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

Slides:

Advertisements

Similar presentations

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

Advertisements

The expression and signaling of FGFR3 in WM cells.

Supplementary Figure 1 Sensitive Resistant Cell Count Propidium Iodide

Figure 5. FK866 caused apoptosis in MCF-7 cells while nicotinamide adenine dinucleotide (NAD+) reversed FK866-induced apoptosis. (A) Representative quadrant.

DNA content flow cytometric histograms of propidium iodide–stained A549 cells. DNA content flow cytometric histograms of propidium iodide–stained A549.

Targeting the PARP DNA repair pathway enhanced cytotoxicity induced by chemotherapy. Targeting the PARP DNA repair pathway enhanced cytotoxicity induced.

IDH1 mutant glioma cells are sensitive to TMZ

Figure 1. Artemisinin derivatives inhibited EOC growth and arrested the cell cycle at the G2/M phase (A) SKOV3 and primary epithelial ovarian cancer (EOC)

(a) (b) SUPPLEMENTARY FIGURE 1:

Fas ligand+ fallopian tube epithelium induces apoptosis in both Fas receptor+ T lymphocytes and endometrial cells Sebastian E. Illanes, M.D., Kevin Maisey,

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.

Effect of expression of constitutively active CAMKK2 on AMPK activation and the cell cycle in G361 cells. Effect of expression of constitutively active.

Confirmation of synergy and cytotoxicity of genotype-selective drug pairs. Confirmation of synergy and cytotoxicity of genotype-selective drug pairs. A,

CD8+ T cells were immunomodulated and required for the efficacy of anti–4-1BB/anti–PD-1 combination treatment. CD8+ T cells were immunomodulated and required.

MI-773 reduces the fraction of CSCs and prevents recurrence in ACC xenograft tumors. MI-773 reduces the fraction of CSCs and prevents recurrence in ACC.

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

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.

Figure 1. Effects of Gal-4 on apoptosis and proliferation of monocytes

Aplf downregulation does not induce cellular arrest.

Dox titration and kinetic analyses of CD19CAR expression upon Dox administration and discontinuation. Dox titration and kinetic analyses of CD19CAR expression.

A, B, apoptosis analysis using Annexin V-FITC/PI was done on 5th, 7th, and 9th day after transfection either with si control or si AEBP1in U87MG and U138MG.

Induction of apoptosis by NS398.

Combined BRAFi and anti-CTLA4 administration leads to prolonged antitumor immunity in a patient with metastatic melanoma. Combined BRAFi and anti-CTLA4.

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

Association between RB pathway alterations and poor prognosis in early-stage lung adenocarcinoma patients. Association between RB pathway alterations and.

Protein expression profile in a dasatinib-resistant cell line.

Fluorescence-activated cell sorting (FACS) and clonogenicity analyses.

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.

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

A, one-step viral growth curves: RT treatment increased the virus yield in MV-CEA–treated U87 cells by up to 2 log as compared with MV-CEA infection only.

Immune responses to 12MP and 6MHP.

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.

Increase in proliferation and activation of immune cells in peripheral blood after NKTR-214 treatment. Increase in proliferation and activation of immune.

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

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.

Xenograft regrowth studies.

Cells lacking CDK6 kinase function are required to mutate p53.

Immunologic and pharmacokinetic studies.

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,

Combination CDN and PD-L1 mAb treatment of established MOC1 tumors produces consistent tumor rejection. Combination CDN and PD-L1 mAb treatment of established.

A, P causes G2-M arrest with apoptosis in asynchronous population of PC-3 when exposed to 1.5 and 5 μmol/L P for various time points. A, P

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

Nested RT-PCR of Mammaglobin and CK19 mRNA in plasma and circulating cells of controls (C) and patients (T) with breast cancer. Nested RT-PCR of Mammaglobin.

A24 induces apoptosis of MCL cells.

IGF-I partially protects Rh30 cells from apoptosis despite simultaneous inhibition of PI3K-Akt and MAP kinase pathways. IGF-I partially protects Rh30 cells.

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

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,

Enhanced expression of Cap43 gene by nickel in breast cancer cell lines. Enhanced expression of Cap43 gene by nickel in breast cancer cell lines. Expression.

ROC analysis of MIC-1 and CA19-9.

A, cellular uptake of AS1411 in MCF-7 and MCF-10A cells.

The activation of PKC-δ and JNK1 is essential for doxorubicin-induced senescence. The activation of PKC-δ and JNK1 is essential for doxorubicin-induced.

RhuαVEGF and rhuαVEGF/paclitaxel mediated growth inhibition in an androgen-independent prostate cancer xenograft model. rhuαVEGF and rhuαVEGF/paclitaxel.

MGA271 exhibits potent in vivo antitumor activity toward tumor cell carcinoma xenografts. MGA271 exhibits potent in vivo antitumor activity toward tumor.

Combination of R848 and anti-CD200R affects activation of tumor-infiltrating myeloid cells. Combination of R848 and anti-CD200R affects activation of tumor-infiltrating.

Induction of PARP cleavage (A) and activation of caspases (B) after treatment with a combination of TRAIL and cisplatin. Induction of PARP cleavage (A)

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

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,

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.

Expression of chemokine receptors in A-498 cell line.

Effect of BCAA on the progression of cell cycle, expression of p21CIP1, and induction of apoptosis in HepG2 cells in the presence and absence of visfatin.

Activation status of NK cells is associated with therapeutic effects of TKIs. PBMCs from CML patients were cocultured with HLA class I–deficient K562 cells.

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

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

Bezafibrate increases the number of effector CTLs by enhancing their survival capacity and proliferation. Bezafibrate increases the number of effector.

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.

Presentation transcript:

Increased apoptotic levels after combined treatment with DXR and imatinib. Increased apoptotic levels after combined treatment with DXR and imatinib. A–D represent significant flow cytometry experiments analyzing Annexin-V-FITC detection. Histograms showing Annexin-V and propidium iodide distribution in presence of FBS (A), 10 μm imatinib (B), and imatinib with doxorubicin (DXR; C) are shown in the top half of the figure. The number of A673 early apoptotic cells (Annexin-V +, propidium iodide −) increased when combined treatment was administered (48%) with respect to DXR alone (33%). D shows curve displacement of imatinib + DXR with respect to DXR alone. Iranzu González et al. Clin Cancer Res 2004;10:751-761 ©2004 by American Association for Cancer Research