Tipifarnib combined with bortezomib induces cell death in diverse multiple myeloma and AML cell lines. Tipifarnib combined with bortezomib induces cell.

Slides:

Advertisements

Similar presentations

Incomplete Treatment Complete Treatment Control Flow Cytometric Cell Cycple Analysis of Propidium Iodide-Stained HPAC Cells ControlComplete TreatmentIncomplete.

Advertisements

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.

IL-1β differentially regulates CXCL5 and CXCL8 protein secretion in NHTBE and NSCLC cells. IL-1β differentially regulates CXCL5 and CXCL8 protein secretion.

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.

SUPPLEMENTAL TABLE 1. Cell cycle profiles of HeLa cells treated

AT-101, a Pan-Bcl-2 Inhibitor, Leads to Radiosensitization of Non-small Cell Lung Cancer Luigi Moretti, MD, Bo Li, MD, Kwang Woon Kim, PhD, Heidi Chen,

The BET inhibitor JQ‐1 in combination with the MEK inhibitor PD synergistically impairs cell proliferation and induces apoptosis of NRAS‐mutant.

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.

Valproic acid (VPA) synergises with VAC (mafosfamide, doxorubicin and vindesine) to induce apoptosis in small cell lung carcinoma (SCLC) cell lines. Valproic.

ROS induction and ATR inhibition synergize in inducing multiple myeloma (MM) cell death. ROS induction and ATR inhibition synergize in inducing multiple.

mpJX-594 effects on tumor burden and leukocyte influx.

AML cells display differential sensitivity to inhibition of IKBKE and TBK1. AML cells display differential sensitivity to inhibition of IKBKE and TBK1.

Fig. 5. Combination of SAHA and ML produces augmented suppression of cellular proliferation with impaired cell cycle progression, enhanced apoptotic.

Induction of apoptosis by nelfinavir and bortezomib

Effects of fAS stimulation on cathepsin-B activity, mitochondrial quality and microglial cell survival after autophagy inhibition. Effects of fAS stimulation.

SW fraction induces S phase arrest and apoptosis.

PKIs block DHT + bombesin-induced transactivation of probasin ARR3 tk-luc and PSA pPUE-E1b-Luc report constructs. PKIs block DHT + bombesin-induced transactivation.

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.

CYP1A1 knockdown increases cell death.

Aplf downregulation does not induce cellular arrest.

Induction of apoptosis by NS398.

Effects of PS-341 on human pancreatic cancer cells in vitro.

CDCP1 is required for invadopodia formation and ECM degradation by human breast cancer cells. CDCP1 is required for invadopodia formation and ECM degradation.

Stimulatory effect induced by docetaxel, gefitinib, and cyclopamine on MMP (A) and (B) cytosolic cytochrome c level. Stimulatory effect induced by docetaxel,

A, chemical structures of PRIMA-1 and PRIMA-1Met.

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.

Radiosensitization by combined Wee1 and PARP inhibition.

Selective delivery of pIC/PPHAffibody decreases the survival of HER2-overexpressing cells. Selective delivery of pIC/PPHAffibody decreases the survival.

Effect of sulindac and atorvastatin on the cell cycle.

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

Immunization regimens that include a GLA-SE-formulated protein vaccine generate memory CD4 T cells. Immunization regimens that include a GLA-SE-formulated.

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

The effects of IAA and glycyrrhizin (Gc) on proliferation and cell-cycle distribution. The effects of IAA and glycyrrhizin (Gc) on proliferation and cell-cycle.

Induction of cell death in prostate cancer cells by SAHA and ZOL

N-3 PUFAs promote endometrial cancer cell apoptosis in vitro and in vivo. n-3 PUFAs promote endometrial cancer cell apoptosis in vitro and in vivo. HEC-1-A.

Bone marrow stroma partially protects multiple myeloma and AML cell lines from tipifarnib- and bortezomib-induced cell death. 8226/S myeloma cells were.

