Academic literature on the topic 'Biphenotypic progenitors'

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Journal articles on the topic "Biphenotypic progenitors"

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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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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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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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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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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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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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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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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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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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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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Dissertations / Theses on the topic "Biphenotypic progenitors"

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Chiron, Andrada-Silvana. "Investigation into the role of erythropoietin in B cell lymphopoiesis." Electronic Thesis or Diss., Université Paris Cité, 2024. http://www.theses.fr/2024UNIP5262.

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L'érythropoïétine (EPO) est une hormone produite principalement par les reins, dont la fonction essentielle consiste à assurer l'érythropoïèse. Sa concentration systémique augmente en réponse à l'anémie ou à l'hypoxie. En plus de cette production endogène, l'EPO humaine recombinante est couramment utilisée pour traiter l'anémie des patients atteints d'insuffisance rénale chronique ou de cancer. Les effets immunomodulateurs/immunosuppresseurs de l'EPO sur les lymphocytes matures et plus généralement sur les cellules immunitaires ont été bien étudiés. Cependant, son rôle dans la lympho-hématopoï
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