Log in

Relevant bibliographies by topics / GMPLS e RWA / Journal articles

To see the other types of publications on this topic, follow the link: GMPLS e RWA.

Journal articles on the topic 'GMPLS e RWA'

Author: Grafiati

Published: 4 June 2021

Last updated: 1 February 2022

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles

Select a source type:

Consult the top 50 journal articles for your research on the topic 'GMPLS e RWA.'

Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.

You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.

Browse journal articles on a wide variety of disciplines and organise your bibliography correctly.

1

Hwang, I.-Shyan, I.-Feng Huang, and Shin-Cheng Yu. "Dynamic Fuzzy Controlled RWA Algorithm for IP/GMPLS over WDM Networks." Journal of Computer Science and Technology 20, no. 5 (2005): 717–27. http://dx.doi.org/10.1007/s11390-005-0717-6.

Full text

APA, Harvard, Vancouver, ISO, and other styles

2

Olsson, Andre, H. Leighton Grimes, Virendra K. Chaudhri, Philip Dexheimer, Bruce J. Aronow, and Harinder Singh. "Single Cell Transcriptome-Based Dissection of Lineage Fate Decisions in Myelopoiesis." Blood 124, no. 21 (2014): 1395. http://dx.doi.org/10.1182/blood.v124.21.1395.1395.

Full text

Abstract:

Abstract In spite of tremendous advances in the analysis of hematopoietic progenitors and transcription factors that give rise to different lineages, molecular insight into the mechanisms that underlie cell fate choice at the level of individual cells is lacking. We utilized single-cell RNA sequencing of murine granulocyte-monocyte progenitors (GMPs) to analyze the molecular basis of cell fate choice. Over 200 libraries were generated with average read depths of 4 million per library and an expressed gene call of over 3,800 genes with FPKM >3. Our data reveal a varied but coherent spectrum

APA, Harvard, Vancouver, ISO, and other styles

3

Ito, Yusuke, Fumio Nakahara, Yuki Kagoya, and Mineo Kurokawa. "CD62L Expression Level Dictates the Cell Fate of Myeloid Progenitors in Mice and Humans." Blood 136, Supplement 1 (2020): 26–27. http://dx.doi.org/10.1182/blood-2020-134753.

Full text

Abstract:

Hematopoietic cells are hierarchically differentiated from hematopoietic stem cells through several progenitors. Recent studies showed that each progenitor population has significant heterogeneity and some of the subsets have skewed differentiation potential. However, it has not been elucidated how and when common myeloid progenitors (CMPs) and granulocyte-monocyte progenitors (GMPs) acquire different fates. We hypothesized that progenitor cells with skewed differentiation potential had acquired a part of gene expression profiles of more differentiated cells. By analyzing publicly available si

APA, Harvard, Vancouver, ISO, and other styles

4

Su, Xi, Chao Feng, Simeng Wang, et al. "The noncoding RNAs SNORD50A and SNORD50B-mediated TRIM21-GMPS interaction promotes the growth of p53 wild-type breast cancers by degrading p53." Cell Death & Differentiation 28, no. 8 (2021): 2450–64. http://dx.doi.org/10.1038/s41418-021-00762-7.

Full text

Abstract:

AbstractSmall nucleolar RNA SNORD50A and SNORD50B (SNORD50A/B) has been reported to be recurrently deleted and function as a putative tumor suppressor in different types of cancer by binding to and suppressing the activity of the KRAS oncoproteins. Its deletion correlates with poorer patient survival. However, in this study, we surprisingly found that SNORD50A/B loss predicted a better survival in breast cancer patients carrying wild-type p53. Functional studies showed that SNORD50A/B deletion strongly inhibited the proliferation, migration, invasion and tumorigenic potential, and induced cell

APA, Harvard, Vancouver, ISO, and other styles

5

Albertioni, Freidoun, Alan Fotoohi, Jamileh Hashemi, Elham Yektaei, and Catharina Larsson. "RNA Interference Targeting Thiopurine Methyl Transferase Gene Alters the Cytotoxic Effect of the 6-Mercaptopurine In Human Leukaemia Cells." Blood 116, no. 21 (2010): 2891. http://dx.doi.org/10.1182/blood.v116.21.2891.2891.

Full text

Abstract:

Abstract Abstract 2891 Thiopurines; mercaptopurine (6-MP) and 6-thioguanine (6-TG) are important drugs in treatment of paediatric cancer patients. The activity of these drugs depends on the activity of several common enzymes in the metabolism pathways such as thiopurine methyl transferase (TPMT) and guanine monphosphate synthetase (GMPS). In the present study the efficacy of thiopurines was investigated upon inhibition of TPMT and GMPS gene expression by RNA interference (siRNA). Treatment of the MOLT4 human T-cell leukemia cells with TPMT and GMPS siRNA resulted in decreased mRNA expression a

APA, Harvard, Vancouver, ISO, and other styles

6

Marega, Manuela, Rocco Piazza, Iris Meneghetti, Sara Redaelli, Angela Mogavero, and Carlo Gambacorti. "BCR and BCR/ABL Regulation during Myeloid Differentiation in Healthy Donors and in Chronic Phase/Blast Crisis CML Patients." Blood 112, no. 11 (2008): 3204. http://dx.doi.org/10.1182/blood.v112.11.3204.3204.

Full text

Abstract:

Abstract The fusion protein BCR/ABL leads to chronic myeloid leukaemia (CML). The corresponding fusion gene is under the transcriptional control of BCR promoter. It is known that in CML progenitors the ability to block myeloid differentiation is directly related to BCR/ABL levels. These observations open new questions about BCR/ABL and BCR expression control. However, up to date only few studies have been focused on the characterization of the BCR promoter, so little is known about the transcriptional regulation of this gene. We studied BCR expression in sorted myeloid precursors in healthy do

APA, Harvard, Vancouver, ISO, and other styles

7

Kfoury, Youmna, Anthony Anselmo, Jefferson Seidl, et al. "Osteoblastic Cell-Derived Extracellular Vesicles Transfer Small RNAs That Alter the Physiology of Hematopoietic Cells In Vivo." Blood 130, Suppl_1 (2017): 93. http://dx.doi.org/10.1182/blood.v130.suppl_1.93.93.