Time course of a G2-M arrest in response to 6-TG compared with IR and VP-16, showing that 6-TG induced a delayed G2-M arrest in MMR+ cells. Time course.

Tipifarnib and bortezomib are synergistic in cytotoxicity assays

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

FACS analyses of the inhibitory effect induced by mixed docetaxel, gefitinib, and cyclopamine on EGF plus SHHNp–stimulated PC3 cells. FACS analyses of.

Cells lacking CDK6 kinase function are required to mutate p53.

Immunologic and pharmacokinetic studies.

Per1 inhibits growth and induces apoptosis in prostate cancer cell lines. Per1 inhibits growth and induces apoptosis in prostate cancer cell lines. LNCaP,

Staurosporine induces changes in MMP

Combined inhibition of Wee1 and PARP causes persistent radiation-induced DNA damage. Combined inhibition of Wee1 and PARP causes persistent radiation-induced.

Induction of DNA strand breaks by artesunate.

SY-1425 induces maturation in RARA-high AML

A24 induces apoptosis of MCL cells.

Effect of siltuximab on paclitaxel sensitivity in ovarian cancer drug resistant cells. Effect of siltuximab on paclitaxel sensitivity in ovarian cancer.

Systemic reovirus treatment targets disseminated human myeloma in vivo

Increased apoptotic levels after combined treatment with vincristine (VCR) and imatinib. Increased apoptotic levels after combined treatment with vincristine.

Increased apoptotic levels after combined treatment with DXR and imatinib. Increased apoptotic levels after combined treatment with DXR and imatinib. A–D.

A, capsid modifications increase the infectivity of gastric cancer cell lines. A, capsid modifications increase the infectivity of gastric cancer cell.

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,

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

The effects of AZD1775 and olaparib on DNA damage response signaling.

CpG oligodeoxynucleotide (CpG ODN)–induced activation of different types of primary malignant B cells. CpG oligodeoxynucleotide (CpG ODN)–induced activation.

Effect of MIF siRNA on the production of MMP-13 induced by LPA

W. chinensis extract induces apoptosis in AR-dependent prostate cancer cells. W. chinensis extract induces apoptosis in AR-dependent prostate cancer cells.

Sorafenib inhibits cell proliferation and induces apoptosis in HCC cells. Sorafenib inhibits cell proliferation and induces apoptosis in HCC cells. A,

Effects of ZOL treatment on pulmonary metastases.

RA-9 induces G2–M cell-cycle arrest and caspase-mediated apoptosis in ovarian cancer cells. RA-9 induces G2–M cell-cycle arrest and caspase-mediated apoptosis.

Effect of dexamethasone on PCDGF/GP88 mRNA and protein expressions and effect of PCDGF/GP88 on dexamethasone-induced cell death. Effect of dexamethasone.

BPDCN cells are dependent on BCL2 and sensitive to venetoclax in vitro

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 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.

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

DQs have superior anticancer efficacy among dimeric antimalarials.

Presentation transcript:

Tipifarnib combined with bortezomib induces cell death in diverse multiple myeloma and AML cell lines. Tipifarnib combined with bortezomib induces cell death in diverse multiple myeloma and AML cell lines. H929 (A), U266 (B), MM1s (C), or KG-1 (D) cell lines were treated with the indicated concentrations of tipifarnib, bortezomib, or the combination for 24 hours in cell suspension. Cell death was determined by flow cytometry after Annexin V/FITC and propidium iodide staining. Specific cell death was calculated relative to untreated controls. Three independent experiments. To identify evidence for greater than additive effect, a simple linear regression (no intercept model) was used that included drug effect for each individual drug and the interaction effect of the combination. SAS software was used in the calculations using Proc REG (n = 9 observations for each cell line). Ps are provided. Columns, mean; bars, SE. Niranjan Yanamandra et al. Clin Cancer Res 2006;12:591-599 ©2006 by American Association for Cancer Research