Database : MEDLINE
Search on : lymphopoiesis [Words]
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[PMID]: 29288704
[Au] Autor:Kurkewich JL; Boucher A; Klopfenstein N; Baskar R; Kapur R; Dahl R
[Ad] Address:Department of Biological Sciences, University of Notre Dame, Notre Dame, IN, USA; Harper Cancer Research Institute, South Bend, IN, USA.
[Ti] Title:The mirn23a and mirn23b microrna clusters are necessary for proper hematopoietic progenitor cell production and differentiation.
[So] Source:Exp Hematol;59:14-29, 2018 Mar.
[Is] ISSN:1873-2399
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:Mice deficient for microRNA (miRNA) cluster mirn23a exhibit increased B lymphopoiesis at the expense of myelopoiesis, whereas hematopoietic stem and progenitor cell (HSPC) populations are unchanged. Mammals possess a paralogous mirn23b gene that can give rise to three mature miRNAs (miR-23b, miR-24-1, and miR-27b) that have identical seed/mRNA-targeting sequences to their mirn23a counterparts. To assess whether compound deletion of mirn23a and mirn23b exacerbates the hematopoietic phenotype observed in mirn23a mice, we generated a compound mirn23a mirn23b :Mx1-Cre conditional knockout mouse and assayed hematopoietic development after excision of mirn23b. Loss of both genes in adult bone marrow further skewed HSPC differentiation toward B cells at the expense of myeloid cells, demonstrating a dosage-dependent effect on regulating cell differentiation. Strikingly, double-knockout (DKO) mice had decreased bone marrow cellularity with significantly decreased hematopoietic stem cell and HSPC populations, a phenotype not observed in mice deficient for mirn23a alone. Competitive transplantation assays showed decreased contribution of mirn23a mirn23b HSPCs to hematopoietic lineages at 6 and 12 weeks after transplantation. Defects in the proliferation of mirn23a b HSPCs was not observed; however, DKO cells were more apoptotic compared with both wild-type and mirn23a cells. Together, our data show that complete loss of mirn23a/mirn23b miRNAs results in decreased blood production and affects lineage output in a concentration-dependent manner.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1712
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:In-Data-Review

  2 / 2583 MEDLINE  
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[PMID]: 29519871
[Au] Autor:Marke R; van Leeuwen FN; Scheijen B
[Ad] Address:Laboratory of Pediatric Oncology, Radboud university medical center, Nijmegen, the Netherlands.
[Ti] Title:The many faces of IKZF1 in B-cell precursor acute lymphoblastic leukemia.
[So] Source:Haematologica;, 2018 Mar 08.
[Is] ISSN:1592-8721
[Cp] Country of publication:Italy
[La] Language:eng
[Ab] Abstract:Transcription factor IKZF1 (IKAROS) acts as a critical regulator of lymphoid differentiation and is frequently deleted or mutated in B-cell precursor acute lymphoblastic leukemia (BCP-ALL). IKZF1 gene defects are associated with inferior treatment outcome in both childhood and adult BCP-ALL and occur in more than 70% of BCR-ABL1 positive and BCR-ABL1-like ALL cases. Over the past few years, much has been learned about the tumor suppressive function of IKZF1 during leukemia development and the molecular pathways that relate to its impact on treatment outcome. In this review, we provide a concise overview on the role of IKZF1 during normal lymphopoiesis and the pathways that contribute to leukemia pathogenesis as a consequence of altered IKZF1 function. Furthermore, we will discuss different mechanisms by which IKZF1 alterations impose therapy resistance to leukemic cells, including enhanced cell adhesion and modulation of glucocorticoid response.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:Publisher

