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Inotuzumab ozogamicin in combination with low-intensity chemotherapy for older patients with Philadelphia chromosome-negative acute lymphoblastic leukaemia: a single-arm, phase 2 study.

Inotuzumab ozogamicin, an anti-CD22 monoclonal antibody bound to a toxin, calicheamicin, has shown single-agent activity in relapsed or refractory acute lymphoblastic leukaemia. We aimed to assess the activity and safety of inotuzumab ozogamicin in combination with low-intensity chemotherapy in older patients with acute lymphoblastic leukaemia.

1726 related Products with: Inotuzumab ozogamicin in combination with low-intensity chemotherapy for older patients with Philadelphia chromosome-negative acute lymphoblastic leukaemia: a single-arm, phase 2 study.

Breast invasive ductal ca Multiple lung carcinoma ( Low density malignant mel Syringe pump can be contr ING1B antisense AKT1 (dn) Inducible Growth Differentiation Fa DNA (cytosine 5) methyltr Human Interleukin-32 alph Human Interleukin-1-alpha Caspase-3 Inhibitor Z-DEV Caspase-Family Inhibitor

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Clinical significance of MUC13 in pancreatic ductal adenocarcinoma.

Poor prognosis of pancreatic cancer (PanCa) is associated with lack of an effective early diagnostic biomarker. This study elucidates significance of MUC13, as a diagnostic/prognostic marker of PanCa.

1304 related Products with: Clinical significance of MUC13 in pancreatic ductal adenocarcinoma.

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Binding of NUFIP2 to Roquin promotes recognition and regulation of ICOS mRNA.

The ubiquitously expressed RNA-binding proteins Roquin-1 and Roquin-2 are essential for appropriate immune cell function and postnatal survival of mice. Roquin proteins repress target mRNAs by recognizing secondary structures in their 3'-UTRs and by inducing mRNA decay. However, it is unknown if other cellular proteins contribute to target control. To identify cofactors of Roquin, we used RNA interference to screen ~1500 genes involved in RNA-binding or mRNA degradation, and identified NUFIP2 as a cofactor of Roquin-induced mRNA decay. NUFIP2 binds directly and with high affinity to Roquin, which stabilizes NUFIP2 in cells. Post-transcriptional repression of human ICOS by endogenous Roquin proteins requires two neighboring non-canonical stem-loops in the ICOS 3'-UTR. This unconventional cis-element as well as another tandem loop known to confer Roquin-mediated regulation of the Ox40 3'-UTR, are bound cooperatively by Roquin and NUFIP2. NUFIP2 therefore emerges as a cofactor that contributes to mRNA target recognition by Roquin.

1852 related Products with: Binding of NUFIP2 to Roquin promotes recognition and regulation of ICOS mRNA.

Rabbit Anti-Rat Androgen Ofloxacin CAS Number [824 Topoisomerase II; Clone Topoisomerase II; Clone Topoisomerase II; Clone ELISA Binding Buffer ELISA Binding Buffer ELISA Binding Buffer Toludine Blue Solution Toludine Blue Solution Toludine Blue Solution Acyl CoA binding Protein

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FcγRIIIB stimulation promotes β1 integrin activation in human neutrophils.

The molecular stimuli involved in receptor-induced integrin activation are still poorly defined. We have investigated the role of receptors for the Fc portion of immunoglobulin G molecules (FcγR) on activation of integrins in human neutrophils. Cross-linking of FcγRIIA induced an increase in surface expression of β2 integrins but had no effect on β1 integrins. In contrast, cross-linking of FcγRIIIB not only increased β2 integrins on the cell surface but also induced β1 integrin activation, as indicated by an increase in binding to fibronectin and the appearance of an activation epitope detected by the monoclonal antibody 15/7. The FcγRIIIB-induced increase of β2 integrins required Src-family tyrosine kinases, Syk kinase, and phosphatidylinositol-3 kinase (PI-3K), as the corresponding, specific inhibitors, PP2, Piceatannol, and LY294002, completely blocked it. Contrary to this, FcγRIIIB-indued β1 integrin activation was not blocked by PP2 or LY294002. It was, however, enhanced by Piceatannol. After FcγRIIIB cross-linking, colocalization of FcγRIIIB and active β1 integrins was detected on the neutrophil membrane. These data show, for the first time, that cross-linking of FcγRIIIB induces an inside-out signaling pathway that leads to β1 integrin activation. This activation is independent of Src-family kinases, and PI-3K and may be induced in part by the interaction of FcγRIIIB with β1 integrins.

