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Journal articles on the topic 'Biphenotypic progenitors'

Author: Grafiati

Published: 24 May 2025

Last updated: 31 July 2025

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1

Anderson, Kristina, Corinne Rusterholz, Robert Månsson, et al. "Ectopic expression of PAX5 promotes maintenance of biphenotypic myeloid progenitors coexpressing myeloid and B-cell lineage-associated genes." Blood 109, no. 9 (2007): 3697–705. http://dx.doi.org/10.1182/blood-2006-05-026021.

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Abstract The transcription factor PAX5 is a critical regulator of B-cell commitment and development. Although normally not expressed in myeloid progenitors, PAX5 has recently been shown to be frequently expressed in myeloid malignancies and to suppress expression of myeloid differentiation genes, compatible with an effect on the differentiation or maintenance of myeloid progenitors. However, previous studies in which PAX5 was ectopically expressed in normal myeloid progenitors in vivo and in vitro provided conflicting results as to the effect of PAX5 on myeloid development. Herein, we demonstr

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2

Sanada, Chad, Juliana Xavier-Ferrucio, Yi-Chien Lu, et al. "Adult human megakaryocyte-erythroid progenitors are in the CD34+CD38mid fraction." Blood 128, no. 7 (2016): 923–33. http://dx.doi.org/10.1182/blood-2016-01-693705.

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3

Simmons, Szandor, Marko Knoll, Christopher Drewell, et al. "Biphenotypic B-lymphoid/myeloid cells expressing low levels of Pax5: potential targets of BAL development." Blood 120, no. 18 (2012): 3688–98. http://dx.doi.org/10.1182/blood-2012-03-414821.

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Abstract The expression of Pax5 commits common lymphoid progenitor cells to B-lymphoid lineage differentiation. Little is known of possible variations in the levels of Pax5 expression and their influences on hematopoietic development. We have developed a retroviral transduction system that allows for the study of possible intermediate stages of this commitment by controlling the levels of Pax5 expressed in Pax5-deficient progenitors in vitro and in vivo. Retroviral transduction of Pax5-deficient pro-/pre-B cell lines with a doxycycline-inducible (TetON) form of the human Pax5 (huPax5) gene yie

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4

Chabannon, C., P. Wood, and B. Torok-Storb. "Expression of CD7 on normal human myeloid progenitors." Journal of Immunology 149, no. 6 (1992): 2110–13. http://dx.doi.org/10.4049/jimmunol.149.6.2110.

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Abstract Existence of biphenotypic leukemias co-expressing CD7 and CD34 has prompted the question of whether a similar population of cells is present in normal human bone marrow. As CD7 is considered to be a T cell-restricted Ag, the co-expression of CD7 with the "human stem cell Ag" CD34 may identify a bipotent stage within hemopoietic differentiation. Cells with this phenotype have previously been isolated from human thymus. In this report we provide evidence that human marrow mononuclear cells also contain a minor subpopulation of cells co-expressing CD7 and CD34. The CD7+/CD34+ cells were

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5

Chou, Stella T., Joanna B. Opalinska, Yu Yao, et al. "Trisomy 21 enhances human fetal erythro-megakaryocytic development." Blood 112, no. 12 (2008): 4503–6. http://dx.doi.org/10.1182/blood-2008-05-157859.

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Abstract Children with Down syndrome exhibit 2 related hematopoietic diseases: transient myeloproliferative disorder (TMD) and acute megakaryoblastic leukemia (AMKL). Both exhibit clonal expansion of blasts with biphenotypic erythroid and megakaryocytic features and contain somatic GATA1 mutations. While altered GATA1 inhibits erythro-megakaryocytic development, less is known about how trisomy 21 impacts blood formation, particularly in the human fetus where TMD and AMKL originate. We used in vitro and mouse transplantation assays to study hematopoiesis in trisomy 21 fetal livers with normal G

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6

Birg, F., M. Courcoul, O. Rosnet, et al. "Expression of the FMS/KIT-like gene FLT3 in human acute leukemias of the myeloid and lymphoid lineages." Blood 80, no. 10 (1992): 2584–93. http://dx.doi.org/10.1182/blood.v80.10.2584.2584.

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Abstract FLT3, a receptor belonging to the FMS/KIT family and localized to 13q12, could play a role in the biology of early hematopoietic progenitor cells. Because FMS and KIT are expressed in both normal progenitors and myeloid leukemias, we looked for FLT3 expression in fresh human leukemic cells using Northern blot analysis. High levels of FLT3 expression were detected in 92% of the cases of acute myeloid leukemia (AML) tested, ranging from the M1 to the M5 stages of differentiation assessed in the French-American-British classification. Immature (MO) AML cells, biphenotypic leukemias, and

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7

Birg, F., M. Courcoul, O. Rosnet, et al. "Expression of the FMS/KIT-like gene FLT3 in human acute leukemias of the myeloid and lymphoid lineages." Blood 80, no. 10 (1992): 2584–93. http://dx.doi.org/10.1182/blood.v80.10.2584.bloodjournal80102584.

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FLT3, a receptor belonging to the FMS/KIT family and localized to 13q12, could play a role in the biology of early hematopoietic progenitor cells. Because FMS and KIT are expressed in both normal progenitors and myeloid leukemias, we looked for FLT3 expression in fresh human leukemic cells using Northern blot analysis. High levels of FLT3 expression were detected in 92% of the cases of acute myeloid leukemia (AML) tested, ranging from the M1 to the M5 stages of differentiation assessed in the French-American-British classification. Immature (MO) AML cells, biphenotypic leukemias, and AML with

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8

Dinndorf, PA, and GH Reaman. "Acute lymphoblastic leukemia in infants: evidence for B cell origin of disease by use of monoclonal antibody phenotyping." Blood 68, no. 4 (1986): 975–78. http://dx.doi.org/10.1182/blood.v68.4.975.975.

