Filtered By:
Specialty: Hematology
This page shows you your search results in order of date. This is page number 2.
Order by Relevance | Date
Total 236 results found since Jan 2013.
The combination of C-Myc rearrangement and 1q21 gain is associated with poor prognosis in multiple myeloma
AbstractThe prognostic value of chromosomal 1q21 gain in newly diagnosed multiple myeloma (NDMM) remains controversial. Add-on Myc aberrations may further worsen the outcome. To investigate whether specific genes located at the 1q21 region, such as myeloid cell leukemia 1 (Mcl-1), are involved in NDMM progression, we examined bone marrow cytogenetic abnormalities in 153 patients with NDMM by fluorescence in situ hybridization. Their response to treatment and survival was also analyzed.C-Myc andMcl-1 expressions in bone marrow samples were analyzed by RT-PCR. The expression of Mcl-1 was evaluated in bone marrow sections by ...
Source: Annals of Hematology - March 8, 2021 Category: Hematology Source Type: research
Targeting of antithrombin in hemophilia A or B with investigational siRNA therapeutic fitusiran - results of the phase 1 inhibitor cohort.
CONCLUSIONS: Monthly fitusiran was generally well tolerated, lowered antithrombin levels from baseline, and resulted in improved thrombin generation. These preliminary results suggest that monthly fitusiran treatment may reduce bleeding episodes and improve QoL in participants with hemophilia A or B with inhibitors.
PMID: 33587824 [PubMed - as supplied by publisher]
Source: Thrombosis and Haemostasis - February 15, 2021 Category: Hematology Authors: Pasi KJ, Lissitchkov T, Mamonov V, Mant T, Timofeeva M, Bagot C, Chowdary P, Georgiev P, Gercheva-Kyuchukova L, Madigan K, Nguyen H, Yu Q, Mei B, Benson CC, Ragni MV Tags: J Thromb Haemost Source Type: research
Expression of inducible NOS is indispensable for the antiproliferative and proapoptotic effect of imatinib in BCR-ABL positive cells.
Abstract
Chronic myeloid leukemia (CML) is characterized by constitutive BCR-ABL kinase activity, an aggressive proliferation of immature cells, and reduced differentiation. Targeting tyrosine kinase activity of BCR-ABL with imatinib is an effective therapy for the newly diagnosed CML patients; however, 20%-30% of the patients initially treated with imatinib eventually experience treatment failure. Therefore, early identification of these patients is of high clinical relevance. In the present study, we by undertaking a direct comparison of inducible NOS (iNOS) status in neutrophils from healthy volunteers, newly d...
Source: Journal of Leukocyte Biology - February 2, 2021 Category: Hematology Authors: Singh AK, Awasthi D, Dubey M, Nagarkoti S, Chandra T, Barthwal MK, Tripathi AK, Dikshit M Tags: J Leukoc Biol Source Type: research
Knockdown of liver-derived factor XII by GalNAc-siRNA ALN-F12 prevents thrombosis in mice without impacting hemostatic function
Plasma coagulation Factor XII (FXII) plays a crucial role in contact activation, ultimately regulating both the kinin-kallikrein system and the intrinsic pathway of coagulation. A growing body of evidence suggests that inhibition of FXII can prevent thrombosis. Given FXII does not appear to modulate hemostasis, targeting FXII is a promising strategy for the prevention of pathological thrombus formation without the hemostatic risks typically associated with anticoagulants. To this end, a subcutaneously administered investigational RNAi therapeutic targeting liver F12 mRNA (ALN-F12) was developed.
Source: Thrombosis Research - August 26, 2020 Category: Hematology Authors: Jingxuan Liu, Brian C. Cooley, Akin Akinc, James Butler, Anna Borodovsky Tags: Full Length Article Source Type: research
Ex vivo Improvement of a von Willebrand Disease Type 2A Phenotype Using an Allele-Specific Small-Interfering RNA.
Abstract
Von Willebrand disease (VWD) is the most common inherited bleeding disorder and is mainly caused by dominant-negative mutations in the multimeric protein von Willebrand factor (VWF). These mutations may either result in quantitative or qualitative defects in VWF. VWF is an endothelial protein that is secreted to the circulation upon endothelial activation. Once secreted, VWF multimers bind platelets and chaperone coagulation factor VIII in the circulation. Treatment of VWD focuses on increasing VWF plasma levels, but production and secretion of mutant VWF remain uninterrupted. Presence of circulating muta...