2792 related Products with: FcγRIIIB stimulation promotes β1 integrin activation in human neutrophils.

Integrin β1 (CD29) Antib LPAM-1(Integrin α4, CD49 Integrin alphaX antibody CD41 Integrin alpha 2b an Integrin alpha6 antibody Human integrin aVb3, affi Mouse Anti-Human Integrin Goat Anti-Human, Mouse In Mouse anti human Integrin Mouse anti human Integrin Mouse anti human Integrin Mouse anti human Integrin

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New Frontiers in Cancer Therapy: Monoclonal Antibody Therapy of Hematologic Malignancies.


1952 related Products with: New Frontiers in Cancer Therapy: Monoclonal Antibody Therapy of Hematologic Malignancies.

Anti AGO2 Human, Monoclon Anti AGO2 Mouse, Monoclon Anti AGO2 Human, Monoclon Anti AGO2 Mouse, Monoclon HIV1 integrase antibody, Anti 3 DG imidazolone Mon Bladder cancer tissue arr Breast cancer tissue arra Breast cancer tissue arra Mouse Anti-Insulin(1G11) Mouse Anti-Insulin(1G11) Mouse Anti-Insulin(1G11)

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Multicenter French harmonization study for PD-L1 IHC testing in non-small cell lung cancer.

Various PD-L1 immunohistochemistry (IHC) assays have been developed and used in clinical trials in association with different drugs. In order to harmonize and make PD-L1 testing in non-small cell lung cancer (NSCLC) widely available, we conducted a multicenter study comparing PD-L1 standardized assays and laboratory-developed tests (LDT).

3000 related Products with: Multicenter French harmonization study for PD-L1 IHC testing in non-small cell lung cancer.

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

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A mathematical model for IL-6-mediated, stem cell driven tumor growth and targeted treatment.

Targeting key regulators of the cancer stem cell phenotype to overcome their critical influence on tumor growth is a promising new strategy for cancer treatment. Here we present a modeling framework that operates at both the cellular and molecular levels, for investigating IL-6 mediated, cancer stem cell driven tumor growth and targeted treatment with anti-IL6 antibodies. Our immediate goal is to quantify the influence of IL-6 on cancer stem cell self-renewal and survival, and to characterize the subsequent impact on tumor growth dynamics. By including the molecular details of IL-6 binding, we are able to quantify the temporal changes in fractional occupancies of bound receptors and their influence on tumor volume. There is a strong correlation between the model output and experimental data for primary tumor xenografts. We also used the model to predict tumor response to administration of the humanized IL-6R monoclonal antibody, tocilizumab (TCZ), and we found that as little as 1mg/kg of TCZ administered weekly for 7 weeks is sufficient to result in tumor reduction and a sustained deceleration of tumor growth.

1016 related Products with: A mathematical model for IL-6-mediated, stem cell driven tumor growth and targeted treatment.

Epidermal Growth Factor ( Epidermal Growth Factor ( Growth Differentiation Fa TCGF (Natural T Cell Grow RABBIT ANTI HUMAN SDF-1 A Mesenchymal Stem Cell Adi Stem cell miRNA Array Skin malignant tumor tiss Bone giant cell tumor tis Human tumor cell array, 1 Human tumor cell array, 1 Stem Cell TF Activation P

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Central inhibition of granulocyte-macrophage colony-stimulating factor is analgesic in experimental neuropathic pain.

With less than 50% of patients responding to the current standard of care and poor efficacy and selectivity of current treatments, neuropathic pain continues to be an area of considerable unmet medical need. Biological therapeutics such as monoclonal antibodies (mAbs) provide better intrinsic selectivity; however, delivery to the central nervous system (CNS) remains a challenge. Granulocyte-macrophage colony-stimulating factor (GM-CSF) is well described in inflammation-induced pain, and early-phase clinical trials evaluating its antagonism have exemplified its importance as a peripheral pain target. Here, we investigate the role of this cytokine in a murine model of traumatic nerve injury and show that deletion of the GM-CSF receptor or treatment with an antagonizing mAb alleviates pain. We also demonstrate enhanced analgesic efficacy using an engineered construct that has greater capacity to penetrate the CNS. Despite observing GM-CSF receptor expression in microglia and astrocytes, the gliosis response in the dorsal horn was not altered in nerve injured knockout mice compared with wild-type littermate controls as evaluated by ionized calcium binding adapter molecule 1 (Iba1) and glial fibrillary acidic protein, respectively. Functional analysis of glial cells revealed that pretreatment with GM-CSF potentiated lipopolysaccharide-induced release of proinflammatory cytokines. In summary, our data indicate that GM-CSF is a proinflammatory cytokine that contributes to nociceptive signalling through driving spinal glial cell secretion of proinflammatory mediators. In addition, we report a successful approach to accessing CNS pain targets, providing promise for central compartment delivery of analgesics.This is an open-access article distributed under the terms of the Creative Commons Attribution-Non Commercial-No Derivatives License 4.0 (CCBY-NC-ND), where it is permissible to download and share the work provided it is properly cited. The work cannot be changed in any way or used commercially without permission from the journal.

