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Combination of anginex gene therapy and radiation decelerates the growth and pulmonary metastasis of human osteosarcoma xenografts.

Investigate whether rAAV-anginex gene therapy combined with radiotherapy could decrease growth and pulmonary metastasis of osteosarcoma in mice and examine the mechanisms involved in this therapeutic strategy. During in vitro experiment, multiple treatment regimes (rAAV-eGFP, radiotherapy, rAAV-anginex, combination therapy) were applied to determine effects on proliferation of endothelial cells (ECs) and G-292 osteosarcoma cells. During in vivo analysis, the same multiple treatment regimes were applied to osteosarcoma tumor-bearing mice. Use microcomputed tomography to evaluate tumor size. Eight weeks after tumor cell inoculation, immunohistochemistry was used to assess the therapeutic efficacy according to microvessel density (MVD), proliferating cell nuclear antigen (PCNA), and terminal-deoxynucleotidyl transferase-mediated nick-end labeling (TUNEL) assays. Metastasis of lungs was also evaluated by measuring number of metastatic nodules and wet weight of metastases. The proliferation of ECs and the tumor volumes in combination therapy group were inhibited more effectively than the other three groups at end point (P < 0.05). Cell clone assay showed anginex had radiosensitization effect on ECs. Immunohistochemistry showed tumors from mice treated with combination therapy exhibited the lowest MVD and proliferation rate, with highest apoptosis rate, as confirmed by IHC staining for CD34 and PCNA and TUNEL assays (P < 0.05). Combination therapy also induced the fewest metastatic nodules and lowest wet weights of the lungs (P < 0.05). rAAV-anginex combined with radiotherapy induced apoptosis of osteosarcoma cells and inhibited tumor growth and pulmonary metastasis on the experimental osteosarcoma models. We conclude that the primary mechanism of this process may be due to sensitizing effect of anginex to radiotherapy.

1149 related Products with: Combination of anginex gene therapy and radiation decelerates the growth and pulmonary metastasis of human osteosarcoma xenografts.

Rabbit Anti-Human Androge Rabbit Anti-Human Androge Rabbit Anti-Human Androge Goat Anti-Human Androgen CAR,CAR,Constitutive acti Recombinant Human Androge Epidermal Growth Factor ( Epidermal Growth Factor ( Epidermal Growth Factor ( Epidermal Growth Factor ( Fibroblast Growth Factor Fibroblast Growth Factor

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Two-step transplantation with adipose tissue-derived stem cells increases follicle survival by enhancing vascularization in xenografted frozen-thawed human ovarian tissue.

Do adipose tissue-derived stem cells (ASCs) enhance vascularization and follicle survival in xenografted ovarian tissue using a two-step transplantation approach?

1561 related Products with: Two-step transplantation with adipose tissue-derived stem cells increases follicle survival by enhancing vascularization in xenografted frozen-thawed human ovarian tissue.

Frozen multiple human org Macrophage Colony Stimula Macrophage Colony Stimula Ovarian cancer tissue arr Human normal bone and ost Human breast invasive duc Human breast invasive duc ELISA kit CLGI,Collagenas Goat Anti-Human Tissue Fa Normal human multiple org Colorectal organ carcinom Frozen colorectal adenoca

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Correlation of Expression of Tenascin C and Blood Vessel Density in Non-small Cell Lung Cancers.

Non-small cell lung cancers are cancer diseases that rank second in terms of incidence and first in terms of mortality, worldwide. Stromal cells of these cancers express tenascin C (TNC) - hexameric glycoprotein, which is also expressed during foetal life. TNC is also observed in stromal cells of most human cancers. In some cancers, TNC was shown to influence proliferation and migration of cancer cells and angiogenesis. The aim of this work was to analyze the correlation of expression of TNC with the markers of vascular endothelial cells, CD31 and CD34, and clinicopathological data in NSCLC.

1148 related Products with: Correlation of Expression of Tenascin C and Blood Vessel Density in Non-small Cell Lung Cancers.

High density non small ce Small cell lung carcinoma Non small cell lung carci Lung non small cell cance Non small cell lung carci Lung small cell carcinoma Middle advanced stage lun Multiple lung carcinoma ( Non-small cell lung cance Non small cell lung carci Non small cell lung carci Non small cell lung carci

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Co-targeting BCL-2 and PI3K induces BAX-dependent mitochondrial apoptosis in AML cells.