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Abstract Since the prognosis of infants with acute lymphoblastic leukemia (ALL) is so poor, it has been suggested that these leukemias may not be lymphoid in origin, but may originate from stem cell, myeloid, or megakaryocytic progenitors. Alternately it has been hypothesized that these leukemias originate in lymphoid cells at the earliest stages of B cell development. Another possibility is that these leukemias may be of more than one lineage. Therefore we examined leukemic blasts from 12 infants with ALL using monoclonal antibodies to myeloid and lymphoid differentiation antigens. The majori

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9

Dinndorf, PA, and GH Reaman. "Acute lymphoblastic leukemia in infants: evidence for B cell origin of disease by use of monoclonal antibody phenotyping." Blood 68, no. 4 (1986): 975–78. http://dx.doi.org/10.1182/blood.v68.4.975.bloodjournal684975.

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Since the prognosis of infants with acute lymphoblastic leukemia (ALL) is so poor, it has been suggested that these leukemias may not be lymphoid in origin, but may originate from stem cell, myeloid, or megakaryocytic progenitors. Alternately it has been hypothesized that these leukemias originate in lymphoid cells at the earliest stages of B cell development. Another possibility is that these leukemias may be of more than one lineage. Therefore we examined leukemic blasts from 12 infants with ALL using monoclonal antibodies to myeloid and lymphoid differentiation antigens. The majority of spe

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10

Sanada, Chad D., Ping-Xia Zhang, Gazelle Zerafati, and Diane S. Krause. "Optimization of a Clonal Assay for Bipotent Megakaryocyte-Erythroid Progenitors (MEP), and Their Enrichment From Mobilized Peripheral Blood." Blood 120, no. 21 (2012): 2310. http://dx.doi.org/10.1182/blood.v120.21.2310.2310.

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Abstract Abstract 2310 Megakaryocyte/Erythroid Progenitor (MEP) cells are bipotent hematopoietic progenitors that undergo a fate decision to commit to either Megakaryocyte (Mk) or Erythroid (E) lineage. How this biphenotypic fate decision is made is not clearly understood. In order to elucidate the epigenetic changes underlying the MEP fate decision in human cells, one must first have a robust approach for purifying the starting population of MEP. Published enrichment strategies for human MEP are suboptimal as they also enrich committed erythroid progenitors, and assays aimed at identifying ME

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11

Ugale, Amol Sanjay, Sofia Adolfsson, Petter Säwén, Monika Dudenhöffer-Pfeifer, and David Bryder. "Probing Co-Operating Somatic Mutations in MLL-ENL Driven Leukemogenesis." Blood 128, no. 22 (2016): 2855. http://dx.doi.org/10.1182/blood.v128.22.2855.2855.

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Abstract Missense mutations and other chromosomal perturbations underlie the heterogeneity of acute leukemia. While Mixed lineage leukemia-1 (MLL1/KMT2A) translocations are recurrent in human acute leukemia, most if not all MLL fusions are permissive for either acute myeloid (AML), acute lymphoid (ALL) or mixed/biphenotypic leukemia (MLL). At the same time, previous work have suggested that MLL rearranged leukemias require few additional mutations to induce transformation(1, 2). The MLL-ENL translocation is apart from being associated with AML also found in human acute T cell leukemia (T-ALL).

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12

Petropoulos, Konstantin, Christina Schessl, Natalia Arseni, et al. "Constitutive Expression of Lef-1 in Murine Hematopoietic Progenitors Causes Myeloid and Lymphoid Leukemias Propagated by a Leukemic Stem Cell Population with Lymphoid Characteristics." Blood 110, no. 11 (2007): 2645. http://dx.doi.org/10.1182/blood.v110.11.2645.2645.

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Abstract Canonical Wnt signaling is critically involved in normal hematopoietic development and the self-renewal process of hematopoietic stem cells. Deregulation of this pathway has been linked to a large variety of cancers including leukemia. Lef-1, a key factor of the Wnt / beta-catenin signaling pathway, plays pivotal roles in lymphoid development, but little is known about the role of Lef-1 in myeloid hematopoiesis and leukemogenesis. We now show that Lef-1 is expressed in murine hematopoietic stem cells (‘LSK’, Sca+cKit+Lin−) and both myeloid and lymphoid subpopulations as well as in dif

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13

Wei, Junping, Wunderlich Mark, Catherine Fox, Jorge F. DiMartino, and James C. Mulloy. "Environmental Factors Determine Lineage Fate in a Human Model of MLL-AF9 Leukemia." Blood 110, no. 11 (2007): 3374. http://dx.doi.org/10.1182/blood.v110.11.3374.3374.

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Abstract The MLL gene is fused to over 30 different fusion partners by reciprocal translocations in human acute leukemias. Some fusion partners are associated almost exclusively with myeloid or lymphoid leukemias while others are found in both. The degree to which the fusion partner contributes to the lineage of the resulting leukemia remains a matter of controversy. Using a novel model system, we demonstrate that myeloid vs lymphoid differentiation of hematopoietic progenitors transformed by MLL-AF9 can be predictably driven by cytokine combinations in vitro and in vivo. The t(9;11)(p22;q23)

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14

Sanada, Chad D., Elizabeth Min, Siying Zou, et al. "Single Cell Transcriptome Profiling of Highly Purified Human Megakaryocyte-Erythroid Progenitors (MEP) Reveals New Insights into the MEP Fate Decision." Blood 124, no. 21 (2014): 2903. http://dx.doi.org/10.1182/blood.v124.21.2903.2903.

