expression predict better.
Inhibition of BCR-mediated signaling by ARQ 531.
Overexpression of SUFU and GLI1 in the poor clinical outcome subgroup was confirmed by real-time PCR along with its association with disease progression.
WEE1 inhibition followed by TRAIL treatment results in apoptotic cell death in MB231 cells. WEE1 inhibition followed by TRAIL treatment results in apoptotic.
Effect of 6-SHO on mouse prostate cancer HMVP2 cells.
DQs have superior anticancer efficacy among dimeric antimalarials.
Inhibition of stromal cell–induced survival of primary B-CLL cells by cyclopamine in vitro. Inhibition of stromal cell–induced survival of primary B-CLL.
Surface expression of chemokine receptors on M
Presentation transcript:

ARQ 531 is cytotoxic to CLL cells, decreases NF-κB function, and inhibits migration. ARQ 531 is cytotoxic to CLL cells, decreases NF-κB function, and inhibits migration. A, Primary CLL cells were continuously treated with increasing concentrations of ARQ 531 for 48 hours to assess cytotoxicity via annexin V/propidium iodide (PI) staining and flow cytometry (n = 9). B, Primary CLL cells were treated daily with ARQ 531 for 2 hours followed by drug washout and media replacement in order to simulate clearance of the reversible BTK inhibitor ARQ 531 (n = 9). C, Transcriptional expression of MYC, CD40, and MCL1 in CLL cells was assessed via real-time PCR following 72 hours of treatment with 1 μmol/L ARQ 531 (n = 7 for MYC; n = 8 for MCL1 and CD40). D and E, The NF-κB–dependent activation markers CD40 and CD86 were measured via flow cytometry 48 hours following treatment with 1 μmol/L ARQ 531 and 3.2 μmol/L CpG in CLL B cells (n = 9). MFI, mean fluorescence intensity. F and G, The number of CLL cells migrating through an 8.0-μm transwell insert toward the chemokines CXCL12 and CXCL13 was counted by flow cytometry (n = 8 for CXCL12; n = 9 for CXCL13). Differences were assessed using linear mixed-effects models (*, 0.05 ≥ P > 0.01; **, 0.01 ≥ P ≥ 0.001; ***, P < 0.001). Sean D. Reiff et al. Cancer Discov 2018;8:1300-1315 ©2018 by American Association for Cancer Research