Full text

Abstract:

Abstract Background The bone marrow microenvironment (BMEV) regulates the highly regenerative hematopoietic system. However, there are a limited number of BMEV-derived molecules with a definitive role in maintaining hematopoietic stem and progenitor cells (HSPCs). Extracellular vesicles (EVs) encapsulate bioactive molecules, and may modify the physiology of their target cells. In hematopoiesis, EVs derived from culture-expanded mesenchymal cells can rescue irradiation damage, expand human umbilical cord blood cells and support HSPCs in vitro . However, in vivo evidence of EV function is lackin

APA, Harvard, Vancouver, ISO, and other styles

8

Mathur, Tushar, Gokhan Sahin, and Donald R. Ucci. "A Performance Comparison of Centralized and Distributed Spectrum Management Techniques in Elastic Optical Networks." Journal of Engineering 2019 (January 1, 2019): 1–13. http://dx.doi.org/10.1155/2019/3860685.

Full text

Abstract:

Elastic optical networks (EONs) have emerged to provide higher spectrum efficiency than traditional Dense Wavelength-Division-Multiplexing (DWDM) by utilizing enabling technologies such as flexible spectrum grid, Orthogonal Frequency Division Multiplexing (OFDM), and distance adaptive rate and modulation. The choice of the control-plane is an important consideration when deploying any new technology, especially in optical networks. This paper considers generic distributed and centralized spectrum assignment policies in conjunction with the accompanying connection set-up signaling protocols in

APA, Harvard, Vancouver, ISO, and other styles

9

Kumar, Ashish R., Wendy A. Hudson, Weili Chen, Rodney A. Staggs, Anne-Francoise Lamblin, and John H. Kersey. "Differential Expression of Mll-AF9 Up-Regulated Genes Correlates with Enhanced Self-Renewal of Hematopoietic Progenitors." Blood 108, no. 11 (2006): 733. http://dx.doi.org/10.1182/blood.v108.11.733.733.

Full text

Abstract:

Abstract In order to understand the pathophysiology of leukemia, we need to study the effects of leukemic oncogenes on the rare hematopoietic stem and progenitor cells. We investigated the self-renewal capabilities of the various hematopoietic cell types derived from Mll-AF9 knock-in mice. We used the murine knock-in model since it offers the advantage of a single copy of the Mll-fusion gene under the control of the endogenous promoter present in every hematopoietic stem/progenitor cell. In methylcellulose cultures, we compared myeloid colony formation of Mll-AF9 cells to wild type progenitor

APA, Harvard, Vancouver, ISO, and other styles

10

Wilson, Daniel J. "Generalized mean p-values for combining dependent tests: comparison of generalized central limit theorem and robust risk analysis." Wellcome Open Research 5 (March 31, 2020): 55. http://dx.doi.org/10.12688/wellcomeopenres.15761.1.

Full text

Abstract:

The test statistics underpinning several methods for combining p-values are special cases of generalized mean p-value (GMP), including the minimum (Bonferroni procedure), harmonic mean and geometric mean. A key assumption influencing the practical performance of such methods concerns the dependence between p-values. Approaches that do not require specific knowledge of the dependence structure are practically convenient. Vovk and Wang derived significance thresholds for GMPs under the worst-case scenario of arbitrary dependence using results from Robust Risk Analysis (RRA). Here I calculate sig

APA, Harvard, Vancouver, ISO, and other styles

11

Wanet, Anaïs, Mahmoud A. Bassal, Sweta B. Patel, et al. "E-cadherin is regulated by GATA-2 and marks the early commitment of mouse hematopoietic progenitors to the basophil and mast cell fates." Science Immunology 6, no. 56 (2021): eaba0178. http://dx.doi.org/10.1126/sciimmunol.aba0178.

Full text

Abstract:

E-cadherin is a calcium-dependent cell-cell adhesion molecule extensively studied for its involvement in tissue formation, epithelial cell behavior, and suppression of cancer. However, E-cadherin expression in the hematopoietic system has not been fully elucidated. Combining single-cell RNA-sequencing analyses and immunophenotyping, we revealed that progenitors expressing high levels of E-cadherin and contained within the granulocyte-monocyte progenitors (GMPs) fraction have an enriched capacity to differentiate into basophils and mast cells. We detected E-cadherin expression on committed prog

APA, Harvard, Vancouver, ISO, and other styles

12

Kfoury, Youmna, Fei Ji, Michael Mazzola, et al. "Niche Transfer of Small Non-Coding RNAs Regulates Hematopoietic Response to Stress." Blood 134, Supplement_1 (2019): 1207. http://dx.doi.org/10.1182/blood-2019-124794.

Full text

Abstract:

The bone marrow (BM) niche, is an extrinsic regulator of hematopoietic stem and progenitor cells (HSPCs) (Morrison and Scadden 2014). The niche can drive disease and loss of HSPC function (Raaijmakers et al., 2010; Kode et al., 2014; Dong et al., 2016). Of particular interest, deletion in specific niche cells of the small RNA processing enzymes, Dicer1 and Angiogenin (Ang1) resulted in hematopoietic transformation (Raaijmakers et al., 2010) and loss of HSC quiescence (Goncalves et al., 2016), respectively. We tested mechanisms by which small non-coding RNAs (sncRNA) from niche cells might cont

APA, Harvard, Vancouver, ISO, and other styles

13

Yamashita, Masayuki, та Emmanuelle Passegué. "Inflammation-Produced TNFα± Protects Hematopoietic Stem Cells from Necroptosis via Canonical NF-κB Pathway". Blood 130, Suppl_1 (2017): 631. http://dx.doi.org/10.1182/blood.v130.suppl_1.631.631.