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Abstract Megakaryocyte-Erythroid Progenitors (MEPs) are bipotent cells capable of generating megakaryocytic (Mk) or erythroid (E) progeny. However, neither the cell fate-determining componentry nor the initial molecular consequences of lineage specification have been defined. To elucidate this, it is critical to rigorously purify MEP from primary cell sources. Unfortunately, existing purification strategies to do this fail to yield pure, bipotent cells. To improve upon existing approaches for the enrichment of primary human MEPs from G-CSF mobilized peripheral blood (MPB) and BM, we used the c

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15

Strehl, Sabine, Karin Nebral, Margit König, et al. "A Novel Fusion between ETV6 and NCOA2 Defines a New Entity of Acute Leukemia with Co-Expression of T-Cell and Myeloid Markers." Blood 108, no. 11 (2006): 804. http://dx.doi.org/10.1182/blood.v108.11.804.804.

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Abstract We have identified a novel recurrent translocation and the genes involved therein, which is associated with both lymphoid and myeloid acute leukemia. Fluorescence in situ hybridization (FISH) and molecular analyses revealed an in-frame fusion of ETV6 (alias TEL) and NCOA2 (alias TIF2) in six cases of childhood acute leukemia. ETV6 encodes an ets transcription repressor and is frequently involved in chromosome rearrangements with a multitude of partners in lymphoid and myeloid leukemia, and to a lesser extent also in solid tumors. NCOA2 is a member of the p160 family of nuclear recepto

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16

King-Underwood, L., and K. Pritchard-Jones. "Wilms' Tumor (WT1) Gene Mutations Occur Mainly in Acute Myeloid Leukemia and May Confer Drug Resistance." Blood 91, no. 8 (1998): 2961–68. http://dx.doi.org/10.1182/blood.v91.8.2961.2961_2961_2968.

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In a previous study of acute leukemia, we have shown thatWT1 gene mutations occur in both myeloid and biphenotypic subtypes, where they are associated with refractoriness to standard induction chemotherapy. We have now extended this study to a total of 67 cases (34 acute myeloid leukemia [AML], 23 acute lymphoblastic leukemia [ALL], 10 acute undifferentiated leukemia [AUL]/biphenotypic) and find that WT1 mutations occur in 14% of AML and 20% of biphenotypic leukemia, but are rare in ALL (one case). In contrast to the findings in Wilms' tumor, where mutations in the WT1 gene usually behave acco

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17

Delaney, Colleen, Filippo Milano, Ian Nicoud, et al. "Dose Dependent Enhancement Of Neutrophil Recovery By Infusion Of Notch Ligand Ex Vivo Expanded Cord Blood Progenitors: Results Of a Multi-Center Phase I Trial." Blood 122, no. 21 (2013): 297. http://dx.doi.org/10.1182/blood.v122.21.297.297.

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Abstract Introduction There is a strong clinical need to overcome the increased early non relapse mortality (NRM) associated with delayed neutrophil recovery following cord blood transplant (CBT). Therefore we established a methodology using Notch ligand (Delta1) as a strategy for increasing the absolute number of marrow repopulating CB hematopoietic stem/progenitor cells (HSPC). We previously reported preliminary results of the first 10 patients in 2010 demonstrating the ability of Notch-expanded CB HSPC to provide rapid myeloid recovery post-CBT.1 Herein we present the updated results on 23

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18

Theodossiou, Chris, Angela Scalise, Kevin Troy, Lewis Silverman, Eva Perdahl-Wallace, and Vesna Najfeld. "del(5q) in acute lymphoblastic leukemia with biphenotypic and early progenitor phenotype." Cancer Genetics and Cytogenetics 63, no. 2 (1992): 89–94. http://dx.doi.org/10.1016/0165-4608(92)90385-l.

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19

Prebet, Thomas, Anne Catherine Lhoumeau, Christine Arnoulet, et al. "Expression of the Cell Polarity Protein PTK7 in Acute Myeloid Leukaemia." Blood 112, no. 11 (2008): 1478. http://dx.doi.org/10.1182/blood.v112.11.1478.1478.

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Abstract The planar cell polarity pathway plays a major role in embryogenesis and tissue organisation. Recent genetic studies have highlighted the role of novel receptors and signaling molecules implicated in this pathway. Amongst the receptors, the pseudo tyrosine kinase receptor 7 (PTK7) is an orphean tyrosine kinase receptor with kinase-dead activity. Knock-out of PTK7 in mice strongly affects embryonic development leading to a major neural tube defect. Presence of PTK7 was previously investigated in epithelial and endothelial cells that both express the receptor. In normal donors, we found

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20

Dastugue, N., E. Kuhlein, E. Duchayne, et al. "t(14;14)(q11;q32) in biphenotypic blastic phase of chronic myeloid leukemia." Blood 68, no. 4 (1986): 949–53. http://dx.doi.org/10.1182/blood.v68.4.949.bloodjournal684949.

