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Experimental Hematology

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https://www.readbyqxmd.com/read/28911908/enhancement-of-mouse-hematopoietic-stem-progenitor-cell-function-via-transient-gene-delivery-using-integration-deficient-lentiviral-vectors
#1
Maria E Alonso-Ferrero, Niek P van Til, Kerol Bartolovic, Márcia F Mata, Gerard Wagemaker, Dale Moulding, David A Williams, Christine Kinnon, Simon N Waddington, Michael D Milsom, Steven J Howe
Integration-deficient lentiviruses (IdLV) effectively deliver genes to tissues but are rapidly lost from dividing cells. This property can be harnessed to transiently express transgenes to manipulate cell biology. Here, we demonstrate the utility of short-term gene expression to improve functional potency of Hematopoietic Stem/Progenitor Cells (HSPC) during transplantation by delivering HOXB4 and Angptl3 using IdLV to enhance the engraftment of HSPC. Constitutive overexpression of either of these genes is likely to be undesirable, but the transient nature of IdLVs reduces this risk and those associated with unsolicited gene expression in daughter cells...
September 11, 2017: Experimental Hematology
https://www.readbyqxmd.com/read/28911907/microrna-22-controls-interferon-alpha-production-and-erythroid-maturation-in-response-to-infectious-stress-in-mice
#2
Claudine S Kadmon, Cameron T Landers, Haiyan S Li, Stephanie S Watowich, Antony Rodriguez, Katherine Y King
MicroRNA-22 (miR-22) is a highly conserved microRNA that can regulate cell proliferation, oncogenesis, and cell maturation, especially during stress. In hematopoietic stem cells (HSCs) miR-22 has been reported to be involved in the regulation of key self-renewal factors including Tet2. Recent work demonstrates that miR-22 also participates in regulation of the interferon response, and expression profiling studies suggest that it is variably expressed at different stages in erythroid differentiation. We thus hypothesized that miR-22 regulates maturation of erythroid progenitors during stress hematopoiesis through its interaction with interferon...
September 11, 2017: Experimental Hematology
https://www.readbyqxmd.com/read/28911906/identification-of-novel-biomarkers-for-mll-translocated-acute-myeloid-leukemia
#3
Karine Lagacé, Fréderic Barabé, Josée Hebert, Sonia Cellot, Brian T Wilhelm
Acute myeloid leukemias (AML) with translocations of the Mixed Lineage Leukemia (MLL/KMT2A) gene are common in young patients and are generally associated with poor clinical outcomes. The molecular biology of MLL fusion genes remains incompletely characterized and is complicated by the fact that over 100 different partner genes have been identified in fusions with MLL. The continually growing list of MLL fusions also represents a clinical challenge with respect to identification of novel fusions and tracking the fusions to monitor progression of the disease after treatment...
September 11, 2017: Experimental Hematology
https://www.readbyqxmd.com/read/28893618/lenalidomide-modulates-gene-expression-in-human-abc-dlbcl-cells-by-regulating-ikaros-interaction-with-an-intronic-control-region-of-spib
#4
Lauren A Solomon, Carolina R Batista, Rodney P DeKoter
Activated B cell diffuse large B cell lymphoma (ABC-DLBCL) has poor prognosis compared to other DLBCL types, and therefore represents a top priority for developing novel therapies. Lenalidomide, an immunomodulatory drug in trials for treatment of ABC-DLBCL, targets the transcription factor IKAROS for degradation by the Cereblon E3 ubiquitin ligase complex. In this study, we determined whether the gene encoding the transcription factor SPI-B is a target of IKAROS. Using cultured ABC-DLBCL cell lines, we found that high levels of SPI-B expression conferred resistance to lenalidomide...
September 8, 2017: Experimental Hematology
https://www.readbyqxmd.com/read/28867537/thermal-injury-of-the-skin-induces-g-csf-dependent-attenuation-of-epo-mediated-stat-signaling-and-erythroid-differentiation-arrest-in-mice
#5
John G Noel, Benjamin J Ramser, Jose A Cancelas, Francis X McCormack, Jason C Gardner
Inflammation mediated impairment of erythropoiesis, plays a central role in the development of the anemia of critical illness (ACI). ACI develops despite elevation of endogenous erythropoietin (EPO), does not respond to exogenous EPO supplementation, and contributes significantly to transfusion requirements in burned patients. We have previously reported that the reduction of red blood cell mass in the bone marrow of a burn-injured ACI mouse model is G-CSF dependent. Given that elevated G-CSF levels have also been associated with lower hemoglobin levels and increased transfusion requirements in trauma victims, we postulated that G-CSF mediates post burn EPO resistance...