Inhibitors targeting BCL-2 apoptotic proteins have significant potential for the treatment of acute myeloid leukemia (AML); however, complete responses are observed in only 20% of patients suggesting targeting BCL-2 alone is insufficient to yield durable responses. Here we assessed the efficacy of co-administration of the PI3K/mTOR inhibitor GDC-0980 or the p110β-sparing PI3K inhibitor taselisib with the selective BCL-2 antagonist venetoclax in AML cells. Tetracycline-inducible downregulation of BCL-2 significantly sensitized MV4-11 and MOLM-13 AML cells to PI3K inhibition. Venetoclax/GDC-0980 co-administration induced rapid and pronounced BAX mitochondrial translocation, cytochrome c release, and apoptosis in various AML cell lines in association with AKT/mTOR inactivation and MCL-1 downregulation; ectopic expression of MCL-1 significantly protected cells from this regimen. Combined treatment was also effective against primary AML blasts from 17 patients, including those bearing various genetic abnormalities. Venetoclax/GDC-0980 markedly induced apoptosis in primitive CD34+/38-/123+ AML cell populations but not in normal hematopoietic progenitor CD34+ cells. The regimen was also active against AML cells displaying intrinsic or acquired venetoclax resistance or tumor microenvironment-associated resistance. Either combinatorial treatment markedly reduced AML growth and prolonged survival in a systemic AML xenograft mouse model and diminished AML growth in two patient-derived xenograft models. Venetoclax/GDC-0980 activity was partially diminished in BAK-/- cells and failed to induce apoptosis in BAX-/- and BAX-/-BAK-/- cells, whereas BIM-/- cells were fully sensitive. Similar results were observed with venetoclax alone in in vitro and in vivo systemic xenograft models. Collectively, these studies demonstrate that venetoclax/GDC-0980 exhibits potent anti-AML activity primarily through BAX and, to a lesser extent, BAK. These findings argue that dual BCL-2 and PI3K inhibition warrants further evaluation in AML.

1913 related Products with: Co-targeting BCL-2 and PI3K induces BAX-dependent mitochondrial apoptosis in AML cells.

ABT-263 Mechanisms: Bcl-2 BEZ-235 Mechanisms: PI3K XL-765 (SAR-245409) Mecha BGT-226 Mechanisms: PI3K GSK-2636771 Mechanisms: P Apoptosis Phospho-Specifi ING1B antisense ING1B sense PI3Kâ„¢ Interferon γ p19 INK4D PI3Kδ

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A reappraisal of CTLA-4 checkpoint blockade in cancer immunotherapy.

It is assumed that anti-CTLA-4 antibodies cause tumor rejection by blocking negative signaling from B7-CTLA-4 interactions. Surprisingly, at concentrations considerably higher than plasma levels achieved by clinically effective dosing, the anti-CTLA-4 antibody Ipilimumab blocks neither B7 trans-endocytosis by CTLA-4 nor CTLA-4 binding to immobilized or cell-associated B7. Consequently, Ipilimumab does not increase B7 on dendritic cells (DCs) from either CTLA4 gene humanized (Ctla4 ) or human CD34 stem cell-reconstituted NSG™ mice. In Ctla4 mice expressing both human and mouse CTLA4 genes, anti-CTLA-4 antibodies that bind to human but not mouse CTLA-4 efficiently induce Treg depletion and Fc receptor-dependent tumor rejection. The blocking antibody L3D10 is comparable to the non-blocking Ipilimumab in causing tumor rejection. Remarkably, L3D10 progenies that lose blocking activity during humanization remain fully competent in inducing Treg depletion and tumor rejection. Anti-B7 antibodies that effectively block CD4 T cell activation and de novo CD8 T cell priming in lymphoid organs do not negatively affect the immunotherapeutic effect of Ipilimumab. Thus, clinically effective anti-CTLA-4 mAb causes tumor rejection by mechanisms that are independent of checkpoint blockade but dependent on the host Fc receptor. Our data call for a reappraisal of the CTLA-4 checkpoint blockade hypothesis and provide new insights for the next generation of safe and effective anti-CTLA-4 mAbs.

2601 related Products with: A reappraisal of CTLA-4 checkpoint blockade in cancer immunotherapy.

Multiple organ cancer tis Kidney disease spectrum ( Bladder cancer tissue arr Bladder cancer tissue arr Breast cancer tissue arra Multiple breast cancer ti Breast cancer tissue arra Breast cancer and normal Breast cancer and normal Breast cancer and normal Breast cancer tissue arra Breast cancer tissue arra

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Mouse and human HSPC immobilization in liquid culture by CD43- or CD44-antibody coating.