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A blastic crisis of chronic myeloid leukemia without a detectable chronic phase is reported. At diagnosis, blast cells present t(9;22)(q34;q11),t(14;14)(q11;q32) translocations and early B cell phenotype (DR +, TdT +, B4 +, BA1 +, J5 +). At relapse, the malignant clone evolves to a biphenotypic expression, the initial markers remain unchanged, and two myeloid antigens (My 7, My 9) appear. The wide overlap in percentages of blast cells displaying lymphoid and myeloid markers shows that a single clone bears antigens of both lineages. Simultaneous occurrence of a t(14;14)(q11;q32) translocation,

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21

Rubnitz, Jeffrey E., Mihaela Onciu, Stanley Pounds, et al. "Acute mixed lineage leukemia in children: the experience of St Jude Children's Research Hospital." Blood 113, no. 21 (2009): 5083–89. http://dx.doi.org/10.1182/blood-2008-10-187351.

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Abstract To characterize the biology and optimal therapy of acute mixed-lineage leukemia in children, we reviewed the pathologic and clinical features, including response to therapy, of 35 patients with mixed-lineage leukemia. The majority of cases (91%) had blasts cells that simultaneously expressed either T-lineage plus myeloid markers (T/myeloid, n = 20) or B-lineage plus myeloid markers (B/myeloid, n = 12). Overall survival rates for the B/myeloid and T/myeloid subgroups were not significantly different from each other or from the rate for acute myeloid leukemia (AML) but were inferior to

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22

Dastugue, N., E. Kuhlein, E. Duchayne, et al. "t(14;14)(q11;q32) in biphenotypic blastic phase of chronic myeloid leukemia." Blood 68, no. 4 (1986): 949–53. http://dx.doi.org/10.1182/blood.v68.4.949.949.

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Abstract A blastic crisis of chronic myeloid leukemia without a detectable chronic phase is reported. At diagnosis, blast cells present t(9;22)(q34;q11),t(14;14)(q11;q32) translocations and early B cell phenotype (DR +, TdT +, B4 +, BA1 +, J5 +). At relapse, the malignant clone evolves to a biphenotypic expression, the initial markers remain unchanged, and two myeloid antigens (My 7, My 9) appear. The wide overlap in percentages of blast cells displaying lymphoid and myeloid markers shows that a single clone bears antigens of both lineages. Simultaneous occurrence of a t(14;14)(q11;q32) transl

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23

Minacapelli, Carlos D., Manisha Bajpai, Xin Geng, et al. "Barrett’s metaplasia develops from cellular reprograming of esophageal squamous epithelium due to gastroesophageal reflux." American Journal of Physiology-Gastrointestinal and Liver Physiology 312, no. 6 (2017): G615—G622. http://dx.doi.org/10.1152/ajpgi.00268.2016.

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Gastroesophageal reflux disease (GERD) clinically predisposes to columnar Barrett’s metaplasia (BM) in the distal esophagus. We demonstrate evidence supporting the cellular origin of BM from reprograming or transcommitment of resident normal esophageal squamous (NES) epithelial cells in response to acid and bile (A + B) exposure using an in vitro cell culture model. The hTERT-immortalized NES cell line NES-B10T was exposed 5 min/day to an A + B mixture for 30 wk. Morphological changes, mRNA, and protein expression levels for the inflammatory marker cyclooxygenase-2; the lineage-determining tra

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24

Pavlova, T. Yu, and T. T. Valiev. "Diagnostic and therapeutic approaches for lymphoblastic lymphomas from progenitor cells in children and adolescents." Oncohematology 18, no. 4 (2023): 135–44. http://dx.doi.org/10.17650/1818-8346-2023-18-4-135-144.

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Lymphoblastic lymphomas (LBL) are the second most common subtype of non-Hodgkin’s lymphomas in children and adolescents, accounting for 25–35 % of all non-Hodgkin’s lymphomas cases. The majority of all lymphoblastic lymphomas (80–85 %) are T-lymphoblastic origin; 15–20 % origins from B-cell precursors, biphenotypic LBL are extremely rare. Currently, the overall and relapse-free survival of children and adolescents with LBL exceeds 80 %, uses of modern therapy programs. However, the survival rates of patients with recurrent or refractory LBL remain low – 10 %. Optimization of therapeutic approa

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25

Saltman, DL, JA Ross, RE Banks, FM Ross, AM Ford, and MJ Mackie. "Molecular evidence for a single clonal origin in biphenotypic concomitant chronic lymphocytic leukemia and multiple myeloma." Blood 74, no. 6 (1989): 2062–65. http://dx.doi.org/10.1182/blood.v74.6.2062.bloodjournal7462062.

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To establish the clonal origin of a case of concomitant B-cell chronic lymphocytic leukemia (IgM kappa) and multiple myeloma (IGA lambda), we analyzed the immunoglobulin (Ig) gene rearrangements in the patient's blood and bone marrow. Despite the different isotypes, pretreatment investigation of the heavy chain gene (JH) revealed a germline fragment and two identical rearrangements in the blood and marrow. Both kappa and lambda light-chain genes were rearranged in the blood, suggesting peripheral blood lymphocyte involvement in the myeloma. Analysis of the Ig genes after chemotherapy demonstra

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26

Saltman, DL, JA Ross, RE Banks, FM Ross, AM Ford, and MJ Mackie. "Molecular evidence for a single clonal origin in biphenotypic concomitant chronic lymphocytic leukemia and multiple myeloma." Blood 74, no. 6 (1989): 2062–65. http://dx.doi.org/10.1182/blood.v74.6.2062.2062.