Full text

Abstract:

Abstract Chronic inflammation is associated with bone marrow (BM) failure, aging and hematological malignancies. TNFα is a major pro-inflammatory cytokine overproduced in many hematological diseases, which is also known as a prototypical death ligand that can trigger programmed cell death in effector cells. Hematopoietic stem cells (HSCs: Lin-cKit+Sca1+Flk2-CD48-CD150+) are highly responsive to an altered cytokine milieu in the BM, and show unique response to cell death stimuli compared to downstream progenitors. Yet, how TNFα regulates HSCs and downstream progenitors remains controversial. In

APA, Harvard, Vancouver, ISO, and other styles

14

Emmrich, Stephan, Franziska Schmidt, Ramesh Chandra Pandey, Aliaksandra Maroz, Dirk Reinhardt, and Jan-Henning Klusmann. "Lncrna Hematlas Defines Blood Lineage-Specific RNA Expression Signatures and Novel Lincrna Biomarkers." Blood 122, no. 21 (2013): 3669. http://dx.doi.org/10.1182/blood.v122.21.3669.3669.

Full text

Abstract:

Abstract Long non-coding RNAs (lncRNAs) recently emerged as central regulators of chromatin and gene expression. We created a comprehensive lncRNA HemAtlas in human and murine blood cells. We sampled RNA from differentiated granulocytes, monocytes, erythroid precursors, in vitro maturated megakaryocytes, CD4-T and CD8-T cells, NK cells, B cells and stem cells (human CD34+ cord blood hematopoietic stem and progenitor cells [CB-HSPCs]) and subjected them to microarray analysis of mRNA and lncRNA expression. Moreover, the human LncRNA HemAtlas was complemented with human hematopoietic stem cells

APA, Harvard, Vancouver, ISO, and other styles

15

Woll, Petter, Una Kjällquist, Onima Chowdhury, et al. "Diverse Genetic Lesions In Myelodysplastic Syndromes Originate Exclusively In Rare MDS Stem Cells." Blood 122, no. 21 (2013): 4195. http://dx.doi.org/10.1182/blood.v122.21.4195.4195.

Full text

Abstract:

Abstract Background The popular concept that human cancers might be driven by rare self-renewing cancer stem cells (CSCs) has extensive implications for cancer biology and modelling, as well for development of more efficient and targeted therapies. However, experimental support for the existence of distinct and rare CSCs in human malignancies remain contentious, particularly in light of compelling evidence that cancer-propagating cells frequently fail to read out in existing human stem cell assays. Therefore, to unequivocally establish the existence and identity of human CSCs, the challenge is

APA, Harvard, Vancouver, ISO, and other styles

16

Ihme, Susann, Hartmut Döhner, Konstanze Döhner, Michaela Feuring-Buske, Christian Buske, and Medhanie A. Mulaw. "Two Long Non-Coding RNAs Are Sufficient to Classify and Significantly Predict In Vivo Engraftment Potential and LSC Properties of Human Acute Myeloid Leukemia Cells." Blood 128, no. 22 (2016): 2880. http://dx.doi.org/10.1182/blood.v128.22.2880.2880.

Full text

Abstract:

Abstract Acute Myeloid Leukemia (AML) is a hematological malignancy with heterogeneous genetics and clinical course. Studies have shown that there is a strong correlation between xenograft in vivo engraftment potential and clinical outcome. Furthermore, such studies have conducted gene expression profiling to identify gene signatures associated with engraftment potential, leukemic stem cell (LSC) property, and prognosis. Most of these analyses were limited to protein coding genes. More recently, advances in next generation sequencing (NGS) have created a paradigm shift on our perception of tra

APA, Harvard, Vancouver, ISO, and other styles

17

Harb, Jason, Paolo Neviani, Claudia Huettner, Guido Marcucci, and Danilo Perrotti. "BCR/ABL Dosage Hierarchically and Temporally Influences hnRNP A1, hnRNP K and hnRNP E2 Expression in Hematopoietic Stem and Progenitor Cells." Blood 114, no. 22 (2009): 191. http://dx.doi.org/10.1182/blood.v114.22.191.191.

Full text

Abstract:

Abstract Abstract 191 The molecular mechanism leading to the progression of chronic myelogenous leukemia (CML) from the indolent chronic phase (CML-CP) to the rapidly fatal blast crisis (CML-BC) are still unclear although a plausible assumption is that enhanced expression of BCR/ABL, as that observed in most of patients undergoing progression, represents the factor promoting clonal evolution of CML. Given that a) BCR/ABL levels are increased in the CML-BC stem/leukemia-initiating cell population; b) a causal relationship exists between levels and activity of the BCR/ABL oncoprotein and aberran

APA, Harvard, Vancouver, ISO, and other styles

18

Kon, Ayana, Yasuhito Nannya, Masahiro Nakagawa, et al. "Biological Characterization of the U2af1 S34F Mutation in the Pathogenesis of Myelodysplasia." Blood 132, Supplement 1 (2018): 3080. http://dx.doi.org/10.1182/blood-2018-99-117453.

Full text

Abstract:

Abstract Recent genetic studies have revealed frequent and specific pathway mutations involving multiple components of the RNA splicing machinery in myelodysplasia. Among these, U2AF1 mutations are more prevalent in MDS without increased ring sideroblasts and AML with myelodysplasia-related changes and are associated with a poor prognosis. Also found in approximately 4% of lung adenocarcinoma, U2AF1 mutations exclusively involved two highly conserved amino acid positions (S34 or Q157) within the amino- and the carboxyl-terminal zinc finger motifs flanking the U2AF homology motif (UHM) domain.

APA, Harvard, Vancouver, ISO, and other styles

19

Upton, Roy T. "Use of High-Performance Thin Layer Chromatography by the American Herbal Pharmacopoeia." Journal of AOAC INTERNATIONAL 93, no. 5 (2010): 1349–54. http://dx.doi.org/10.1093/jaoac/93.5.1349.

Full text

Abstract:

Abstract TLC characterizations are among the key identity tests in most pharmacopoeial monographs. Pharmacopoeial standards are typically used by industry as a basis for meeting QC requirements and current good manufacturing practices (cGMPs). TLC is a relatively low-cost, highly versatile tool for developing specifications for raw materials, as well as for the various preparations for which pharmacopoeial standards are created. In addition to its use in the development of identity tests, TLC is a valuable tool for screening plant samples that pharmacopoeias must review in the development of m

APA, Harvard, Vancouver, ISO, and other styles

20

Funk, Ryan, Patrick Cahan, Masayo Izumi, and Timothy Graubert. "Bcl2, a Candidate Murine Therapy-Related Acute Myeloid Leukemia Susceptibility Factor, Exhibits Strain-Dependent and Alkylator-Responsive Expression." Blood 112, no. 11 (2008): 1499. http://dx.doi.org/10.1182/blood.v112.11.1499.1499.

