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Establishment and characterization of immortalized erythroid progenitor cell lines derived from a common cell sourceOpen in a New Window

Recently, attempts have been made to produce large quantities of red blood cells (RBCs) in vitro using cell culture techniques [1-5] Although hematopoietic stem/progenitor cells or pluripotent stem cells have been considered primary candidates for in vitro RBC production, as they possess excellent characteristics for this technology [6-11], we have successfully established immortalized erythroid progenitor cell lines (imERYPCs) that can differentiate into enucleated RBCs [12]. The main advantage of these cell lines is that they can proliferate indefinitely, rapidly produce enucleated RBCs, and can be handled with ease.


Loss of EfnB1 in the osteogenic lineage compromises their capacity to support haematopoietic stem/ progenitor cell maintenanceOpen in a New Window

The haematopoietic stem/ progenitor cell (HSPC) niche is composed of diverse cellular components that contribute to HSPC maintenance and niche function within the bone marrow. These include arterioles, sinusoidal endothelial cells, Nestin+ mesenchymal stem cells, stromal populations including bone marrow stromal stem cells (BMSC)/ perivascular reticular cells and cells of the osteogenic lineage [1–9]. These cells are key mediators of HSC maintenance, proliferation, differentiation and maturation, acting in a non-cell-autonomous manner through membrane dependent or soluble chemokines and growth factors.


Interleukin-18 plays a dispensable role in murine and likely also human bone marrow failureOpen in a New Window

Acquired aplastic anemia (AA) is a bone marrow (BM) failure syndrome characterized by peripheral blood (PB) pancytopenia and BM hypoplasia [1-2]. Success of immunosuppressive therapy (IST), among other clinical and laboratory clues, is compelling evidence of immune pathophysiology of AA [3]. In most cases, AA is an immune-mediated disorder with active destruction of hematopoietic cells by effector T lymphocytes. Increased production of interferon gamma (IFN-γ), tumor necrosis factor-alpha (TNF-α), and interleukin (IL)-2 by patients’ T cells suggests important roles for a type 1 immune response in BM hematopoietic cell destruction [4-6].


TCF4 promotes erythroid developmentOpen in a New Window

Transcription factor 4 (TCF4, ITF2, E2-2), is a basic helix-loop-helix (bHLH) transcription factor that belongs to the family of E-box binding proteins. These proteins recognize CANNTG (Ephrussi-box) DNA sequences, present in a variety of tissue-specific enhancers and promoters. E-proteins are widely expressed and can form both homodimers with other E-proteins or heterodimers with tissue specific bHLH proteins. Dimerization of bHLH transcription factors results in the formation of a four helix bundle, which allows the DNA binding domains to associate with the E-box recognition site, to regulate transcription [1].


Distinct Pathways Affected by Menin versus MLL1/MLL2 in MLL-rearranged Acute Myeloid LeukemiaOpen in a New Window

Patients with chromosomal translocations involving the Mixed Lineage Leukemia 1 gene (MLL, MLL1, KMT2A) represent an exception to overall favorable outcomes for children with acute leukemia [1]. Menin, encoded by the Men1 gene, is a tumor suppressor in neuroendocrine tissues but is essential for MLL1 fusion oncoprotein (MLL-FP)-mediated leukemogenesis. MLL-FP binding to Menin bridges an interaction with Lens Epithelium-Derived Growth Factor (LEDGF), which in turn binds histone H3 dimethyl lysine 36 (H3K36me2) modified chromatin [2,3].


Aptamer-based proteomics of serum and plasma in acquired aplastic anemiaOpen in a New Window

Acquired aplastic anemia (AA), a bone marrow (BM) failure syndrome characterized by pancytopenia and BM hypocellularity, is caused by hematopoietic stem and progenitor cells (HSPCs) destruction by immune cells [1]. BM transplantation remains the first therapeutic choice for young patients with a matched sibling donor. Immunosuppressive therapies (IST), with or without the thrombopoietin (TPO) receptor agonist eltrombopag (EPAG), are considered the standard of care in older patients, and therapeutic option for younger patients without a matched sibling donor [1-2].