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Abstract To establish the clonal origin of a case of concomitant B-cell chronic lymphocytic leukemia (IgM kappa) and multiple myeloma (IGA lambda), we analyzed the immunoglobulin (Ig) gene rearrangements in the patient's blood and bone marrow. Despite the different isotypes, pretreatment investigation of the heavy chain gene (JH) revealed a germline fragment and two identical rearrangements in the blood and marrow. Both kappa and lambda light-chain genes were rearranged in the blood, suggesting peripheral blood lymphocyte involvement in the myeloma. Analysis of the Ig genes after chemotherapy

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27

Morgan, GJ, F. Cotter, FE Katz, et al. "Breakpoints at 11q23 in infant leukemias with the t(11;19)(q23;p13) are clustered." Blood 80, no. 9 (1992): 2172–75. http://dx.doi.org/10.1182/blood.v80.9.2172.2172.

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Abstract We have analyzed a series of nine infant leukemias that carry a t(11;19)(q23;p13). They had the morphologic features of acute lymphoblastic leukemia (ALL) and expressed markers typical of B-cell progenitor ALL or pre-B ALL; one coexpressed myeloid markers in addition to lymphoid markers (biphenotypic). Two probes (P/S4 and 98.40) subcloned from a yeast artificial chromosome (YAC) known to span the breakpoint in the t(4;11) were used to investigate DNA isolated from the leukemic cells of these patients. A total of approximately 15 kb of genomic DNA in the vicinity of the probes was exa

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28

Morgan, GJ, F. Cotter, FE Katz, et al. "Breakpoints at 11q23 in infant leukemias with the t(11;19)(q23;p13) are clustered." Blood 80, no. 9 (1992): 2172–75. http://dx.doi.org/10.1182/blood.v80.9.2172.bloodjournal8092172.

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We have analyzed a series of nine infant leukemias that carry a t(11;19)(q23;p13). They had the morphologic features of acute lymphoblastic leukemia (ALL) and expressed markers typical of B-cell progenitor ALL or pre-B ALL; one coexpressed myeloid markers in addition to lymphoid markers (biphenotypic). Two probes (P/S4 and 98.40) subcloned from a yeast artificial chromosome (YAC) known to span the breakpoint in the t(4;11) were used to investigate DNA isolated from the leukemic cells of these patients. A total of approximately 15 kb of genomic DNA in the vicinity of the probes was examined by

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29

Lee, Po-Shing, Ching-Nan Lin, Chientzu Liu, Chien-Tai Huang, and Wei-Shiou Hwang. "Acute Leukemia With Myeloid, B-, and Natural Killer Cell Differentiation." Archives of Pathology & Laboratory Medicine 127, no. 2 (2003): e93-e95. http://dx.doi.org/10.5858/2003-127-e93-alwman.

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Abstract Biphenotypic acute leukemias account for 4% to 8% of all acute leukemias. Most of these leukemias are of myeloid–B-cell or myeloid–T-cell lineage. Acute myeloid–natural killer cell leukemia has been recognized recently. We report the first case, to our knowledge, of CD56+ acute leukemia showing unequivocal myeloid and B-cell differentiation in a 20-year-old woman, whose blast cells were positive for myeloperoxidase, CD13, CD33, CD117, terminal deoxynucleotidyl transferase, CD19, CD20, CD22, CD34, HLA-DR, and CD56 but negative for CD3, CD5, CD7, and CD10. Rare Auer rods were identified

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30

Calvo, Katherine R., David B. Sykes, Martina Pasillas, and Mark P. Kamps. "Hoxa9 Immortalizes a Granulocyte-Macrophage Colony-Stimulating Factor-Dependent Promyelocyte Capable of Biphenotypic Differentiation to Neutrophils or Macrophages, Independent of Enforced Meis Expression." Molecular and Cellular Biology 20, no. 9 (2000): 3274–85. http://dx.doi.org/10.1128/mcb.20.9.3274-3285.2000.

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ABSTRACT The genes encoding Hoxa9 and Meis1 are transcriptionally coactivated in a subset of acute myeloid leukemia (AML) in mice. In marrow reconstitution experiments, coexpression of both genes produces rapid AML, while neither gene alone generates overt leukemia. Although Hoxa9 and Meis1 can bind DNA as heterodimers, both can also heterodimerize with Pbx proteins. Thus, while their coactivation may result from the necessity to bind promoters as heterodimers, it may also result from the necessity of altering independent biochemical pathways that cooperate to generate AML, either as monomers

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31

Zhang, Yanming, Wu Depei, Aining Sun, et al. "Clinical, Biological Profile and Outcome of Biphenotypic Acute Leukemia: a Case Series." Blood 116, no. 21 (2010): 1683. http://dx.doi.org/10.1182/blood.v116.21.1683.1683.

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Abstract Abstract 1683 Biphenotypic acute leukemia (BAL) is a very rare type of acute leukemia, which presents a high heterogeneity and poor prognosis. We identified 51 cases (3.0%) BAL from 1693 newly diagnosed acute leukemia patients according to the EGIL scoring system between January 2003 and July 2009. The biological features, treatment and outcome of 39 evaluable BAL patients were analyzed retrospectively. There were 23 (59.0%) cases of myeloid and B-lymphoid (M/B) phenotype, 14 (35.9%) cases of myeloid and T-lymphoid (M/T) phenotype, one case (2.6%) of trilineage phenotype or B-lymphoid

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32

Pereira-Martins, Diego A., Vincent Van Den Boom, Isabel Weinhaeuser, et al. "The Oncogenic Function of the Intrinsically Disordered Transcriptional Regulator MN1 Depends on the Chaperone DNAJB6b." Blood 144, Supplement 1 (2024): 4321. https://doi.org/10.1182/blood-2024-207421.