August 31, 2017: Experimental Hematology
https://www.readbyqxmd.com/read/28866324/effects-of-in-vivo-deletion-of-gata2-in-bone-marrow-stromal-cells
#6
Shin Hasegawa, Tohru Fujiwara, Yoko Okitsu, Hiroki Kato, Yuki Sato, Noriko Fukuhara, Yasushi Onishi, Ritsuko Shimizu, Masayuki Yamamoto, Hideo Harigae
The bone marrow (BM) microenvironment comprises multiple stem cell niches derived from BM mesenchymal stem cells (BM-MSCs). Previous in vitro analyses have suggested that transcription factor GATA2 plays an important role in adipocyte differentiation of BM-mesenchymal stem cells as well as in hematopoietic support, but the role of GATA2 in vivo remains unknown. We evaluated GATA2 effects in BM-MSC in vivo. Expression profiling analysis of Gata2 knockout Ter119(-)CD45(-) mesenchymal stromal cells obtained from compact bone from tamoxifen-treated Gata2 conditional knockout mice (Gata2(f/f)/ER-Cre mice) revealed upregulation of 110 genes and downregulation of 141 by a factor of 2...
August 30, 2017: Experimental Hematology
https://www.readbyqxmd.com/read/28826860/the-microenvironment-in-myelodysplastic-syndromes-niche-mediated-disease-initiation-and-progression
#7
REVIEW
Allison J Li, Laura M Calvi
Myelodysplastic syndromes (MDS) are clonal disorders of hematopoietic stem and progenitor cells and represent the most common cause of acquired marrow failure. Hallmarked by ineffective hematopoiesis, dysplastic marrow, and risk of transformation to acute leukemia, MDS remains a poorly treated disease. Although identification of hematopoietic aberrations in human MDS has contributed significantly to our understanding of MDS pathogenesis, evidence now identify the bone marrow microenvironment (BMME) as another key contributor to disease initiation and progression...
August 18, 2017: Experimental Hematology
https://www.readbyqxmd.com/read/28826859/tet2-restrains-inflammatory-gene-expression-in-macrophages
#8
Alyssa H Cull, Brooke Snetsinger, Rena Buckstein, Richard A Wells, Michael J Rauh
Tet methylcytosine dioxygenase 2 (TET2) is one of the earliest and most frequently mutated genes in clonal hematopoiesis of aging (CHIP) and myeloid cancers, including myelodysplastic syndromes (MDS) and chronic myelomonocytic leukemia (CMML). TET2 catalyzes the oxidation of 5-methylcytosine to 5-hydroxymethylcytosine, leading to DNA demethylation. TET2 also affects transcription by recruiting histone modifiers. Inactivating TET2 mutations cause epigenetic dysregulation, clonal hematopoietic stem cell dominance and monocytic lineage skewing...
August 18, 2017: Experimental Hematology
https://www.readbyqxmd.com/read/28822771/pge2-pulsing-of-murine-bone-marrow-cells-reduces-migration-of-daughter-monocytes-macrophages-in-vitro-and-in-vivo
#9
Terence A McGonigle, Amy R Dwyer, Eloise L Greenland, Naomi M Scott, Kevin N Keane, Philip Newsholme, Helen S Goodridge, Leonard I Zon, Fiona J Pixley, Prue H Hart
Monocytes/macrophages differentiating from bone marrow cells pulsed for 2 hours at 37(o)C with a stabilised derivative of prostaglandin E2, 16,16-dimethyl PGE2 (dmPGE2), migrated less efficiently towards a chemoattractant than monocytes/macrophages differentiated from bone marrow cells pulsed with vehicle. To confirm that the effect on bone marrow cells was long-lasting and to replicate human bone marrow transplantation, chimeric mice were established with donor bone marrow cells pulsed for 2 hours with dmPGE2 before injection into marrow-ablated congenic recipient mice...
August 16, 2017: Experimental Hematology
https://www.readbyqxmd.com/read/28760689/comprehensive-discovery-of-noncoding-rnas-in-acute-myeloid-leukemia-cell-transcriptomes
#10
Jin Zhang, Malachi Griffith, Christopher A Miller, Obi L Griffith, David H Spencer, Jason R Walker, Vincent Magrini, Sean D McGrath, Amy Ly, Nichole M Helton, Maria Trissal, Daniel C Link, Ha X Dang, David E Larson, Shashikant Kulkarni, Matthew G Cordes, Catrina C Fronick, Robert S Fulton, Jeffery M Klco, Elaine R Mardis, Timothy J Ley, Richard K Wilson, Christopher A Maher
To detect diverse and novel RNA species comprehensively, we compared deep small RNA and RNA sequencing (RNA-seq) methods applied to a primary acute myeloid leukemia (AML) sample. We were able to discover previously unannotated small RNAs using deep sequencing of a library method using broader insert size selection. We analyzed the long noncoding RNA (lncRNA) landscape in AML by comparing deep sequencing from multiple RNA-seq library construction methods for the sample that we studied and then integrating RNA-seq data from 179 AML cases...