  3 / 2583 MEDLINE  
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[PMID]: 29476393
[Au] Autor:Patel VS; Ete Chan M; Rubin J; Rubin CT
[Ad] Address:Department of Biomedical Engineering, Stony Brook University, Stony Brook, NY, 11794-2580, USA.
[Ti] Title:Marrow Adiposity and Hematopoiesis in Aging and Obesity: Exercise as an Intervention.
[So] Source:Curr Osteoporos Rep;, 2018 Feb 23.
[Is] ISSN:1544-2241
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:PURPOSE OF REVIEW: Changes in the bone marrow microenvironment, which accompany aging and obesity, including increased marrow adiposity, can compromise hematopoiesis. Here, we review deleterious shifts in molecular, cellular, and tissue activity and consider the potential of exercise to slow degenerative changes associated with aging and obesity. RECENT FINDINGS: While bone marrow hematopoietic stem cells (HSC) are increased in frequency and myeloid-biased with age, the effect of obesity on HSC proliferation and differentiation remains controversial. HSC from both aged and obese environment have reduced hematopoietic reconstitution capacity following bone marrow transplant. Increased marrow adiposity affects HSC function, causing upregulation of myelopoiesis and downregulation of lymphopoiesis. Exercise, in contrast, can reduce marrow adiposity and restore hematopoiesis. The impact of marrow adiposity on hematopoiesis is determined mainly through correlations. Mechanistic studies are needed to determine a causative relationship between marrow adiposity and declines in hematopoiesis, which could aid in developing treatments for conditions that arise from disruptions in the marrow microenvironment.
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Em] Entry month:1802
[Cu] Class update date: 180307
[Lr] Last revision date:180307
[St] Status:Publisher
[do] DOI:10.1007/s11914-018-0424-1

  4 / 2583 MEDLINE  
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[PMID]: 29496554
[Au] Autor:Kjeldsen E; Veigaard C; Aggerholm A; Hasle H
[Ad] Address:HemoDiagnostic Laboratory, Cancer Cytogenetics Section, Department of Hematology, Aarhus University Hospital, Tage-Hansens Gade 2, Ent. 4A, DK-8000 Aarhus C, Denmark. Electronic address: Eigil.Kjeldsen@clin.au.dk.
[Ti] Title:Congenital hypoplastic bone marrow failure associated with a de novo partial deletion of the MECOM gene at 3q26.2.
[So] Source:Gene;, 2018 Feb 26.
[Is] ISSN:1879-0038
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:Congenital hypoplastic bone marrow failure is a rare condition in neonates. The genetics and mechanisms behind are largely obscure. Here we characterize a neonate presenting with congenital thrombocytopenia and anemia. During the first 2-4 weeks after birth the neonate developed severe neutropenia while the lymphoid lineages were unaffected. The neonate was without dysmorphic signs. A de novo mono-allelic constitutional microdeletion of 175.1 kb at 3q26.2 affecting exon 2 of MECOM, involving MDS1 but not EVI1, was identified as the only copy number alteration by oligo-based array-CGH analysis. Expression analysis showed profoundly reduced expression of multiple MECOM transcripts in the bone marrow cells. Whole exome sequencing detected no pathogenic mutations in genes known to be associated with inherited bone marrow failure syndromes. The patient was successfully treated with hematopoietic stem cell transplantation at 5 months of age. Interstitial deletions encompassing the 3q26.2 region are very rare. A literature search revealed two previous cases with microdeletions involving this region, and the cases were associated with congenital thrombocytopenia and anemia, but unaffected lymphopoiesis. Together these data indicate that MECOM may be important for normal myeloid hematopoiesis in humans but dispensable for lymphoid differentiation. We suggest that partial deletion in MECOM may be a primary event associated with congenital pancytopenia.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180302
[Lr] Last revision date:180302
[St] Status:Publisher