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Meningioma 1 (MN1) overexpression (OE) is associated with the progression from myelodysplastic syndrome to acute myeloid leukemia (AML) and correlates with poor survival in AML patients. In murine models, MN1-OE in common myeloid progenitors has been shown to drive AML transformation. Molecularly, MN1-induced inhibition of myeloid differentiation is linked to the over-stabilization of the BAF complex at binding sites of transcription factors involved in hematopoietic differentiation. However, the exact mechanisms through which MN1 promotes AML development remain unclear. We performed single-ce

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33

Guilhot, Francois, Francoise Rigal-Huguet, Joelle Guilhot та ін. "Long Term Outcome of Chronic Phase Chronic Myeloid Leukemia (CP CML) Patients (pts) from the French Spirit Study Comparing Imatinib (IM) 400 Mg to Higher Dose Imatinib or Combination with Peg-interferonα2a (PegIFN) or Cytarabine (Ara-C) : A Trial of the FI LMC (France intergroupe de la leucemie myéloïde chronique)". Blood 124, № 21 (2014): 1793. http://dx.doi.org/10.1182/blood.v124.21.1793.1793.

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Abstract Although they produce high rate of molecular response second generation tyrosine kinase inhibitors or imatinib cannot eradicate CML primitive progenitors. Interferon has been shown to modulate gene expression, inhibits leukemic cell growth and induces an immunomodulatory response. In vitro studies support the use of combination of IM plus interferon. We designed a phase III randomised multicenter open-label prospective trial comparing IM 400 mg/d (n=223) with 3 experimental arms: IM 600 mg/d (n=171), IM 400 mg/d combined to s/c Peg-IFN2a (90 µg/wk) (n=221) and IM 400 mg/d combined to

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Lange, B., M. Valtieri, D. Santoli, et al. "Growth factor requirements of childhood acute leukemia: establishment of GM-CSF-dependent cell lines." Blood 70, no. 1 (1987): 192–99. http://dx.doi.org/10.1182/blood.v70.1.192.192.

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Abstract Eight permanent cell lines were established from cells of 50 consecutive patients with childhood acute leukemia. Three cell lines required growth factor-containing conditioned media. Analysis using blocking antisera and recombinant granulocytic macrophage (GM) colony- stimulating factor (CSF) identified GM-CSF as a growth factor required to establish the latter three cell lines and necessary for their continuous proliferation in chemically defined medium. Two of the GM- CSF-dependent cell lines were derived from patients with undifferentiated T- and a biphenotypic B-myelomonocytic leu

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Lange, B., M. Valtieri, D. Santoli, et al. "Growth factor requirements of childhood acute leukemia: establishment of GM-CSF-dependent cell lines." Blood 70, no. 1 (1987): 192–99. http://dx.doi.org/10.1182/blood.v70.1.192.bloodjournal701192.

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Eight permanent cell lines were established from cells of 50 consecutive patients with childhood acute leukemia. Three cell lines required growth factor-containing conditioned media. Analysis using blocking antisera and recombinant granulocytic macrophage (GM) colony- stimulating factor (CSF) identified GM-CSF as a growth factor required to establish the latter three cell lines and necessary for their continuous proliferation in chemically defined medium. Two of the GM- CSF-dependent cell lines were derived from patients with undifferentiated T- and a biphenotypic B-myelomonocytic leukemia, wh

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Weinberg, Olga K. "How to think about acute leukemia of ambiguous lineage." Hematology 2024, no. 1 (2024): 287–92. https://doi.org/10.1182/hematology.2024000554.

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Abstract Classification of acute leukemia involves assigning lineage by resemblance of blasts to normal progenitor cells. This approach provides descriptive information that is useful for disease monitoring, provides clues to pathogenesis, and can help to select effective chemotherapeutic regimens. Acute leukemias of ambiguous lineage (ALAL) are those leukemias that either fail to show evidence of myeloid, B-lymphoid, or T-lymphoid lineage commitment or show evidence of commitment to more than 1 lineage, including mixed-phenotype acute leukemia (MPAL). The different treatment regimens for acut

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Gough, Sheryl M., Christopher I. Slape, and Peter D. Aplan. "NUP98 gene fusions and hematopoietic malignancies: common themes and new biologic insights." Blood 118, no. 24 (2011): 6247–57. http://dx.doi.org/10.1182/blood-2011-07-328880.

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Abstract Structural chromosomal rearrangements of the Nucleoporin 98 gene (NUP98), primarily balanced translocations and inversions, are associated with a wide array of hematopoietic malignancies. NUP98 is known to be fused to at least 28 different partner genes in patients with hematopoietic malignancies, including acute myeloid leukemia, chronic myeloid leukemia in blast crisis, myelodysplastic syndrome, acute lymphoblastic leukemia, and bilineage/biphenotypic leukemia. NUP98 gene fusions typically encode a fusion protein that retains the amino terminus of NUP98; in this context, it is impor

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Hawley, Teresa S., Andrew Z. C. Fong, Henrik Griesser, Stewart D. Lyman, and Robert G. Hawley. "Leukemic Predisposition of Mice Transplanted With Gene-Modified Hematopoietic Precursors Expressing flt3 Ligand." Blood 92, no. 6 (1998): 2003–11. http://dx.doi.org/10.1182/blood.v92.6.2003.