July 28, 2017: Experimental Hematology
https://www.readbyqxmd.com/read/28760688/the-oligodendrocyte-lineage-transcription-factor-2-olig2-is-epigenetically-regulated-in-acute-myeloid-leukemia
#11
Arzu Yalcin, Marlon Kovarbasic, Julius Wehrle, Rainer Claus, Heiko Becker, Mahmoud Abdelkarim, Verena I Gaidzik, Andrea Schmidts, Ralph Wäsch, Heike L Pahl, Konstanze Döhner, Lars Bullinger, Justus Duyster, Michael Lübbert, Björn Hackanson
DNA methylation differences between normal tissue and cancerous tissue resulting in differential expression of genes are a hallmark of acute myeloid leukemia (AML) and can provide malignant cells with a growth advantage via silencing of specific genes, for example, transcription factors. Oligodendrocyte lineage transcription factor 2 (OLIG2) was reported to be differentially methylated and associated with prognosis in AML and, as reported for acute lymphoblastic leukemia and malignant glioma, may play a role in malignant transformation...
July 28, 2017: Experimental Hematology
https://www.readbyqxmd.com/read/28757432/genetic-risk-of-prediabetes-and-diabetes-development-in-chronic-myeloid-leukemia-patients-treated-with-nilotinib
#12
Bruno Martino, Corrado Mammì, Claudia Labate, Silvia Rodi, Domenica Ielo, Manuela Priolo, Maurizio Postorino, Giovanni Tripepi, Francesca Ronco, Carmelo Laganà, Caterina Musolino, Marianna Greco, Giorgio La Nasa, Giovanni Caocci
Impaired fasting glucose and type 2 diabetes represent adverse events in patients with chronic myeloid leukemia (CML) treated with the second generation tyrosine kinase inhibitor nilotinib. An unweighted genetic risk score (uGRS) for the prediction of insulin resistance, consisting of 10 multiple single-nucleotide polymorphisms, has been proposed. We evaluated uGRS predictivity in 61 CML patients treated with nilotinib. Patients were genotyped for IRS1, GRB14, ARL15, PPARG, PEPD, ANKRD55/MAP3K1, PDGFC, LYPLAL1, RSPO3, and FAM13A1 genes...
July 28, 2017: Experimental Hematology
https://www.readbyqxmd.com/read/28751190/septin-6-regulates-engraftment-and-lymphoid-differentiation-potential-of-murine-long-term-hematopoietic-stem-cells
#13
Katharina Senger, Gina Marka, Karin Soller, Vadim Sakk, Maria Carolina Florian, Hartmut Geiger
Septins are a family of filament-forming GTP-binding proteins that serve as scaffolds and diffusion barriers in various cellular processes. Septin 6 is known as a fusion partner of mixed-lineage leukemia in infant acute myeloid leukemia. The occurrence of the fusion gene is associated with a reduced expression of septin 6 itself. The role of septin 6 in hematopoiesis and whether it is involved in scaffolds within hematopoietic cells is not known. Septin 6-deficient hematopoietic stem cells (HSCs) present with an increased engraftment potential but altered lymphoid differentiation with a reduced contribution to the T-cell compartment and an increased B-cell contribution...
July 24, 2017: Experimental Hematology
https://www.readbyqxmd.com/read/28751189/targeted-therapies-in-hematological-malignancies-using-therapeutic-monoclonal-antibodies-against-eph-family-receptors
#14
REVIEW
Sara Charmsaz, Andrew M Scott, Andrew W Boyd
The use of monoclonal antibodies (mAbs) and molecules derived from them has achieved considerable attention and success in recent years, establishing this mode of therapy as an important therapeutic strategy in many cancers, in particular hematological tumors. mAbs recognize cell surface antigens expressed on target cells and mediate their function through various mechanisms such as antibody-dependent cellular cytotoxicity, complement-dependent cytotoxicity, or immune system modulation. The efficacy of mAb therapy can be improved when they are conjugated to a highly potent payloads, including cytotoxic drugs and radiolabeled isotopes...