Skewed ratio between type 1 and type 2 CALR mutations in Essential Thrombocytosis patients with concomitant JAK2 V617F mutationOpen in a New Window

The classical Philadelphia-negative myeloproliferative neoplasms (MPNs), including polycythemia vera (PV), essential thrombocytosis (ET) and primary myelofibrosis (PMF), are a group of clonal hematopoietic stem cell disorders characterized by the overproduction of terminally differentiated and fully functional hematopoietic cells. Major molecular diagnostic criteria for the MPNs, include presence of somatic mutations in cardinal driver genes; JAK2 V617F or JAK2 exon 12 in PV and JAK2 V617F, CALR exon 9 or MPL exon 10 in ET and PMF [1].


A rare subgroup of leukemia stem cells harbors relapse-inducing potential in acute lymphoblastic leukemiaOpen in a New Window

After initially successful chemotherapy, relapse frequently jeopardizes the outcome of patients with acute leukemia. Because of their adverse characteristics of self-renewal and dormancy, leukemia stem cells have been hypothesized to play a critical role in resistance to antiproliferative chemotherapy and the development of relapse. The high abundance of stem-like cells in acute lymphoblastic leukemia (ALL), however, suggests that not all leukemia-initiating cells carry these adverse characteristics, complicating the biological characterization of relapse-inducing cells in this malignancy.


The Human Cell Atlas bone marrow single-cell interactive web portalOpen in a New Window

The advent of new innovative technologies for single-cell genomics provides nearly limitless opportunities for exploring tissue cellular variation at single-molecule resolution. Single-cell RNA profiling has already revealed hidden heterogeneity within presumed homogenous populations, novel intermediates, and developmental trajectories [1–5]. Although thousands of cells can be readily captured and profiled with these technologies, the cellular composition of in vivo cellular niches are complex, currently requiring selective strategies for isolation such as flow cytometry sorting and a priori defined surface markers to capture and profile sufficient depths of rare cell populations [3,5–8].


Upregulated microRNA-146a expression induced by granulocyte colony-stimulating factor enhanced low-dosage chemotherapy response in aged acute myeloid leukemia patientsOpen in a New Window

Acute myeloid leukemia (AML) is a heterogeneous group of aggressive malignancies characterized by the uncontrolled proliferation of leukemia cells. Among patients with AML younger than 60 years, the complete remission (CR) rate is approximately 60% and the 5-year overall survival (OS) is approximately 40% after intensive chemotherapy and progressive, supportive treatment [1]. Unfortunately, the median age of patients with AML is approximately 65 years [2] and the CR and long-term disease-free survival rates remain low in this population.


Platelet engraftment after allogenic stem cell transplantation is monitoredby digital polymerase chain reaction without interferencebyplatelet supportOpen in a New Window

Leukocyte and platelet counts after transplantation with hematopoietic stem cells (HSCs) serve as an early and relevant sign for the success of transplantation. The time to leukocyte and platelet engraftment appears to be a valid predictor of the probability of complications in transplanted patients, especially for those receiving allogeneic HSC transplantation [1]. The Center for International Blood & Marrow Transplant Research (CIBMTR) and the European Society for Blood and Marrow Transplantation (EBMT) agree in the definition of leukocyte engraftment as the third day of 3 consecutive days with absolute neutrophil counts (ANC) >500/mm3.


miR-217 sensitizes chronic myelogenous leukemia cells to tyrosine kinase inhibitors by targeting pro-oncogenic anterior gradient 2Open in a New Window

Chronic myelogenous leukemia (CML), characterized by the presence of the Philadelphia chromosome (Ph+), is a hematopoietic stem cell malignancy. Translocation of chromosome 9 and chromosome 22 leads to formation of BCR-ABL1 fusion gene, the gene product of which drives and maintains pathogenesis of CML [1,2]. Tyrosine kinase inhibitor (TKI) treatment has improved the outcome of CML patients dramatically since its first application more than a decade ago [3]. However, despite receiving more potent second-generation TKIs such as dasatinib and nilotinib, some patients still experienced resistance and relapse [4,5].


Ponatinib evaluation and safety in real-life chronic myelogenous leukemia patients failing more than two tyrosine kinase inhibitors: The PEARL observational studyOpen in a New Window

Chronic myelogenous leukemia (CML) is induced by the onset of a unique molecular hit, the BCR-ABL oncogene, in a discrete population of hematopoietic stem cells and results in a considerable expansion of the myeloid compartment, compromised apoptotic process, recirculation of progenitors, and genetic instability [1]. This chimeric oncogene is the consequence of a reciprocal translocation the t(9;22)(q34;q11), the Philadelphia (Ph) chromosome [1]. The first tyrosine kinase inhibitor (TKI), imatinib mesylate, was introduced in 1998 and reversed the poor prognosis of this disease, particularly in chronic phase (CP) [2].