Full text

Abstract:

Abstract Identification and characterization of therapy-related acute myeloid leukemia (tAML) susceptibility factors could help distinguish between high- and low-risk patients and suggest logical targets for prevention and control strategies. Our lab recently identified the anti-apoptotic gene Bcl2 as a candidate tAML susceptibility gene based its proximity to a quantitative trait locus (QTL) peak (Mleu1.1) associated with time-to-leukemia in B6C3F1 × SWR/J F2 intercross mice treated with the potent alkylator N-ethyl-N-nitrosourea (ENU). Recent studies have shown that, in addition to its anti-

APA, Harvard, Vancouver, ISO, and other styles

21

Aruljothi, Charlesantony, Subin S. George, Patrick Somers, et al. "Regulation of Ribosomal RNA Synthesis in Myeloid Progenitors By Cell Type Specific Transcription Factors." Blood 136, Supplement 1 (2020): 11–12. http://dx.doi.org/10.1182/blood-2020-138776.

Full text

Abstract:

Haematopoiesis relies on the ability of hematopoietic stem cells to progress through a systematic hierarchy to produce lineage-restricted progenitors that terminally differentiate into phenotypically distinct types of mature hematopoietic cells. This process is precisely coordinated by the combinatorial activity of lineage-specifying transcription factors (TFs). Indeed, the critical transcriptional program of every hematopoietic cell type, and indeed of all cell types throughout the body, requires a set of core TFs for its proper execution. A frequently-overlooked component of the cellular tra

APA, Harvard, Vancouver, ISO, and other styles

22

Rodrigues, Neil P., Ashleigh S. Boyd, Cristina Fugazza, et al. "GATA-2 Regulates Granulocyte-Macrophage Progenitor Cell Function." Blood 112, no. 11 (2008): 1411. http://dx.doi.org/10.1182/blood.v112.11.1411.1411.

Full text

Abstract:

Abstract The zinc finger transcription factor GATA-2 has been implicated in the regulation of hematopoietic stem cells. Herein we explored the role of GATA-2 as a candidate regulator of the hematopoietic progenitor cell compartment. We showed that bone marrow from GATA-2 heterozygote (GATA-2+/-) mice displayed attenuated granulocyte-macrophage progenitor function in colony-forming cell (CFC) and serial replating CFC assays. This defect was mapped to the Lin−CD117+Sca-1−CD34+CD16/32high granulocyte-macrophage progenitor (GMP) compartment of GATA-2+/− marrow, which was reduced in size and functi

APA, Harvard, Vancouver, ISO, and other styles

23

Kon, Ayana, Satoshi Yamazaki, Yasunori Ota, et al. "Srsf2 P95H Mutation Causes Impaired Stem Cell Repopulation and Hematopoietic Differentiation in Mice." Blood 126, no. 23 (2015): 1649. http://dx.doi.org/10.1182/blood.v126.23.1649.1649.

Full text

Abstract:

Abstract Recent genetic studies have revealed frequent and specific pathway mutations involving multiple components of the RNA splicing machinery in myelodysplasia. Among these, SRSF2 mutations are more prevalent in CMML subtype and are associated with poor prognosis. Mutations showed a prominent hotspot involving proline 95, causing either P95H, P95L, or P95 conversion. Comprehensive analysis in our large cohort of MDS revealed that SRSF2 mutations showed a significant trend to coexist with TET2, STAG2, ASXL1 and RUNX1 mutations, while being mutually exclusive with EZH2 mutations. On the othe

APA, Harvard, Vancouver, ISO, and other styles

24

Fung, Tsz Kan, Bernd Zeisig, Magdalena Zarowiecki, et al. "Reconstruction of Human AML Reveals Stem Cell Origin and Therapeutic Targets for Treatment Resistant CD34-/Lo MLL-Rearranged Leukemia." Blood 134, Supplement_1 (2019): 3203. http://dx.doi.org/10.1182/blood-2019-125078.

Full text

Abstract:

Identification of the origins of acute myeloid leukemia (AML) stem cells has been a holy grail for a better understanding of the developmental biology of the disease and the design of effective treatments. Studies using primary AML samples on patient-derived xenograft models identified AML stem cells in multiple different CD34/CD38 cellular fractions, which shared similar immunophenotypes of hematopoietic stem/progenitor cells including hematopoietic stem cells (HSCs), lymphoid-primed multipotent progenitors (LMPPs) and granulocyte-macrophage progenitors (GMPs). However inference of cells-of-o

APA, Harvard, Vancouver, ISO, and other styles

25

Spiecker, Lisa, Ines Witte, Julia Mehlig, et al. "Deficiency of Antioxidative Paraoxonase 2 (Pon2) Leads to Increased Number of Phenotypic LT-HSCs and Disturbed Erythropoiesis." Oxidative Medicine and Cellular Longevity 2021 (June 25, 2021): 1–18. http://dx.doi.org/10.1155/2021/3917028.

Full text

Abstract:

Background. Long-term hematopoietic stem cells (LT-HSCs) reside in bone marrow niches with tightly controlled reactive oxygen species (ROS) levels. ROS increase results into LT-HSC differentiation and stem cell exhaustion. Paraoxonase 2 (PON2) has been shown to be important for ROS control. Objectives. We investigate the effects of inactivation of the PON2 gene on hematopoietic cell differentiation and activity. Methods and Results. In young mice with inactivated Pon2 gene (Pon2-/-, <3 months), we observed an increase of LT-HSCs and a reduced frequency of progenitor cells. In competitive tr

APA, Harvard, Vancouver, ISO, and other styles

26

Mian, Syed A., Kevin Rouault-Pierre, Alexander E. Smith, et al. "SF3B1 Mutant Clones From Patients With Refractory Anaemia With Ringed Sideroblasts (RARS) Originate From The Early Haematopoietic Stem Cells and Maintain Their Engraftment Potential." Blood 122, no. 21 (2013): 262. http://dx.doi.org/10.1182/blood.v122.21.262.262.