July 24, 2017: Experimental Hematology
https://www.readbyqxmd.com/read/28732189/erratum-to-blos2-maintains-hematopoietic-stem-cells-in-the-fetal-liver-via-repressing-notch-signaling
#15
Qiuping He, Suwei Gao, Junhua Lv, Wei Li, Feng Liu
No abstract text is available yet for this article.
July 18, 2017: Experimental Hematology
https://www.readbyqxmd.com/read/28705639/genetic-and-epigenetic-heterogeneity-and-the-impact-on-cancer-relapse
#16
REVIEW
Ciaran Hassan, Ebrahim Afshinnekoo, Sheng Li, Shixiu Wu, Christopher E Mason
Acute myeloid leukemia (AML) is an aggressive hematopoietic malignancy with an exceedingly poor prognosis: a 5-year overall survival rate of 40%-45% in the young and a 5-year survival rate of less than 10% in the elderly (>60 years of age). Although a high percentage of patients enters complete remission after chemotherapeutic intervention, the majority of patients relapse within 3 years. Such stark prognostic outcomes highlight the need for additional clinical research, basic discovery, and molecular delineation of the etiologies and mechanisms behind responses to therapy that lead to relapse...
July 10, 2017: Experimental Hematology
https://www.readbyqxmd.com/read/28690072/identity-of-gli1-cells-in-the-bone-marrow
#17
REVIEW
Isadora F G Sena, Pedro H D M Prazeres, Gabryella S P Santos, Isabella T Borges, Patrick O Azevedo, Julia P Andreotti, Viviani M Almeida, Ana E Paiva, Daniel A P Guerra, Luiza Lousado, Luanny Souto, Akiva Mintz, Alexander Birbrair
Bone marrow fibrosis is a critical component of primary myelofibrosis in which normal bone marrow tissue and blood-forming cells are gradually replaced with scar tissue. The specific cellular and molecular mechanisms that cause bone marrow fibrosis are not understood. A recent study using state-of-the-art techniques, including in vivo lineage tracing, provides evidence that Gli1(+) cells are the cells responsible for fibrotic disease in the bone marrow. Strikingly, genetic depletion of Gli1(+) cells rescues bone marrow failure and abolishes myelofibrosis...
July 6, 2017: Experimental Hematology
https://www.readbyqxmd.com/read/28668351/utility-of-crispr-cas9-systems-in-hematology-research
#18
REVIEW
Daniel Lucas, Heather A O'Leary, Benjamin L Ebert, Chad A Cowan, Cedric S Tremblay
Since the end of the 20th century, novel approaches have emerged to manipulate experimental models of hematological disorders so that they more accurately mirror what is observed in the clinical setting. Despite these technological advances, the characterization of crucial genes for benign or malignant hematological disorders remains challenging, given the dynamic nature of the hematopoietic system and the genetic heterogeneity of these disorders. To overcome this limitation, genome-editing technologies have been developed to manipulate the genome specifically via deletion, insertion, or modification of targeted loci...
June 28, 2017: Experimental Hematology
https://www.readbyqxmd.com/read/28668350/unlocking-the-potential-of-anti-cd33-therapy-in-adult-and-childhood-acute-myeloid-leukemia
#19
REVIEW
Alison A Laing, Christine J Harrison, Brenda E S Gibson, Karen Keeshan
Acute myeloid leukemia (AML) develops when there is a block in differentiation and uncontrolled proliferation of myeloid precursors, resulting in bone marrow failure. AML is a clinically, morphologically, and genetically heterogeneous disease, and biological differences between adult and childhood AML have been identified. AML comprises 15%-20% of all children <15 years of age diagnosed with acute leukemia. Relapse occurs in up to 40% of children with AML and is the most common cause of death. Relapse arises from leukemic stem cells (LSCs) that persist after conventional chemotherapy...
June 28, 2017: Experimental Hematology
https://www.readbyqxmd.com/read/28666967/signaling-via-smad2-and-smad3-is-dispensable-for-adult-murine-hematopoietic-stem-cell-function-in%C3%A2-vivo
#20
Matilda Billing, Emma Rörby, Maria Dahl, Ulrika Blank, Silja Andradottír, Mats Ehinger, Stefan Karlsson
Transforming growth factor-β (TGFβ) is a member of a large family of polypeptide growth factors. TGFβ signals mainly through the intracellular proteins Smad2 and Smad3, which are highly similar in amino acid sequence identity. A number of studies have shown that these proteins, dependent on context, have distinct roles in the TGFβ signaling pathway. TGFβ is one of the most potent inhibitors of hematopoietic stem and progenitor cell proliferation in vitro, but its role in hematopoiesis in vivo is still being determined...
June 27, 2017: Experimental Hematology
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