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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].


A Fond Salute to George Stamatoyannopoulos – Scholar Leader Mentor Colleague FriendOpen in a New Window

George Stam, as the world came to know him, slipped away from us on June 16 of this year. This marked over half a century of major achievements that revolutionized our understanding of the science of genetics and hematology. His unique and persistent, typically impatient, approach to make progress was surpassed by none. He will also be remembered for his lifelong leadership and commitment to the pursuit of truth, to the creation of a deeper understanding of how blood cells are normally generated, and the development of better treatments for diseases that arise when this process goes awry.


Up-regulated miR-146a expression induced by G-CSF 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 rate is approximately 60% and the 5-year overall survival 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 complete remission and long-term disease-free survival rates remain low in this population.


Platelet engraftment after allogenic stem cell transplantation is monitored by digital PCR without interference by platelet supportOpen in a New Window

Leucocyte and platelet counts after transplantation with hematopoietic stem cells (HSC) serve as an early and relevant sign for the success of transplantation. The time to leucocyte and platelet engraftment appears to be a valid predictor of the probability of complications in transplanted patients and especially for allogeneic HSC transplantation.1 EBMT and CIBMTR agree in the definition of leucocyte engraftment as the third day of three 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 Philadelphia (Ph+) chromosome is a haematopoietic stem cell malignancy. Translocation of chromosome 9 and chromosome 22 leads to formation of BCR-ABL1 fusion gene, whose gene product drives and maintains pathogenesis of CML [1,2]. Tyrosine kinase inhibitors (TKIs) treatment have improved outcome of CML patients dramatically since its first application more than a decade ago [3]. Although 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].


Crosstalk between BCR-ABL and protease-activated receptor 1 (PAR1) suggests a novel target in chronic myeloid leukemiaOpen in a New Window

Chronic myeloid leukemia (CML) is a myeloproliferative neoplasm characterized by the presence of the Philadelphia chromosome (Ph) and the BCR-ABL1 oncogene [1]. This gene encodes the chimeric BCR-ABL oncoprotein, which has constitutive kinase activity and is responsible for the malignant phenotype of leukemic cells [2,3]. Activation of various signaling pathways by BCR-ABL can lead to the malignant transformation of cells by interfering with basic cellular processes such as cell proliferation, differentiation, adhesion, and survival [4,5].


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].


Germline mutations in the bone marrow microenvironment and dysregulated hematopoiesisOpen in a New Window

The relationship between the hematopoietic stem cell (HSC) population and its surrounding bone marrow microenvironment, which is generally thought of as a collection of functional “niches,” is a rapidly evolving area of research. Gains and losses of function within the microenvironment compartment have been repeatedly linked to leukemic and myelodysplastic conditions affecting adjacent HSCs or more differentiated marrow progenitor cells. In this review, we discuss the interactions between HSCs and the marrow microenvironment in hematopoietic dysfunction and chemotherapy resistance, as well as the therapeutic implications, including targeted agents, HSC transplantation, mesenchymal stem cell (MSC) infusions, and genetic modification, for dysregulated hematopoiesis associated with germline mutations.


Open access? Widening access to chimeric antigen receptor (CAR) therapy for ALLOpen in a New Window

Although standard therapy leads to a long-term event-free survival in childhood acute lymphoblastic leukemia (ALL) approaching 90% [1,2], the outcomes of the 10% that relapse are much poorer, with a predicted long-term survival of 40–50% [3–5]. Within relapsed patients, high-risk groups are identifiable by timing and site of relapse and have a long-term event-free survival of 30% or less even with allogeneic stem cell transplantation (allo-SCT) [3,5,6]. The outcomes of those relapsing following allo-SCT are dismal, with long-term survival of only 10–20% in those undergoing second transplantation procedures [7–9], which are also associated with significant adverse toxicity.


Inverse and correlative relationships between TRIBBLES genes indicate non-redundant functions during normal and malignant hemopoiesisOpen in a New Window

TRIBBLES proteins are pseudokinases that bind and modulate the activity of several signaling molecules, including kinases, phosphatases, transcription factors and components of the ubiquitin proteasome system. From their first identification in mammalian cells, TRIBBLES have been recognized as inducible genes modulated by a wide range of mitogens and stressors and associated with downstream regulation of key signaling pathways, including those of AKT, ATF4, NF-kB, and MAPKs [1–3]. TRIBBLES pseudokinases are involved in different disease pathways and in many cancer types, including solid tumors such as melanoma, liver, and lung cancer [4,5].


Genetic variants of GCH1 associate with chronic and acute crisis pain in African Americans with sickle cell diseaseOpen in a New Window

Sickle cell disease (SCD) affects millions of individuals worldwide, including about 100,000 Americans [1,2]. It is an autosomal-recessive disorder in which a single nucleotide mutation of the beta-globin gene causes the deoxygenated form of hemoglobin to polymerize. This results in rigid, sickle-shaped red blood cells that aggregate and occlude microvasculature. Therefore, blood flow to organs is obstructed, culminating in frequent episodes of severe acute pain, also referred to as acute crisis pain [3,4].


Functional analysis of Fanconi anemia mutations in ChinaOpen in a New Window

Fanconi anemia (FA) is a genetically and phenotypically heterogeneous condition characterized by progressive bone marrow failure (BMF) during childhood, congenital abnormalities, and increased cancer susceptibility. FA is a rare disease with an estimated incidence of one to five in 1,000,000 live births [1,2]. To date, 22 FANC genes have been identified, including 18 well-known bona fide FA genes (FANC-A, B, C, D1, D2, E, F, G, I, J, L, N, P, Q, T, U, V, and W) and four FA-like genes (FANC-M, O, R, and S) [3–9].


Bone marrow eosinophils in plasma cell disordersOpen in a New Window

Experimental data indicate that eosinophils are important for the survival, proliferation, and retention of plasma cells (PCs) in the bone marrow (BM) and they tend to accumulate in the same BM niches [1–3]. Eosinophils might function as antigen-presenting cells (APCs) [4,5] and have been shown to have immunomodulatory properties that could affect tumor growth [6–8]. Recently, Lingblom et al. found a subset of “regulatory eosinophils” with a T-cell-suppressive effect mediated by the protein galectin-10 [9].


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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