  5 / 2583 MEDLINE  
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[PMID]: 29475522
[Au] Autor:Smirnova OA; Cucinotta FA
[Ad] Address:Federal State Unitary Enterprise Research and Technical Center of Radiation-Chemical Safety and Hygiene, Moscow, Russian Federation.
[Ti] Title:Dynamical modeling approach to risk assessment for radiogenic leukemia among astronauts engaged in interplanetary space missions.
[So] Source:Life Sci Space Res (Amst);16:76-83, 2018 Feb.
[Is] ISSN:2214-5532
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:A recently developed biologically motivated dynamical model of the assessment of the excess relative risk (ERR) for radiogenic leukemia among acutely/continuously irradiated humans (Smirnova, 2015, 2017) is applied to estimate the ERR for radiogenic leukemia among astronauts engaged in long-term interplanetary space missions. Numerous scenarios of space radiation exposure during space missions are used in the modeling studies. The dependence of the ERR for leukemia among astronauts on several mission parameters including the dose equivalent rates of galactic cosmic rays (GCR) and large solar particle events (SPEs), the number of large SPEs, the time interval between SPEs, mission duration, the degree of astronaut's additional shielding during SPEs, the degree of their additional 12-hour's daily shielding, as well as the total mission dose equivalent, is examined. The results of the estimation of ERR for radiogenic leukemia among astronauts, which are obtained in the framework of the developed dynamical model for various scenarios of space radiation exposure, are compared with the corresponding results, computed by the commonly used linear model. It is revealed that the developed dynamical model along with the linear model can be applied to estimate ERR for radiogenic leukemia among astronauts engaged in long-term interplanetary space missions in the range of applicability of the latter. In turn, the developed dynamical model is capable of predicting the ERR for leukemia among astronauts for the irradiation regimes beyond the applicability range of the linear model in emergency cases. As a supplement to the estimations of cancer incidence and death (REIC and REID) (Cucinotta etal., 2013, 2017), the developed dynamical model for the assessment of the ERR for leukemia can be employed on the pre-mission design phase for, e.g., the optimization of the regimes of astronaut's additional shielding in the course of interplanetary space missions. The developed model can also be used on the phase of the real-time responses during the space mission to make the decisions on the operational application of appropriate countermeasures to minimize the risks of occurrences of leukemia, especially, for emergency cases.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180224
[Lr] Last revision date:180224
[St] Status:In-Process

  6 / 2583 MEDLINE  
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[PMID]: 29458123
[Au] Autor:Divieti Pajevic P; Krause DS
[Ad] Address:Goldman School of Dental Medicine, Boston University, Boston, MA 02118, USA. Electronic address: pdivieti@bu.edu.
[Ti] Title:Osteocyte regulation of bone and blood.
[So] Source:Bone;, 2018 Feb 16.
[Is] ISSN:1873-2763
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:This past decade has witnessed a renewed interest in the function and biology of matrix-embedded osteocytes and these cells have emerged as master regulators of bone homeostasis. They secrete two very powerful proteins, sclerostin, a Wnt-inhibitor, that suppresses bone formation, and receptor-activator of NF-kB ligand (RANKL), a cytokine required for osteoclastogenesis. Neutralizing antibodies against these proteins are currently used for the treatment of osteoporosis. Recent studies however, ascribed yet another function to osteocytes: the control of hematopoiesis and the HSPC niche, directly and through secreted factors. In the absence of osteocytes there is an increase in HSC mobilization and abnormal lymphopoiesis whereas in the absence of G α signaling in these cells there is an increase of myeloid cells. How exactly osteocytes control hematopoiesis or the HSPC niche is still not completely understood. In this review we summarize the actions of osteocytes in bone and then analyze the effects of these cells on hematopoiesis. Future directions and gaps in current knowledge are further discussed.
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Em] Entry month:1802
[Cu] Class update date: 180224
[Lr] Last revision date:180224
[St] Status:Publisher