Full text

Abstract:

Abstract Introduction Defects in pre-mRNA splicing have recently been implicated in the pathogenesis of myelodysplastic syndrome, particularly RARS where SF3B1, a key component of the spliceosome machinery is mutated in up to 83% of the cases. Moreover, as homozygosity is the exception to the rule for these mutations and SF3B1 homozygous systems have been previously reported as lethal, then such aberrations are most certainly not benign bystanders and are likely to play a significant role in pathogenesis of the disease. Besides the strong correlation of SF3B1 mutations and the presence of ring

APA, Harvard, Vancouver, ISO, and other styles

27

Kaplan, Ian M., Sebastien Morisot, Diane Heiser, Wen-Chih Cheng, Christina LaDana, and Curt I. Civin. "The Hematopoietic Stem Cell (HSC) Compartment in Tristetraprolin (TTP) Knock-out Mice Is Abnormal Phenotypically but Normal Functionally." Blood 114, no. 22 (2009): 2541. http://dx.doi.org/10.1182/blood.v114.22.2541.2541.

Full text

Abstract:

Abstract Abstract 2541 Poster Board II-518 The RNA binding protein TTP binds to AU-rich elements (AREs) located in the 3′UTR of mRNAs and dramatically reduces their half-life through exosome-mediated RNA degradation. TTP provides a conserved mechanism for the temporal and fine-tuning regulation of gene expression. We found that the Lin−Kit+Sca+ (KSL) population, a phenotypic marker combination that enriches for HSCs, in adult (6–8 week old) C57Bl/6 marrow expressed TTP mRNA at a level 25-fold higher than whole bone marrow mononucuclear cells. Furthermore, adult TTP KO mice had twice the number

APA, Harvard, Vancouver, ISO, and other styles

28

Shinoda, Daisuke, Yaeko Nakajima-Takagi, Motohiko Oshima, et al. "Insufficiency of Non-Canonical PRC1 Complex Cooperates with an Activating JAK2 Mutation in the Pathogenesis of Myelofibrosis." Blood 132, Supplement 1 (2018): 100. http://dx.doi.org/10.1182/blood-2018-99-117741.

Full text

Abstract:

Abstract Introduction: PcG proteins form two main multiprotein complexes, Polycomb repressive complex 1 (PRC1) and PRC2. They repress the transcription of target genes. Polycomb group ring finger protein1 (PCGF1) is a component of PRC1.1, a non-canonical PRC1.1 that monoubiquitylates H2A at lysine 119 in a manner independent of H3K27me3. Several groups including ours showed that the loss of Ezh2, a component of PRC2, promotes the development of JAK2 V617F-induced Myelofibrosis (MF) in mice. However, the role of PRC1.1 in hematologic malignancies is still not fully understood. We found that the

APA, Harvard, Vancouver, ISO, and other styles

29

Jeffrey, Kurkewich, Justin Hansen, Emmanuel Bikorimani, Tan Nguyen, and Richard Dahl. "Mirn23a Inhibits B Lymphopoiesis through Antagonism of the B Cell Transcription Factor Network." Blood 124, no. 21 (2014): 4340. http://dx.doi.org/10.1182/blood.v124.21.4340.4340.

Full text

Abstract:

Abstract Transcription factors (TFs) regulate genetic networks to direct the differentiation of hematopoietic stem and progenitor cells (HSPCs) to mature blood lineages. Historically studies have focused on identifying genes activated by TFs that act as master hematopoietic regulators. Recently, it has become appreciated that these regulatory TFs direct one distinct differentiation program while simultaneously directing the repression of genes associated with alternative blood lineages. MicroRNAs (miRNAs) are short (~22nt) non-coding RNA molecules that negatively regulate gene expression at th

APA, Harvard, Vancouver, ISO, and other styles

30

Ramdas, Baskar, Lakshmi Reddy Palam, Raghuveer Singh Mali, Zhigang Cai, Ruchi Pandey, and Reuben Kapur. "Combined Heterozygous Loss of Tet2 and Dnmt3a Along with Expression of Flt3ITD/WT results in Acute Myeloid Leukemia Which Responds to a Combination of FLT3 Inhibitor, APE1 Inhibitor and Decitabine." Blood 134, Supplement_1 (2019): 3754. http://dx.doi.org/10.1182/blood-2019-131172.

Full text

Abstract:

Heterozygous mutations in FLT3ITD, TET2 and DNMT3A are associated with human neoplasms. Whole exome sequencing of patients demonstrate co-occurrence of several of these mutations in myeloid malignancies; however it is unclear if and how these mutations cooperate and how does this cooperation manifest in disease. We assessed the consequence of co-existence of TET2, DNMT3A and FLT3ITD/WT mutations on AML development and overall survival. Mice were bred to obtain eight distinct genotypes WT, Tet2+/-, Flt3ITD/WT, Dnmt3aFlox/- MxCre, double het Tet2+/-; Dnmt3aFlox/- MxCre (TD), double het Tet2+/-;

APA, Harvard, Vancouver, ISO, and other styles

31

Wu, Kai, Qianyi Ma, Darren King, Jun Li, and Sami Malek. "Paired Analyses of AML at Diagnosis and Relapse By Single-Cell RNA Sequencing Identifies Two Distinct Relapse Patterns." Blood 134, Supplement_1 (2019): 183. http://dx.doi.org/10.1182/blood-2019-124170.

Full text

Abstract:

Introduction: Despite achievement of complete remission (CR) following chemotherapy, Acute Myelogenous Leukemia (AML) relapses in the majority of adult patients. While relapsed AML is almost always clonally related to the disease at diagnosis, the actual molecular and cellular contributors to chemotherapy resistance and to AML relapse remain incompletely understood. Some molecular determinants of relapse have been identified in genomic, epigenetic and proteomic aberrations, while cellular relapse reservoirs have been identified in leukemia stem cells as well as in more mature leukemic cell com

APA, Harvard, Vancouver, ISO, and other styles

32

Han, Lin, Vikas Madan, Anand Mayakonda, et al. "ARID1A Is Critical for Maintaining Normal Hematopoiesis in Mice." Blood 132, Supplement 1 (2018): 3833. http://dx.doi.org/10.1182/blood-2018-99-117993.