Keeping track of individual cell identifications is imperative to the study of dynamic single-cell behavior over time. Highly motile hematopoietic stem and progenitor cells (HSPCs) migrate quickly and do not adhere, and thus must be imaged very frequently to keep cell identifications. Even worse, they are also flushed away during medium exchange. To overcome these limitations, we tested antibody coating for reducing HSPC motility in vitro. Anti-CD43- and anti-CD44-antibody coating reduced the cell motility of mouse and human HSPCs in a concentration-dependent manner. This enables 2-dimensional (2D) colony formation without cell mixing in liquid cultures, massively increases time-lapse imaging throughput, and also maintains cell positions during media exchange. Anti-CD43 but not anti-CD44 coating reduces mouse HSPC proliferation with increasing concentrations. No relevant effects on cell survival or myeloid and megakaryocyte differentiation of hematopoietic stem cells and multipotent progenitors 1-5 were detected. Human umbilical cord hematopoietic CD34 cell survival, proliferation, and differentiation were not affected by either coating. This approach both massively simplifies and accelerates continuous analysis of suspension cells, and enables the study of their behavior in dynamic rather than static culture conditions over time.

1501 related Products with: Mouse and human HSPC immobilization in liquid culture by CD43- or CD44-antibody coating.

Integrin β1 (CD29) Antib Rabbit Anti-intestinal FA Rabbit Anti-Orexin-A Poly Rabbit Anti-APIP Apaf1 In Rabbit Anti-APIP Apaf1 In Rabbit Anti-TNIP2 ABIN2 T Rabbit Anti-TNIP2 ABIN2 T Rabbit Anti-Cell death in Rabbit Anti-Cell death in Inhibitory mouse monoclo Anti AGO2 Human, Monoclon Anti AGO2 Mouse, Monoclon

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Antibiotic ivermectin selectively induces apoptosis in chronic myeloid leukemia through inducing mitochondrial dysfunction and oxidative stress.

Mitochondria has been a promising target in blood cancer given their unique dependencies on mitochondrial functions compared to normal hematopoietic cells. In line with this concept, we show that an anthelminthic drug ivermectin selectively kills chronic myeloid leukemia (CML) cells via inducing mitochondrial dysfunctions and oxidative stress. Ivermectin is significantly more effective in inducing caspase-dependent apoptosis in CML cell line K562 and primary CML CD34 than normal bone marrow (NBM) CD34 cells. Ivermectin also augments in vitro and in vivo efficacy of standard CML tyrosine kinase inhibitors. Mechanistically, ivermectin inhibits respiratory complex I activity and suppresses mitochondrial respiration in K562 and CML CD34 cells. Interestingly, we demonstrate that mitochondrial respiration are lower in NBM CD34 compared to malignant CD34 cells. In addition, ivermectin also induces mitochondrial dysfunctions in NBM CD34 cells in a similar manner as in CML CD34 cells whereas NBM CD34 cells are significantly less sensitive to ivermectin than CML CD34 cells. These suggest that NBM CD34 cells are more tolerable to mitochondrial dysfunctions than CML CD34 cells. Consistently, ivermectin induces higher levels of oxidative stress and damage in CML than normal counterparts. Antioxidant NAC rescues ivermectin's effects, confirming oxidative stress as the mechanism of its action in CML. Our work provides the fundamental evidence to repurpose ivermectin for CML treatment. Our work also highlights the therapeutic value of targeting mitochondria respiration in CML.

1828 related Products with: Antibiotic ivermectin selectively induces apoptosis in chronic myeloid leukemia through inducing mitochondrial dysfunction and oxidative stress.

Anti-Apoptosis-Inducing F Anti Apoptosis Inducing F Apoptosis Inducing Factor Apoptosis Inducing Factor Apoptosis Inducing Factor Apoptosis Inducing Factor OXI TEK (Oxidative Stress Anti 3 DG imidazolone Mon Anti beta3 AR Human, Poly 8 Isoprostane oxidative s Apoptosis antibody array Apoptosis Phospho-Specifi

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Inhibition of Aldehyde Dehydrogenase-Activity Expands Multipotent Myeloid Progenitor Cells with Vascular Regenerative Function.