  7 / 2583 MEDLINE  
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[PMID]: 29290585
[Au] Autor:Biers C; Richardson SE; Laycock E; Zriwil A; Turati VA; Brown J; Wray JP; Wang D; James C; Herrero J; Sitnicka E; Karlsson S; Smith AJH; Jacobsen SEW; Enver T
[Ad] Address:Department of Cancer Biology, UCL Cancer Institute, UCL, London, UK; Lund Stem Cell Center, Lund University, Lund, Sweden.
[Ti] Title:A Human IPS Model Implicates Embryonic B-Myeloid Fate Restriction as Developmental Susceptibility to BAcute Lymphoblastic Leukemia-Associated ETV6-RUNX1.
[So] Source:Dev Cell;44(3):362-377.e7, 2018 Feb 05.
[Is] ISSN:1878-1551
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:ETV6-RUNX1 is associated with childhood acute B-lymphoblastic leukemia (cALL) functioning as a first-hit mutation that initiates a clinically silent pre-leukemia in utero. Because lineage commitment hierarchies differ between embryo and adult, and the impact of oncogenes is cell-context dependent, we hypothesized that the childhood affiliation of ETV6-RUNX1 cALL reflects its origins in a progenitor unique to embryonic life. We characterize the firstemerging B cells in first-trimester human embryos, identifying a developmentally restricted CD19 IL-7R progenitor compartment, which transitions from a myeloid to lymphoid program during ontogeny. This developmental series is recapitulated in differentiating human pluripotent stem cells (hPSCs), thereby providing a model for the initiation of cALL. Genome-engineered hPSCs expressing ETV6-RUNX1 from the endogenous ETV6 locus show expansion of the CD19 IL-7R compartment, show a partial block in B lineage commitment, andproduce proB cells with aberrant myeloid geneexpression signatures and potential: features (collectively) consistent with a pre-leukemic state.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1801
[Cu] Class update date: 180216
[Lr] Last revision date:180216
[St] Status:In-Data-Review

  8 / 2583 MEDLINE  
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[PMID]: 29321277
[Au] Autor:Rodrigues PM; Ribeiro AR; Serafini N; Meireles C; Di Santo JP; Alves NL
[Ad] Address:Instituto de Investigao e Inovao em Sade, Universidade do Porto, 4200-135 Porto, Portugal.
[Ti] Title:Intrathymic Deletion of IL-7 Reveals a Contribution of the Bone Marrow to Thymic Rebound Induced by Androgen Blockade.
[So] Source:J Immunol;200(4):1389-1398, 2018 Feb 15.
[Is] ISSN:1550-6606
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Despite the well-documented effect of castration in thymic regeneration, the singular contribution of the bone marrow (BM) versus the thymus to this process remains unclear. The chief role of IL-7 in pre- and intrathymic stages of T lymphopoiesis led us to investigate the impact of disrupting this cytokine during thymic rebound induced by androgen blockade. We found that castration promoted thymopoiesis in young and aged wild-type mice. In contrast, only young germline IL-7-deficient ( ) mice consistently augmented thymopoiesis after castration. The increase in T cell production was accompanied by the expansion of the sparse medullary thymic epithelial cell and the peripheral T cell compartment in young mice. In contrast to young and wild-type mice, the poor thymic response of aged mice after castration was associated with a defect in the expansion of BM hematopoietic progenitors. These findings suggest that BM-derived T cell precursors contribute to thymic rebound driven by androgen blockade. To assess the role of IL-7 within the thymus, we generated mice with conditional deletion of IL-7 ( conditional knockout [cKO]) in thymic epithelial cells. As expected, cKO mice presented a profound defect in T cell development while maintaining an intact BM hematopoietic compartment across life. Unlike mice, castration promoted the expansion of BM precursors and enhanced thymic activity in cKO mice independently of age. Our findings suggest that the mobilization of BM precursors acts as a prime catalyst of castration-driven thymopoiesis.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1801
[Cu] Class update date: 180212
[Lr] Last revision date:180212
[St] Status:In-Data-Review
[do] DOI:10.4049/jimmunol.1701112