Long noncoding RNA HOTAIR promotes the self-renewal of leukemia stem cells through epigenetic silencing of p15Open in a New Window

Acute myeloid leukemia (AML) is characterized by the blockage of differentiation and uncontrolled proliferation. Although conventional chemotherapy and stem cell transplantation markedly improve the overall survival (OS) in AML patients, half of adult patients and more than 80% of older patients (>60 years) die as a result of primary refractoriness, relapse, or treatment-related mortality [1]. Various genetic mutations, such as c-Kit, FLT3, and WT1, lead to the initiation and development of AML [2].


Comparative utility of NRG and NRGS mice for the study of normal hematopoiesis, leukemogenesis, and therapeutic responseOpen in a New Window

Immune-deficient mice have revolutionized biomedical research, including the study of both normal human hematopoiesis and leukemogenesis [1–3]. Capable of harboring both normal and malignant human xenografts without rejection, highly immune-deficient mice are indispensable in hematological research, allowing differentiation and proliferation of these cells in vivo [4]. Xenograft mouse models consistently better predict the success of experimental chemotherapeutics in clinical trials [5], likely because of the complex and dynamic interaction between the bone marrow (BM) microenvironment and heterogeneous populations of leukemic cells [6].


Oral administration of the LSD1 inhibitor ORY-3001 increases fetal hemoglobin in sickle cell mice and baboonsOpen in a New Window

Increased levels of fetal hemoglobin (HbF) lessen the severity of symptoms and increase the life span of patients with sickle cell disease (SCD). More effective strategies to increase HbF are needed because the current standard of care, hydroxyurea, is not effective in a significant proportion of patients. Treatment of the millions of patients projected worldwide would best be accomplished with an orally administered drug therapy that increased HbF. LSD1 is a component of corepressor complexes that repress γ-globin gene expression and are a therapeutic target for HbF reactivation.


Epigenetic modification enhances the cytotoxicity of busulfan and4-hydroperoxycyclophosphamide in AML cellsOpen in a New Window

Busulfan (Bu) is a bifunctional DNA-alkylating agent commonly used in combination with other agents for high-dose pretransplantation conditioning therapy for hematopoietic stem cell transplantation (HSCT) [1]. Its combination with cyclophosphamide (Cy) has been used as an alternative to a Cy plus total body irradiation (Cy+TBI)-containing myeloablative regimen and found to be effective for acute leukemias [2–7]. The “BuCy2” preparative regimen is more effective than Cy+TBI in patients ≤40years old [6,8].


Fluorescent genetic barcoding for cellular multiplex analysesOpen in a New Window

Hematopoiesis depends on the hierarchical production of mature cells from a pool of self-renewing hematopoietic stem cells (HSCs). Due to their high regenerative capacity, great interest focuses on the understanding of HSC biology, which can be best assessed in functional transplantation assays that allow for the read-out of HSC numbers and their potential to produce cells of disparate lineages. To track individual HSC fate decisions, initial transplantation studies employed retroviral gene marking of bulk cells and subsequent Southern blot analyses to assess clonal hematopoietic contributions [1–3].


Philadelphia-Like acute lymphoblastic leukemia: diagnostic dilemma and management perspectivesOpen in a New Window

Acute lymphoblastic leukemia (ALL) is an aggressive hematologic malignancy treated with intensive chemotherapy [1]. In children, ALL therapy was a success story [2]; however, in adults, outcomes remain poor [3]. The poor prognosis of adult ALL is attributed to the accumulation of poor prognostic features, including, but not limited to, the higher frequency of poor-risk genomic subgroups, the lower tolerability to prolonged courses of intensive chemotherapy, and the high therapy-related mortality after hematopoietic cell transplantation (HCT) [4].


WITHDRAWN: Assessment of hematopoietic and neurologic pathophysiology of HCLS1-associated protein X-1 deficiency in a Hax1-knockout mouse modelOpen in a New Window

This article has been withdrawn at the request of the author(s) and/or editor. The Publisher apologizes for any inconvenience this may cause.The full Elsevier Policy on Article Withdrawal can be found at


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