Full text

Abstract:

Abstract ARID1A is a key component of ATP-dependent SWI/SNF complex involved in chromatin remodeling. Chromatin remodeling mediated by SWI/SNF complex is crucial for gene expression and affects a broad range of biological processes including hematopoietic development. ARID1A is frequently mutated across several solid tumors as well as hematopoietic malignancies, including Burkitt's lymphoma, diffuse large B-cell lymphoma and acute promyelocytic leukemia. Nevertheless, function of ARID1A in adult hematopoiesis and implications of its deficiency in development and progression of hematopoietic di

APA, Harvard, Vancouver, ISO, and other styles

33

Magidey-Klein, Ksenia, Tim J. Cooper, Ksenya Kveler, et al. "IL-6 contributes to metastatic switch via the differentiation of monocytic-dendritic progenitors into prometastatic immune cells." Journal for ImmunoTherapy of Cancer 9, no. 6 (2021): e002856. http://dx.doi.org/10.1136/jitc-2021-002856.

Full text

Abstract:

BackgroundMetastasis is the major cause of death in patients with cancer. Myeloid skewing of hematopoietic cells is a prominent promoter of metastasis. However, the reservoir of these cells in the bone marrow (BM) compartment and their differentiation pattern from hematopoietic stem and progenitor cells (HSPCs) have not been explored.MethodsWe used a unique model system consisting of tumor cell clones with low metastatic potential or high metastatic potential (met-low and met-high, respectively) to investigate the fate of HSPC differentiation using murine melanoma and breast carcinoma. Single-

APA, Harvard, Vancouver, ISO, and other styles

34

Ries, Rhonda E., Timothy Junius Triche, Jenny L. Smith, et al. "Genome and Transcriptome Profiling of Monosomy 7 AML Defines Novel Risk and Therapeutic Cohorts." Blood 136, Supplement 1 (2020): 20–21. http://dx.doi.org/10.1182/blood-2020-137244.

Full text

Abstract:

Monosomy 7 (mono7) alterations in acute myeloid leukemia (AML) are associated with poor outcome and disease progression. Through advancements in multi-omic approaches, more specific treatment strategies may be available for high-risk cohorts. Here we describe pediatric cases of AML with mono7, co-occurring fusions, associated outcome, and potential therapeutic treatments. Of the 2200 patients treated in 3 consecutive Children's Oncology Group protocols (AAML03P1, AAML0531, and AAML1031), 45 patients (2%) had karyotypic evidence of mono7 with full complement of clinical data for analysis. RNA s

APA, Harvard, Vancouver, ISO, and other styles

35

Ganan-Gomez, Irene, Ana Alfonso, Hui Yang, et al. "Cell-Type Specific Mechanisms of Hematopoietic Stem Cell (HSC) Expansion Underpin Progressive Disease in Myelodysplastic Syndromes (MDS) and Provide a Rationale for Targeted Therapies." Blood 132, Supplement 1 (2018): 1798. http://dx.doi.org/10.1182/blood-2018-99-116881.

Full text

Abstract:

Abstract The mechanisms of HMA failure in MDS remain unclear, as recent advances in sequencing approaches did not enable the molecular characterization of the cells that survive therapy and drive resistance and disease progression. Here, through combined functional and transcriptomic analyses of highly-purified hematopoietic populations isolated from the BM of 132 MDS patients enrolled in clinical trials of single drug HMA therapy, we show that 2 immunophenotypically and molecularly distinct cell types maintain the disease and expand at progression, and we propose therapeutic approaches to ove

APA, Harvard, Vancouver, ISO, and other styles

36

Chatain, Nicolas, Juliane Lüscher-Firzlaff, Chao-Chung Kuo, et al. "Hematopoietic Stem and Progenitor Cell Proliferation and Differentiation Requires the Trithorax Protein Ash2l In Vivo." Blood 132, Supplement 1 (2018): 2566. http://dx.doi.org/10.1182/blood-2018-99-115950.

Full text

Abstract:

Abstract Gene transcription is controlled by post-translational modifications of core histones. Methylation of lysine 4 of histone H3 (H3K4), together with acetylation of H3K27, is closely associated with open chromatin and gene transcription. H3K4 methylation is catalyzed by KMT2 lysine methyltransferases that include the mixed-lineage leukemia 1-4 (MLL1-4) and SET1A and B enzymes. For efficient catalysis all six require a core complex of four proteins, WDR5, RBBP5, ASH2L, and DPY30. In a newly-generated pIC-inducible Mx1-Cre mouse model, we report that targeted disruption of Ash2l in the hem

APA, Harvard, Vancouver, ISO, and other styles

37

Holm, Frida L., Eva Hellqvist, Cayla N. Mason, et al. "Malignant Reprogramming of Progenitors into Leukemia Stem Cells Is Enhanced By Upregulation of CD44 Transcript Variant 3 in Malignant Microenvironments." Blood 124, no. 21 (2014): 511. http://dx.doi.org/10.1182/blood.v124.21.511.511.

Full text

Abstract:

Abstract Introduction Malignant reprogramming, first described in chronic myeloid leukemia (CML), occurs upon activation of the Wnt/b-catenin pathway in granulocyte-macrophage progenitors (GMPs) that gain the capacity to self-renew and contribute to the emergence of BCR-ABL1 tyrosine kinase inhibitor (TKI) resistant blast crisis CML. Deregulation of the Wnt/b-catenin target gene, CD44, plays a vital role in leukemia stem cell (LSC) maintenance in the malignant microenvironment in mouse models of CML. However, extensive alternative mRNA splicing in humans results in expression of multiple CD44

APA, Harvard, Vancouver, ISO, and other styles

38

Spitzer, Barbara, Olga A. Guryanova, Omar Abdel-Wahab, et al. "Characterizing Transcriptional and Epigenetic Signatures Induced By FLT3-ITD Activation." Blood 124, no. 21 (2014): 2186. http://dx.doi.org/10.1182/blood.v124.21.2186.2186.