Source: Thrombosis and Haemostasis - August 14, 2020 Category: Hematology Authors: de Jong A, Dirven RJ, Boender J, Atiq F, Anvar SY, Leebeek FWG, van Vlijmen BJM, Eikenboom J Tags: Thromb Haemost Source Type: research
Hypoxia induced up-regulation of tissue factor is mediated through extracellular RNA activated Toll-like receptor 3-activated protein 1 signalling.
Abstract
Sterile Inflammation (SI), a condition where damage associated molecular patterns (DAMPs) released from dying cells, leads to TLR (Toll-like receptor) activation and triggers hypoxemia in circulation leading to venous thrombosis (VT) through tissue factor (TF) activation, but its importance under acute hypoxia (AH) remains unexplored. Thus, we hypothesized that eRNA released from dying cells under AH activates TF via the TLR3-ERK1/2-AP1 pathway, leading to VT. Animals were exposed to stimulate hypoxia for 0-24 h at standard temperature and humidity. RNaseA and DNase1 were injected immediately before expo...
Source: Blood Cells, Molecules and Diseases - June 10, 2020 Category: Hematology Authors: Bhagat S, Biswas I, Ahmed R, Khan GA Tags: Blood Cells Mol Dis Source Type: research
SLC44A2 deficient mice have a reduced response in stenosis but not in hypercoagulability driven venous thrombosis.
CONCLUSIONS: These studies corroborate the original GWAS findings and establish a contributing role for SLC44A2 during the initiation of VT, with indications that this may be related to platelet-neutrophil interaction. The precise mechanism however remains elusive and warrants further investigation.
PMID: 32297475 [PubMed - as supplied by publisher]
Source: Thrombosis and Haemostasis - April 14, 2020 Category: Hematology Authors: Tilburg J, Coenen DM, Zirka G, Dólleman S, van Oeveren-Rietdijk AM, Karel MFA, de Boer HC, Cosemans JMEM, Versteeg HH, Morange PE, van Vlijmen BJM, Maracle CX, Thomas GM Tags: J Thromb Haemost Source Type: research
Plasmodium falciparum histidine rich protein HRPII inhibits the antiinflammatory function of antithrombin.
CONCLUSION: We postulate that Pf-derived HRPII and polyphosphate can contribute to the pathogenesis of malaria infection by downregulating the AT-dependent antiinflammatory and anticoagulant pathways.
PMID: 31858717 [PubMed - as supplied by publisher]
Source: Thrombosis and Haemostasis - December 18, 2019 Category: Hematology Authors: Dinarvand P, Yang L, Biswas I, Giri H, Rezaie AR Tags: J Thromb Haemost Source Type: research
P14. Abstract Title: Modulating Fibrinolysis using siRNA against Coagulation Factor XIII
High specificity, easy reversibility, and a half-life on the order of weeks; these are all major advantages that gene therapy has over traditional anticoagulants, add to that a strategy that weakens clots rather than preventing clotting altogether and prophylaxis of thrombosis may become much safer. Currently, anticoagulant drugs are used as a preventative measure for people susceptible to developing disease causing thrombi (which manifest as heart attacks, strokes, and pulmonary embolism), but they require frequent administration and their strict inhibition of clotting increases the risk of uncontrolled bleeding.
Source: Thrombosis Research - September 30, 2019 Category: Hematology Authors: A. Strilchuk, E. Conway, E. Pryzdial, P. Cullis, C. Kastrup Source Type: research
RNF144B inhibits LPS-induced inflammatory responses via binding TBK1.
Abstract
Innate immune responses need to be precisely controlled to avoid prolonged inflammation and prevent unwanted damage to the host. Here, we report that RNF144B responded dynamically to LPS stimulation and negatively regulated LPS-induced inflammation. We found that RNF144B interacted with the scaffold/dimerization domain (SDD) of TANK binding kinase 1 (TBK1) through the in between RING (IBR) domain to inhibit its phosphorylation and K63-linked polyubiquitination, which led to TBK1 inactivation, IRF3 dephosphorylation, and IFN-β reduction. RNF144B knockdown with siRNA increased IRF3 activation and IFN-β pr...