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Abstract flt3/flk-2 ligand (FL) is a cytokine that exhibits synergistic activities in combination with other early acting factors on subpopulations of hematopoietic stem/progenitor cells. In addition to normal hematopoietic precursors, expression of the FL receptor, flt3R, has been frequently demonstrated on the blast cells from patients with acute B-lineage lymphoblastic, myeloid, and biphenotypic (also known as hybrid or mixed) leukemias. Because many of these leukemic cell types express FL, the possibility has been raised that altered regulation of FL-mediated signaling might contribute to

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Hawley, Teresa S., Andrew Z. C. Fong, Henrik Griesser, Stewart D. Lyman, and Robert G. Hawley. "Leukemic Predisposition of Mice Transplanted With Gene-Modified Hematopoietic Precursors Expressing flt3 Ligand." Blood 92, no. 6 (1998): 2003–11. http://dx.doi.org/10.1182/blood.v92.6.2003.418k11_2003_2011.

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flt3/flk-2 ligand (FL) is a cytokine that exhibits synergistic activities in combination with other early acting factors on subpopulations of hematopoietic stem/progenitor cells. In addition to normal hematopoietic precursors, expression of the FL receptor, flt3R, has been frequently demonstrated on the blast cells from patients with acute B-lineage lymphoblastic, myeloid, and biphenotypic (also known as hybrid or mixed) leukemias. Because many of these leukemic cell types express FL, the possibility has been raised that altered regulation of FL-mediated signaling might contribute to malignant

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40

Schiff, C., M. Milili, D. Bossy, et al. "Lambda-like and V pre-B genes expression: an early B-lineage marker of human leukemias." Blood 78, no. 6 (1991): 1516–25. http://dx.doi.org/10.1182/blood.v78.6.1516.1516.

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Abstract V pre-B and lambda-like genes are selectively expressed in human pre-B cells and encode polypeptide chains that associate in a mu-pseudolight chain complex that may regulate some crucial steps of early B-cell differentiation. We have followed by polymerase chain reaction and Northern blot analysis the expression of these “pre-B-specific” genes in correlation with the status (rearranged v germline) of Ig gene loci (H, kappa, lambda) in a panel of 32 leukemias pertaining mostly to the B lineage and including a number of ambiguously characterized samples. All cells that had rearranged th

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Schiff, C., M. Milili, D. Bossy, et al. "Lambda-like and V pre-B genes expression: an early B-lineage marker of human leukemias." Blood 78, no. 6 (1991): 1516–25. http://dx.doi.org/10.1182/blood.v78.6.1516.bloodjournal7861516.

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V pre-B and lambda-like genes are selectively expressed in human pre-B cells and encode polypeptide chains that associate in a mu-pseudolight chain complex that may regulate some crucial steps of early B-cell differentiation. We have followed by polymerase chain reaction and Northern blot analysis the expression of these “pre-B-specific” genes in correlation with the status (rearranged v germline) of Ig gene loci (H, kappa, lambda) in a panel of 32 leukemias pertaining mostly to the B lineage and including a number of ambiguously characterized samples. All cells that had rearranged the H locus

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So, Chi Wai Eric, Piu Wong, Min Lin, and Michael L. Cleary. "Disease Models and Transformation Mechanisms Mediated by MLL-AF4 Family Oncoproteins in Human Leukemia." Blood 104, no. 11 (2004): 467. http://dx.doi.org/10.1182/blood.v104.11.467.467.

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Abstract The Mixed Lineage Leukemia (MLL) gene codes for a histone methyltransferase that is required for hematopoietic development. As a consequence of chromosomal translocations, MLL is fused with over 40 different genes to yield in-frame fusion proteins in acute leukemias. AF4, the most common fusion partner, accounts for 40% of MLL leukemias. The AF4-related proteins, LAF4 and AF5q31, are also fusion partners for MLL in rare cases of leukemia, whereas a fourth family member, FMR2, is a candidate protein for fragile X mental retardation syndrome. MLL fusions with AF4 family proteins manifes

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Stachura, David L., Stella T. Chou, and Mitchell J. Weiss. "An Early Block to Erythro-Megakaryocytic Development Conferred by Loss of Transcription Factor GATA-1." Blood 106, no. 11 (2005): 1732. http://dx.doi.org/10.1182/blood.v106.11.1732.1732.

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Abstract Transcription factor GATA-1 is essential at multiple stages of hematopoiesis. Murine gene targeting and analysis of naturally occurring human mutations demonstrate that GATA-1 is required for the maturation of committed erythroid precursors and megakaryocytes. Prior studies also suggest additional, poorly defined, roles for GATA-1 at earlier stages of erythro-megakaryocytic development. To investigate these functions further, we studied hematopoietic differentiation of Gata1− murine embryonic stem cells on OP9 stroma with the cytokine thrombopoietin (TPO) present. Initially, the Gata1

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Kotani, Ai, Kazuki Okuyama, Bidisha Chanda, et al. "Mir-126 and Mir-195-Mediated Control of B Cell Fate in Leukemic and Normal Cells As a Potential Alternative for Transcriptional Factor." Blood 120, no. 21 (2012): 3533. http://dx.doi.org/10.1182/blood.v120.21.3533.3533.