Blood-derived progenitor cell transplantation holds potential for the treatment of severe vascular diseases. Human umbilical cord blood (UCB)-derived hematopoietic progenitor cells purified using high aldehyde dehydrogenase (ALDH ) activity demonstrate pro-angiogenic functions following intramuscular (i.m.) transplantation into immunodeficient mice with hind-limb ischemia. Unfortunately, UCB ALDH cells are rare and prolonged ex vivo expansion leads to loss of high ALDH-activity and diminished vascular regenerative function. ALDH-activity generates retinoic acid, a potent driver of hematopoietic differentiation, creating a paradoxical challenge to expand UCB ALDH cells while limiting differentiation and retaining pro-angiogenic functions. We investigated whether inhibition of ALDH-activity during ex vivo expansion of UCB ALDH cells would prevent differentiation and expand progeny that retained pro-angiogenic functions after transplantation into non-obese diabetic/severe combined immunodeficient mice with femoral artery ligation-induced unilateral hind-limb ischemia. Human UCB ALDH cells were cultured under serum-free conditions for 9 days, with or without the reversible ALDH-inhibitor, diethylaminobenzaldehyde (DEAB). Although total cell numbers were increased >70-fold, the frequency of cells that retained ALDH /CD34+ phenotype was significantly diminished under basal conditions. In contrast, DEAB-inhibition increased total ALDH /CD34+ cell number by ≥10-fold, reduced differentiation marker (CD38) expression, and enhanced the retention of multipotent colony-forming cells in vitro. Proteomic analysis revealed that DEAB-treated cells upregulated anti-apoptotic protein expression and diminished production of proteins implicated with megakaryocyte differentiation. The i.m. transplantation of DEAB-treated cells into mice with hind-limb ischemia stimulated endothelial cell proliferation and augmented recovery of hind-limb perfusion. DEAB-inhibition of ALDH-activity delayed hematopoietic differentiation and expanded multipotent myeloid cells that accelerated vascular regeneration following i.m. transplantation in vivo. Stem Cells 2018.

2842 related Products with: Inhibition of Aldehyde Dehydrogenase-Activity Expands Multipotent Myeloid Progenitor Cells with Vascular Regenerative Function.

Rabbit Anti-Aldehyde Dehy Mouse Anti-Lipoprotein Li Mouse Anti-Human CD34 Tar Lactate Dehydrogenase Act Isocitrate Dehydrogenase Glucose-6-Phosphate Dehyd Glucose Dehydrogenase Act Alcohol Dehydrogenase Act MarkerGeneTM in vivo lacZ MarkerGeneTM Live Dead As MarkerGeneTM Chemilumines MarkerGeneTM Live Cell Gl

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Systemic multilineage engraftment in mice after in utero transplantation with human hematopoietic stem cells.

IUHCT of human cord blood-derived CD34 cells into fetal NSG mice results in systemic multilineage engraftment with human cells.Preconditioning with in utero injection of an anti-c-Kit receptor antibody (ACK2) results in an improved rate of engraftment.

2264 related Products with: Systemic multilineage engraftment in mice after in utero transplantation with human hematopoietic stem cells.

Macrophage Colony Stimula Macrophage Colony Stimula Human Small Intestine Mic Human Large Intestine Mic Human Internal Mammary Ar GFP Expressing Human Inte Anti C Reactive Protein A Anti AGO2 Human, Monoclon Anti AGO2 Human, Monoclon anti HSV (II) gB IgG1 (mo anti HCMV IE pp65 IgG1 (m anti HCMV gB IgG1 (monocl

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Modeling Anti-HIV-1 HSPC-Based Gene Therapy in Humanized Mice Previously Infected with HIV-1.

Investigations of anti-HIV-1 human hematopoietic stem/progenitor cell (HSPC)-based gene therapy have been performed by HIV-1 challenge after the engraftment of gene-modified HSPCs in humanized mouse models. However, the clinical application of gene therapy is to treat HIV-1-infected patients. Here, we developed a new method to investigate an anti-HIV-1 HSPC-based gene therapy in humanized mice previously infected with HIV-1. First, humanized mice were infected with HIV-1. When plasma viremia reached >10 copies/mL 3 weeks after HIV-1 infection, the mice were myeloablated with busulfan and transplanted with anti-HIV-1 gene-modified CD34 HSPCs transduced with a lentiviral vector expressing two short hairpin RNAs (shRNAs) against CCR5 and HIV-1 long terminal repeat (LTR), along with human thymus tissue under the kidney capsule. Anti-HIV-1 vector-modified human CD34 HSPCs successfully repopulated peripheral blood and lymphoid tissues in HIV-1 previously infected humanized mice. Anti-HIV-1 shRNA vector-modified CD4 T lymphocytes showed selective advantage in HIV-1 previously infected humanized mice. This new method will be useful for investigations of anti-HIV-1 gene therapy when testing in a more clinically relevant experimental setting.

1710 related Products with: Modeling Anti-HIV-1 HSPC-Based Gene Therapy in Humanized Mice Previously Infected with HIV-1.

anti HIV 2 gp36 IgG1 (mon anti HIV 1 p55 17 IgG1 (m anti HIV 1 p17 IgG1 (mono anti HCMV IE pp65 IgG1 (m anti HCMV gB IgG1 (monocl Anti HIV 1 p24 Clone 38 8 MONOBODIES (Monoclonal An Anti-HIV-1 p17 Clone 32 5 Anti HIV 1 p17 Clone 32 5 MONOBODIES (Monoclonal An Anti-HIV-1 gp41 Clone 10E Anti HIV 1 gp41 Clone 10E

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