Source: Journal of Leukocyte Biology - September 10, 2019 Category: Hematology Authors: Zhang Z, Zhang L, Wang B, Zhu X, Zhao L, Chu C, Guo Q, Wei R, Yin X, Zhang Y, Li X Tags: J Leukoc Biol Source Type: research
MN1 is indispensable for MLL-rearranged acute myeloid leukemia.
Abstract
Mixed lineage leukemia (MLL/KMT2A) rearrangements (MLL-r) are one of the most frequent chromosomal aberrations in acute myeloid leukemia. We evaluated the function of Meningioma 1 (MN1), a cofactor of HOXA9 and MEIS1, in human and murine MLL-rearranged leukemia by CRISPR-Cas9 mediated deletion of MN1. MN1 was required for in vivo leukemogenicity of MLL positive murine and human leukemia cells. Loss of MN1 inhibited cell cycle and proliferation, promoted apoptosis and induced differentiation of MLL-rearranged cells. Expression analysis and chromatin immunoprecipitation with sequencing from previously repor...
Source: Haematologica - August 13, 2019 Category: Hematology Authors: Sharma A, Jyotsana N, Gabdoulline R, Heckl D, Kuchenbauer F, Slany RK, Ganser A, Heuser M Tags: Haematologica Source Type: research
Functional analysis of cd99 upregulation in acute myeloid leukemia
Outcome of patients with Acute Myeloid Leukemia (AML) remains dismal and the need for new therapies is high. We recently found CD99 to be upregulated in AML and showed that CD99 loss of function by siRNA or anti-CD99 antibody decreased proliferation of AML cells. Here, we investigate the functional role of CD99 wild type isoform (WT) in AML with the hypothesis that CD99 ectopic expression results in more aggressive leukemia.We found that transducing cells with CD99 lentivirus resulted in initial increase in cell proliferation in THP-1, U937 and MOLM-13 (CD99OE vs EV: 1-56-1.78 fold, p
Source: Experimental Hematology - July 31, 2019 Category: Hematology Authors: Houda Alachkar, Vijaya Vaikari, yang Du, Sharon Wu, Tian Zhang, Klaus Metzeler, Tobias Herold, Wolfgang Hiddemann, Mojtaba Akhtari Tags: 3012 Source Type: research
A Genome Wide Association Study on plasma FV levels identified PLXDC2 as a new modifier of the coagulation process.
CONCLUSION: Our study identified PLXDC2 as a new molecular player of the coagulation process. This article is protected by copyright. All rights reserved.
PMID: 31271701 [PubMed - as supplied by publisher]
Source: Thrombosis and Haemostasis - July 3, 2019 Category: Hematology Authors: Thibord F, Hardy L, Ibrahim-Kosta M, Saut N, Pulcrano-Nicolas AS, Goumidi L, Civelek M, Eriksson P, Deleuze JF, Le Goff W, Trégouët DA, Morange PE Tags: J Thromb Haemost Source Type: research
Inhibition of γ/β Globin Gene Switching in CD 34 + Derived Erythroid Cells by BCL11A RNA Silencing
In this study, the possibility of increasing HbF in the CD34+ derived erythroid cells was investigated by BCL11A inhibition using specific small-interfering RNAs (siRNAs). Human peripheral blood-derived hematopoietic stem cells were isolated and differentiated to erythroid cells. Erythroid maturation was investigated using cell morphology parameters and flow cytometry analysis of CD235a expression On day 20, siRNA complementary to BCL11A was transfected to differentiating cells via electroporation. BCL11A expression was evaluated through real-time quantitative reverse transcription polymerase chain reaction (qRT-PCR) and e...
Source: Indian Journal of Hematology and Blood Transfusion - May 12, 2019 Category: Hematology Source Type: research
CSF1R inhibitors exhibit antitumor activity in acute myeloid leukemia by blocking paracrine signals from support cells
This study identifies CSF1R as a novel therapeutic target of AML and provides a mechanism of paracrine cytokine/growth factor signaling in this disease.
Source: Blood - February 7, 2019 Category: Hematology Authors: Edwards, D. K., Watanabe-Smith, K., Rofelty, A., Damnernsawad, A., Laderas, T., Lamble, A., Lind, E. F., Kaempf, A., Mori, M., Rosenberg, M., dAlmeida, A., Long, N., Agarwal, A., Sweeney, D. T., Loriaux, M., McWeeney, S. K., Tyner, J. W. Tags: Myeloid Neoplasia Source Type: research