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Abstract Abstract 3533 microRNAs (miRNAs) control many developmental and physiological processes. However, it is assumed to work as a fine tuner in cell fate determination, which has been shown to be regulated by transcription factors. Here, we challenge this canonical notion. miR-126 is downregulated in MLL-AF4 ALL, biphenotypic leukemia expressing both B cell and myeloid markers, compared with other types of ALLs. CD19 and CD20, B cell differentiation markers, were upregulated when miR-126 is reexpressed in MLL-AF4 ALLs (Figure 1). Interestingly, we found that miR-126, in leukemic cells, ind

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Patel, Bhumika, Caner Saygin, Bartlomiej P. Przychodzen, et al. "Molecular and Immunophenotypic Characteristics of Adult Acute Leukemias of Ambiguous Lineage." Blood 128, no. 22 (2016): 1659. http://dx.doi.org/10.1182/blood.v128.22.1659.1659.

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Abstract Acute undifferentiated leukemia (AUL) and mixed phenotype acute leukemia (MPAL) are acute leukemias of ambiguous lineage representing less than 5% of all adult leukemias. Ontogenetically, they are thought to be caused by precursor lesions in early pluripotent hematopoietic progenitor cells having the ability to differentiate into both lymphoid and myeloid lineages. In contrast, common lymphoid and myeloid leukemias are likely derived from precursor lesions in committed progenitor cells. The molecular characteristics of the cell of origin of these leukemias have not been fully characte

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Zuckerman, Tsila, Polina Stepensky, Dana Yehudai-Ofir, Israel Henig, Moshe Kamar, and Jerry Stein. "Safety and Preliminary GvHD Mitigation in First in Human Clinical Trial of Apograft in Match Related Stem Cell Transplantation (SCT)." Blood 138, Supplement 1 (2021): 2893. http://dx.doi.org/10.1182/blood-2021-149419.

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Abstract Graft versus host disease (GvHD) is a major frequent adverse event (AE) and the primary cause of morbidity and mortality following allogeneic stem cell transplantation (ASCT). Numerous attempts to reduce incidence and severity of GvHD using a variety of cell selection methods have been employed, but they all suffer from a risk/benefit trade-off where reduction of GvHD-causing cells leads to reduced engraftment and/or reduced graft vs. tumor (GvT) effect. We have previously reported development of a new method for cell selection, which take advantage of cells' differential sensitivity

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Kawashima, Naomi, Yasuo Kubota, Carmelo Gurnari, et al. "Biallelic Landscape of DNMT3A Mutant Myeloid Neoplasia." Blood 142, Supplement 1 (2023): 1469. http://dx.doi.org/10.1182/blood-2023-181793.

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The structure of DNMT3A comprises an N-terminal regulatory part promoting nuclear localization and targeting chromatin and a C-terminal domain, mainly involved in DNA binding and methylation catalysis. 1DNMT3A mutations in myeloid neoplasia (MN) and clonal hematopoiesis are mostly heterozygous. Homozygous null Dnmt3amice are born runted and Dnmt3a-/- cells express a hypomethylation phenotype. 2 An invariant detection of heterozygous mutations without homozygous, hemizygous, or biallelic configurations suggests absence of acquisition of more malignant phenotypes by progressive inactivation of D

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Peng, Jiayin, Fei Li, Jia Wang, et al. "Identification of a rare Gli1+ progenitor cell population contributing to liver regeneration during chronic injury." Cell Discovery 8, no. 1 (2022). http://dx.doi.org/10.1038/s41421-022-00474-3.

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AbstractIn adults, hepatocytes are mainly replenished from the existing progenitor pools of hepatocytes and cholangiocytes during chronic liver injury. However, it is unclear whether other cell types in addition to classical hepatocytes and cholangiocytes contribute to hepatocyte regeneration after chronic liver injuries. Here, we identified a new biphenotypic cell population that contributes to hepatocyte regeneration during chronic liver injuries. We found that a cell population expressed Gli1 and EpCAM (EpCAM+Gli1+), which was further characterized with both epithelial and mesenchymal ident

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Kim, Minwook, Fatima Rizvi, Donghun Shin, and Valerie Gouon-Evans. "Update on Hepatobiliary Plasticity." Seminars in Liver Disease, February 10, 2023. http://dx.doi.org/10.1055/s-0042-1760306.

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The liver field has been debating for decades the contribution of the plasticity of the two epithelial compartments in the liver, hepatocytes and biliary epithelial cells (BECs), to derive each other as a repair mechanism. The hepatobiliary plasticity has been first observed in diseased human livers by the presence of biphenotypic cells expressing hepatocyte and BEC markers within bile ducts and regenerative nodules or budding from strings of proliferative BECs in septa. These observations are not surprising as hepatocytes and BECs derive from a common fetal progenitor, the hepatoblast, and, a

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Li, Qinjin, Yuqing Gong, Yi Wang та ін. "Sirt1 Promotes the Restoration of Hepatic Progenitor Cell (HPC)-Mediated Liver Fatty Injury in NAFLD Through Activating the Wnt/β-Catenin Signal Pathway". Frontiers in Nutrition 8 (15 грудня 2021). http://dx.doi.org/10.3389/fnut.2021.791861.

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Non-alcoholic fatty liver disease (NAFLD) has developed into the world's largest chronic epidemic. In NAFLD, hepatic steatosis causes hepatocytes dysfunction and even apoptosis. The liver has a strong restoration or regeneration ability after an injury, however, it is unclear through which pattern fatty liver injury in NAFLD is repaired and what the repair mechanism is. Here, we found that in the high-fat diet (HFD)-induced NAFLD mice model, fatty liver injury caused the significant ductular reaction (DR), which is a marker to promote the repair of liver injury. SOX9+ and HNF4α+ biphenotype al

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