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KLF1 Mutation E325K Induces Cell-cycle Arrest in Erythroid Cells Differentiated from Congenital Dyserythropoietic Anemia (CDA) Patient-specific Induced Pluripotent Stem CellsOpen in a New Window

Krüppel-like factor 1 (KLF1), also known as erythroid Krüppel-like factor (EKLF), is a transcription factor controlling erythroid lineage commitment and differentiation. Analysis of KLF1-deficient human neonates showed that KLF1 regulated more than 800 erythroid genes directly or indirectly [1]. KLF1 knockout mice were embryonic lethal due to critical roles of KLF1 in the fate decision and maturation of erythroid cells [2,3]. Erythroid progenitor cells accumulate in the fetal liver of the KLF1 knockout mice, and their cell-cycle defect is attributable to reduced expression of E2F transcription factor 2 (E2F2) [4,5].


Activin A contributes to the definition of a pro-oncogenic bone marrow microenvironment in t(12;21) preleukemiaOpen in a New Window

The t(12;21) is the most frequent chromosomal lesion in pediatric B-cell precursor acute lymphoblastic leukemia (BCP-ALL) [1]. The translocation gives rise to the TEL-AML1 fusion gene, which results in the generation of a persistent preleukemic clone [2]. Because this alteration is insufficient for leukemogenesis, additional secondary postnatal genetic events are necessary for the transition of silent preleukemic cells to overt ALL [3]. Previous epidemiological and experimental studies have demonstrated the impact of infections and inflammation in the definition of an oncogenic environment able to favor TEL-AML1–expressing clones [4].


Difference in megakaryocyte expression of GATA-1, IL-6, and IL-8 associated with maintenance of platelet counts in patients with plasma cell neoplasm with dysmegakaryopoiesisOpen in a New Window

Abnormal proliferation and maturation of megakaryocytes lead to dysmegakaryopoiesis, which subsequently results in the abnormal morphology of megakaryocytes. The mechanism underlying these effects is unknown. Dysmegakaryopoiesis is a key feature in diagnosing myelodysplastic syndrome (MDS), which is accompanied by peripheral thrombocytopenia. Moreover, dysmegakaryopoiesis is associated with plasma cell neoplasm (PCN), which is not accompanied by thrombocytopenia [1].


DNA damage response-related alterations define the genetic background of patients with chronic lymphocytic leukemia and chromosomal gainsOpen in a New Window

The presence of chromosomal gains other than trisomy 12 suggesting a hyperdiploid karyotype is extremely rare in chronic lymphocytic leukemia (CLL) and is associated with a dismal prognosis. However, the genetic mechanisms and mutational background of these patients have not been fully explored. To improve our understanding of the genetic underpinnings of this subgroup of CLL, seven CLL patients with several chromosomal gains were sequenced using a next-generation sequencing (NGS)-targeted approach.


ATP produced by anaerobic glycolysis is essential for enucleation of human erythroblastsOpen in a New Window

Mammalian erythropoiesis culminates in enucleation, a still partially understood process that entails the expulsion of the nucleus from the cytoplasm of erythroblasts. During erythropoiesis, stem cells undergo lineage-specific commitment and generate erythroid progenitor cells through cellular division events, which include nuclear (mitosis) and cytoplasmic (cytokinesis) components. These progenitor cells consist of burst-forming units–erythroid (BFU-Es) and their progeny, colony-forming units–erythroid (CFU-Es) [1,2].


Vorinostat synergizes with antioxidant therapy to target myeloproliferative neoplasmsOpen in a New Window

BCR-ABL-negative myeloproliferative neoplasms (MPNs) are driven by JAK-STAT pathway activation, but epigenetic alterations also play an important pathophysiological role. These can be pharmacologically manipulated with histone deacetylase inhibitors (HDACIs), which have proven to be clinically effective in the treatment of MPNs but exhibit dose-limiting toxicity. The treatment of primary MPN cells with vorinostat modulates the expression of genes associated with apoptosis, cell cycle, inflammation, and signaling.


Alternative translation initiation generates the N-terminal truncated form of RUNX1 that retains hematopoietic activityOpen in a New Window

The mammalian Runx transcription factors RUNX1, RUNX2, and RUNX3 are key regulators of lineage-specific gene expression in diverse developmental processes [1,2]. The RUNX proteins contain a conserved 128-amino acid Runt domain responsible for sequence-specific DNA binding. The Runt domain is also required to form a heterodimeric complex with a partner protein, CBFB. RUNX1 is a master regulator of hematopoiesis, and disruption of RUNX1 function either through mutations or generation of fusion genes leads to the development of hematopoietic diseases [3–6].


Erratum to “Engineered humanized bone organs maintain human hematopoiesis in vivo”Open in a New Window

The publisher regrets that one of the authors, Sébastien Pigeot (2nd author), was not acknowledged as a co-first author. The publisher would like to apologize for any inconvenience caused.


Sphingosine-1-phosphate signaling modulates terminal erythroid differentiation through the regulation of mitophagyOpen in a New Window

Erythropoiesis, the process of differentiation from hematopoietic/stem progenitor cells (HSPCs) to mature red blood cells (RBCs), is responsible for the daily production of ∼2 × 1011 RBCs to maintain homeostatic oxygen supply to various tissues [1,2]. Adult erythropoiesis occurs in the bone marrow (BM) via three stages: early erythropoiesis, terminal erythroid differentiation, and reticulocyte maturation [1,3]. Early erythropoiesis involves the differentiation of HSPCs into megakaryocyte–erythroid progenitors (MEPs), followed by burst-forming unit-erythroid cells, colony-forming unit-erythroid (CFU-E) cells and finally pro-erythroblasts [4].


USP44 is dispensable for normal hematopoietic stem cell function, lymphocyte development, and B-cell-mediated immune response in a mouse modelOpen in a New Window

Most cells of our blood and immune system are produced from hematopoietic stem cells (HSCs) in the bone marrow through the process of cell proliferation and differentiation, which is known as hematopoiesis. Immune response against infection or immunization involves multiple further cell proliferation, differentiation, and activation checkpoints. Dysregulation in the molecular mechanisms controlling cell cycle progression, gene expression, and genomic stability in hematopoietic and immune cells is commonly linked to bone marrow failure, immunodeficiency, and cancer.


Compounds targeting class II histone deacetylases do not cause panHDACI-associated impairment of megakaryocyte differentiationOpen in a New Window

The first generation of histone deacetylase inhibitors (HDACIs) has shown significant efficacy in the inhibition of cancer cell proliferation both in in vitro and in xenograft in vivo models. These inhibitors are generally broad acting (pan), inhibiting a number of histone deacetylases (HDACs) with increasing class preference depending on the concentration. Currently, four panHDACIs—suberoyl anilide hydroxamic acid (SAHA), panobinostat, romidepsin, and belinostat—have been approved by the Food and Drug Administration as epigenetic therapies, mainly for the treatment of T-cell lymphomas and multiple myelomas.


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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