Full text

Abstract:

Abstract Molecular studies have shown that specific somatic mutations impact therapeutic response and overall outcome in acute myeloid leukemia (AML) and have informed the development of molecularly targeted therapies. Previous studies have shown that the FLT3-ITD mutant disease allele predicts a poor prognosis in AML. Despite this important insight and the established role of FLT3-ITD mutations in AML pathogenesis, the impact of this mutation on gene regulation has not been extensively investigated. We hypothesized that transcriptional and epigenetic studies using genetically accurate murine

APA, Harvard, Vancouver, ISO, and other styles

39

Kon, Ayana, Masahiro Marshall Nakagawa, Ryosaku Inagaki, et al. "Functional Characterization of Compound DDX41 Germline and Somatic R525H Mutations in the Development of Myeloid Malignancies." Blood 136, Supplement 1 (2020): 21–22. http://dx.doi.org/10.1182/blood-2020-143318.

Full text

Abstract:

DDX41 is a newly identified leukemia predisposition gene encoding an RNA helicase, whose germline mutations are tightly associated with late-onset myeloid malignancies. Importantly, germline DDX41 mutations were also found in as many as ~7 % of sporadic cases of high-risk MDS, conferring the largest germline risk for myeloid malignancies. In typical cases, a germline loss-of-function allele (most commonly p.A500fs or p.D140fs, depending on the ethnicity) is compounded by a somatic missense mutation affecting the helicase domain in the remaining allele (p.R525H). However, the molecular mechanis

APA, Harvard, Vancouver, ISO, and other styles

40

Gaudreau, Marie-Claude, Damien Grapton, Florian Heyd, Charles Vadnais, Brian T. Wilhelm, and Tarik Moroy. "The Splicing Factor Heterogeneous Nuclear Ribonucleoprotein L (hnRNPL) Restricts p53 Dependent and p53 Independent Cell Death Pathways In Hematopoietic Stem Cells." Blood 122, no. 21 (2013): 2445. http://dx.doi.org/10.1182/blood.v122.21.2445.2445.

Full text

Abstract:

Abstract Hematopoiesis is sustained by a pool of multipotent hematopoietic stem cells (HSCs) that have the capacity to differentiate into cells of all blood cell lineages. The pool of long-lived HSCs is maintained throughout life by the self-renewal ability of HSCs. New evidence suggests the process of alternative splicing is an important regulator of the maturation and activation of blood and immune effector cells. It is presently estimated that almost all multi-exon genes in human genome undergo alternative pre-mRNA splicing, and aberrant splicing has been linked to a variety of human pathol

APA, Harvard, Vancouver, ISO, and other styles

41

Park, Sun Mi, Mithat Gönen, Ly P. Vu, et al. "Msi2 Maintains the MLL Leukemia Stem Cell Regulatory Program." Blood 124, no. 21 (2014): 836. http://dx.doi.org/10.1182/blood.v124.21.836.836.

Full text

Abstract:

Abstract Leukemia stem cells (LSCs) are found in most aggressive myeloid diseases and contribute to therapeutic resistance. LSCs are characterized by their gain of a self-renewal program that is normally associated with hematopoietic stem cells (HSCs). Previously we have shown that the RNA binding protein, Msi2 contributes to both HSC and myeloid leukemia function. Elevated MSI2 expression predicts a poor prognosis in a variety of leukemias and shRNA-mediated depletion in human AML cell lines reduces proliferation, increases differentiation and induces apoptosis. Despite these in vitroand corr

APA, Harvard, Vancouver, ISO, and other styles

42

Maeda, Takahiro, Taha Merghoub, Robin Hobbs, et al. "Conditional Inactivation of the Proto-Oncogene Pokemon Results in Block of Differentiation in Multiple Hematopoietic Lineages." Blood 106, no. 11 (2005): 121. http://dx.doi.org/10.1182/blood.v106.11.121.121.

Full text

Abstract:

Abstract We recently reported a role of the POK transcription factor Pokemon in oncogenesis (Nature. 433, 278–85). To elucidate its function in fetal and adult hematopoiesis, we studied the hematopoiesis in Pokemon knockout mice (Pokemon−/−) and the conditional knockout mutants (Pokemonflox/flox) respectively. We generated the Pokemonflox/floxMx−1cre+ mice, in which Exon 2 of the Pokemon genomic locus can be excised in vivo upon pIpC (polyinosinic-polycytidylic ribonucleic acid) injections. &lt;Erythroid&gt; Pokemon−/− mice died around 16.5 d.p.c due to severe anemia. Flow cytometric a

APA, Harvard, Vancouver, ISO, and other styles

43

Ha, Caryn J., Wenhuo Hu, Harold K. Elias, Sohini Chakraborty, and Christopher Y. Park. "Mir-29 Maintains the Acute Myeloid Leukemia Epigenome By Regulating CBX2." Blood 134, Supplement_1 (2019): 1236. http://dx.doi.org/10.1182/blood-2019-131518.

Full text

Abstract:

Epigenetic regulators in normal and malignant hematopoiesis have been shown to be important in normal and malignant stem cell self-renewal function and myeloid leukemogenesis. While epigenetic dysregulation can occur through activating and/or loss-of-function mutations, these regulators can also be modulated by other regulators, such as microRNAs. Specifically, miR-29 has been previously identified as an "epi-mir" for contributing to epigenetic regulation by altering expression of DNMT3a and TET. We and others have previously shown that in the hematopoietic system, miR-29 is a positive regulat

APA, Harvard, Vancouver, ISO, and other styles

44

Kurkewich, Jeffrey, Justin Hansen, Nathan Klopfenstein, et al. "Regulation of Hematopoietic Stem and Progenitor Cell Differentiation By Mirn23a/b Micrornas." Blood 128, no. 22 (2016): 3880. http://dx.doi.org/10.1182/blood.v128.22.3880.3880.