  9 / 2583 MEDLINE  
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[PMID]: 29309056
[Au] Autor:Velardi E; Tsai JJ; Radtke S; Cooper K; Argyropoulos KV; Jae-Hung S; Young LF; Lazrak A; Smith OM; Lieberman S; Kreines F; Shono Y; Wertheimer T; Jenq RR; Hanash AM; Narayan P; Lei Z; Moore MA; Kiem HP; van den Brink MRM; Dudakov JA
[Ad] Address:Department of Immunology, Memorial Sloan Kettering Cancer Center, New York, New York, USA.
[Ti] Title:Suppression of luteinizing hormone enhances HSC recovery after hematopoietic injury.
[So] Source:Nat Med;24(2):239-246, 2018 Feb.
[Is] ISSN:1546-170X
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:There is a substantial unmet clinical need for new strategies to protect the hematopoietic stem cell (HSC) pool and regenerate hematopoiesis after radiation injury from either cancer therapy or accidental exposure. Increasing evidence suggests that sex hormones, beyond their role in promoting sexual dimorphism, regulate HSC self-renewal, differentiation, and proliferation. We and others have previously reported that sex-steroid ablation promotes bone marrow (BM) lymphopoiesis and HSC recovery in aged and immunodepleted mice. Here we found that a luteinizing hormone (LH)-releasing hormone antagonist (LHRH-Ant), currently in wide clinical use for sex-steroid inhibition, promoted hematopoietic recovery and mouse survival when administered 24 h after an otherwise-lethal dose of total-body irradiation (L-TBI). Unexpectedly, this protective effect was independent of sex steroids and instead relied on suppression of LH levels. Human and mouse long-term self-renewing HSCs (LT-HSCs) expressed high levels of the LH/choriogonadotropin receptor (LHCGR) and expanded ex vivo when stimulated with LH. In contrast, the suppression of LH after L-TBI inhibited entry of HSCs into the cell cycle, thus promoting HSC quiescence and protecting the cells from exhaustion. These findings reveal a role of LH in regulating HSC function and offer a new therapeutic approach for hematopoietic regeneration after hematopoietic injury.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1801
[Cu] Class update date: 180210
[Lr] Last revision date:180210
[St] Status:In-Data-Review
[do] DOI:10.1038/nm.4470

  10 / 2583 MEDLINE  
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[PMID]: 29399633
[Au] Autor:Zeng H; Yu M; Tan H; Li Y; Su W; Shi H; Dhungana Y; Guy C; Neale G; Cloer C; Peng J; Wang D; Chi H
[Ad] Address:Department of Immunology, St. Jude Children's Research Hospital, Memphis, TN 38105, USA.
[Ti] Title:Discrete roles and bifurcation of PTEN signaling and mTORC1-mediated anabolic metabolism underlie IL-7-driven B lymphopoiesis.
[So] Source:Sci Adv;4(1):eaar5701, 2018 Jan.
[Is] ISSN:2375-2548
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Interleukin-7 (IL-7) drives early B lymphopoiesis, but the underlying molecular circuits remain poorly understood, especially how Stat5 (signal transducer and activator of transcription 5)-dependent and Stat5-independent pathways contribute to this process. Combining transcriptome and proteome analyses and mouse genetic models, we show that IL-7 promotes anabolic metabolism and biosynthetic programs in pro-B cells. IL-7-mediated activation of mTORC1 (mechanistic target of rapamycin complex 1) supported cell proliferation and metabolism in a Stat5-independent, Myc-dependent manner but was largely dispensable for cell survival or and gene expression. mTORC1 was also required for Myc-driven lymphomagenesis. PI3K (phosphatidylinositol 3-kinase) and mTORC1 had discrete effects on Stat5 signaling and independently controlled B cell development. PI3K was actively suppressed by PTEN (phosphatase and tensin homolog) in pro-B cells to ensure proper IL-7R expression, Stat5 activation, heavy chain rearrangement, and cell survival, suggesting the unexpected bifurcation of the classical PI3K-mTOR signaling. Together, our integrative analyses establish IL-7R-mTORC1-Myc and PTEN-mediated PI3K suppression as discrete signaling axes driving B cell development, with differential effects on IL-7R-Stat5 signaling.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180208
[Lr] Last revision date:180208
[St] Status:In-Data-Review
[do] DOI:10.1126/sciadv.aar5701


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