2635 related Products with: Central inhibition of granulocyte-macrophage colony-stimulating factor is analgesic in experimental neuropathic pain.

Human Granulocyte Macroph Macrophage Colony Stimula Macrophage Colony Stimula Rat Granulocyte Macrophag CELLKINES MACROPHAGE COLO MACROPHAGE COLONY STIMULA CELLKINES MACROPHAGE COLO MACROPHAGE COLONY STIMULA Human Macrophage Colony S Human Granulocyte Colony Macrophage Colony Stimula Macrophage Colony Stimula

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ABP 501 for the treatment of Rheumatoid Arthritis.

Rheumatoid arthritis (RA) is an autoimmune disease, which has a negative impact on the ability to perform activities daily. Tumour necrosis factor α (TNF) is a cytokine with diverse cellular effects, and a key regulator of the inflammatory response. ABP 501 is a biosimilar to adalimumab, a TNF inhibitor. Areas covered: In this review, we examined ABP 501, as a biosimilar candidate to adalimumab in the treatment of RA focusing on the available data. Current data indicate that ABP 501 is a highly similar alternative to adalimumab in terms of safety, efficacy, tolerability and immunogenicity. ABP 501 has already been approved by health authorities in Europe and the United States of America, as a subcutaneous (s.c.) therapy option for the treatment of patients with RA, but also for the full spectrum approved for its bio-originator adalimumab. Expert opinion: Current body of evidence suggests that all biologic activities have been demonstrated to be equivalent between ABP 501 and the originator, including binding rates and affinity to TNF, and also the effector functions such as antibody-dependent cell-mediated cytotoxicity (ADCC). Therefore, it is fully expected to have same efficacy and safety in all indications.

2162 related Products with: ABP 501 for the treatment of Rheumatoid Arthritis.

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Safety and efficacy of denosumab in osteoporotic patients previously treated with other medications: a systematic review and meta-analysis.

Denosumab is a monoclonal antibody that received approval by the FDA for the treatment of osteoporosis in 2010. Available higher level research evidence concerns the treatment of patients that have not received any anti-osteoporotic medication in the past. Further investigation is warranted, since clinicians often face the challenge of administering the most efficacious drug in patients, pretreated with other medications. Areas Covered: We conducted a systematic review and meta-analysis to evaluate the efficacy and safety of denosumab compared to other active anti-osteoporotic agents in patients formerly receiving other treatments. We searched MEDLINE, EMBASE, CENTRAL, the metaRegister of Controlled Trials (mRCT) and clinicaltrials.gov up to April 2017 to identify eligible trials in patients with primary osteoporosis. Expert opinion: Our meta-analysis included 6 Randomised Controlled Trials encompassing 2968 patients formerly treated with anti-osteoporotic medications. Quantitative data synthesis demonstrated superiority of denosumab in augmenting Bone Mineral Density in all skeletal sites studied compared to controls [treatment difference in total hip: 1.59% (95% CI 1.01, 2.17)], whereas the overall incidence of serious adverse events was not increased (OR 1.12, 95% CI 0.85 to 1.47, p = 0.42). Future research geared towards the fracture incidence, quality of life and patient reported outcomes is warranted.

1160 related Products with: Safety and efficacy of denosumab in osteoporotic patients previously treated with other medications: a systematic review and meta-analysis.

Androgen Receptor (Phosph Androgen Receptor (Phosph Rabbit Anti-Human Androge Rabbit Anti-Human Androge Androgen Receptor (Ab 650 AZD-3514 Mechanisms: Andr 17β-Acetoxy-2α-bromo-5 (5α,16β)-N-Acetyl-16-[2 (5α,16β)-N-Acetyl-16-ac 5α-N-Acetyl-2'H-androst- 5α-N-Acetyl-2'H-androst- 3-O-Acetyl 5,14-Androstad

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