Full text

Abstract:

Abstract Differentiation from hematopoietic stem and progenitor cells (HSPCs) to committed blood lineages is dependent on lineage specific transcription factors that simultaneously promote gene expression that commits progenitors to specific lineages while repressing genes associated with alternative lineages. In addition to transcription factors, small non-coding microRNAs (miRNAs) also have the potential to influence cell fate decisions through negative regulation of lineage specific genes. We previously observed that germline knockout of the mirn23a miRNA cluster (which codes for mature miR

APA, Harvard, Vancouver, ISO, and other styles

45

Chu, Yajing, Yangpeng Chen, Huidong Guo, et al. "Suv39h1 Represses the Progression of MLL-Rearranged Myeloid Leukemia Via Hoxb13." Blood 132, Supplement 1 (2018): 3878. http://dx.doi.org/10.1182/blood-2018-99-113732.

Full text

Abstract:

Abstract Acute myeloid leukemia (AML) is the most frequent and heterogeneous malignancy in adult leukemic patients. Genome-wide analyses revealed that genes involved in epigenetic modifications are among the most often re-occurring mutations in AML, suggesting a crucial role of epigenetic regulation in leukemogenesis and leukemia relapse. As a mammalian lysine methyltransferase, SUV39H1 catalyzes di- and tri-methylation of histone 3 lysine 9, and is the predominant H3K9 methyltransferase expressed in hematopoietic stem cells (HSCs). Previous studies have shown that in MLL-rearranged leukemic c

APA, Harvard, Vancouver, ISO, and other styles

46

Yao, Juo-Chin, Terrence Neal Wong, Maria Trissal, et al. "Loss-of-Function Mutations of MIR142 May Contribute to Leukemogenesis By Expanding the Pool of Myeloid-Biased HSCs." Blood 126, no. 23 (2015): 1254. http://dx.doi.org/10.1182/blood.v126.23.1254.1254.

Full text

Abstract:

Abstract MicroRNA (miRNA) expression is sometimes dysregulated in acute myelogenous leukemia (AML), and this dysregulation has been suggested to play a role in leukemic transformation. However, somatic mutations in miRNAs are infrequent in AML. Through whole genome or exome sequencing of 200 cases of de novo AML, The Cancer Genome Atlas (NEJM 2013) identified recurring point mutations in MIR142. Heterozygous point mutations of MIR142 were identifiedin 3 cases, and bi-allelic mutations in 1 case (total incidence of 2%). All of these mutations localized to the "seed" sequence of miR-142-3p, whic

APA, Harvard, Vancouver, ISO, and other styles

47

Lewis, Andrew, Chun Shik Park, Monica Puppi, and H. Daniel Lacorazza. "KLF4 Controls Leukemic Stem Cell Self-Renewal in MLL-AF9-Induced Acute Myeloid Leukemia." Blood 134, Supplement_1 (2019): 1231. http://dx.doi.org/10.1182/blood-2019-129164.

Full text

Abstract:

Acute myeloid leukemia (AML) develops from sequential mutations which transform hematopoietic stem and progenitor cells (HSPCs) in the bone marrow into leukemic stem cells (LSCs) which drive the progression of frank leukemia. Especially poor outcomes in elderly patients coupled with frequent relapse have led to a dismal 28.3% 5-year survival, warranting the need for innovative therapeutic approaches. Successful targeted therapy will selectively eliminate LSCs, which possess distinct characteristics enabling self-renewal and chemotherapeutic resistance, while sparing normal HSPCs. We theorized

APA, Harvard, Vancouver, ISO, and other styles

48

Obenauer, Julia C., Paulina M. H. van Strien, Remco M. Hoogenboezem, Marry M. van den Heuvel-Eibrink, and Ivo P. Touw. "RUNX1 TAD and RHD Mutations Found in SCN/AML Differentially Affect HSPC Expansion in Conjunction with Truncated CSF3 Receptors." Blood 126, no. 23 (2015): 3606. http://dx.doi.org/10.1182/blood.v126.23.3606.3606.

Full text

Abstract:

Abstract Severe congenital neutropenia (SCN) is characterized by a maturation arrest at the promyelocyte stage and consequently a severe reduction of peripheral neutrophils. Administration of colony stimulating factor 3 (CSF3) restores neutrophil levels in over 90% of SCN patients, leading to an improved survival rate. SCN patients have an increased risk to develop secondary MDS or AML. Leukemic progression of SCN frequently involves the acquisition of a mutation in the gene encoding CSF3 receptor (CSF3R) in the neutropenic phase, followed by a mutation in runt-related transcription factor 1 (

APA, Harvard, Vancouver, ISO, and other styles

49

Martin, Gaëlle H., Alexis Desrichard, Stephen S. Chung, et al. "CD97 Is a Critical Regulator of Acute Myeloid Leukemia Stem Cell Function." Blood 128, no. 22 (2016): 1077. http://dx.doi.org/10.1182/blood.v128.22.1077.1077.

Full text

Abstract:

Abstract Despite recent advances in our understanding of the genetic origins of acute myeloid leukemia (AML), clinical outcomes remain poor. While standard induction chemotherapy induces remission in most patients, the majority of patients eventually relapses and dies from progressive disease. A number of cell surface proteins have been shown to be expressed at high levels on AML stem cells compared to normal HSCs including CD47, CD44, CD96, TIM3, CD123, CD25 and IL1RAP. Despite the attention these antigens have received, data supporting their roles as cell-intrinsic regulators of LSCs are mor

APA, Harvard, Vancouver, ISO, and other styles

50

Sloma, Ivan, Philip Beer, Christophe Desterke, et al. "NUP98-HOXA9-Initiates Molecular and Biologic Features of Disease Progression in a Humanized Model of CML." Blood 134, Supplement_1 (2019): 4139. http://dx.doi.org/10.1182/blood-2019-127839.

Full text

Abstract:

Acute myeloid leukemias (AMLs) are heterogenous diseases often resulting from the acquisition of multiple genetic alterations that deregulate hematopoietic precursor proliferation and block normal differentiation. Chronic myeloid leukemia offers a unique opportunity to identify molecular mechanisms that interfere with normal differentiation in the context of a highly proliferative hematopoietic stem cell clone that produces massive number of functional differentiated myeloid cells due to the presence of a BCR-ABL1 fusion gene. Since the NUP98-HOXA9 (NA9) fusion gene has been identified in some

APA, Harvard, Vancouver, ISO, and other styles

We offer discounts on all premium plans for authors whose works are included in thematic literature selections. Contact us to get a unique promo code!