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Journal articles on the topic 'B-acute lymphoblastic leukemia'

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1

Juárez-Avendaño, Gerardo, Nuria Citlalli Luna-Silva, Euler Chargoy-Vivaldo, et al. "Poor Prognosis Biomolecular Factors Are Highly Frequent in Childhood Acute Leukemias From Oaxaca, Mexico." Technology in Cancer Research & Treatment 19 (January 1, 2020): 153303382092843. http://dx.doi.org/10.1177/1533033820928436.

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Objective: To investigate the cellular and molecular epidemiology of acute leukemias in vulnerable populations of children and adolescents in Oaxaca de Juarez, Mexico. Material and Methods: Descriptive, cross-sectional and retrospective study, conducted from 2014 to 2018 in which profiles of molecular and immunophenotypic aberrations were investigated in children and adolescents diagnosed with acute leukemia, by evaluating 28 molecular abnormalities by HemaVision-Q28 multiplex RT-PCR kit and standardized EuroFlow Immunophenotyping of bone marrow cells. Results: We included 218 patients, with 8
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2

Sugisaki, Manato, Kenji Imamura, Yukie Terasaki, et al. "Slowly progressing acute lymphoblastic leukemia with prolonged leukopenia." SAGE Open Medical Case Reports 11 (January 2023): 2050313X2311777. http://dx.doi.org/10.1177/2050313x231177758.

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Acute lymphoblastic leukemia is typically characterized by leukocytosis, resulting from the uncontrolled proliferation of malignant cells. However, we report an atypical case of acute lymphoblastic leukemia that presented with leukopenia and exhibited a protracted clinical course spanning 6 months. The patient, a 45-year-old female, initially presented to our hospital with recurrent fever and was found to have lymphoblasts in a hypoplastic bone marrow. Upon further investigation, the patient was diagnosed with B-cell lymphoblastic leukemia, not otherwise specified, based on cell surface antige
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3

Loghavi, Sanam, Jeffery L. Kutok, and Jeffrey L. Jorgensen. "B-Acute Lymphoblastic Leukemia/Lymphoblastic Lymphoma." American Journal of Clinical Pathology 144, no. 3 (2015): 393–410. http://dx.doi.org/10.1309/ajcpan7bh5dnywzb.

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4

Adamaki, Maria, Spiros Vlahopoulos, George I. Lambrou, Athanasios G. Papavassiliou, and Maria Moschovi. "Aberrant AML1 gene expression in the diagnosis of childhood leukemias not characterized by AML1-involved cytogenetic abnormalities." Tumor Biology 39, no. 3 (2017): 101042831769430. http://dx.doi.org/10.1177/1010428317694308.

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The AML1 ( acute myeloid leukemia 1) gene, a necessary prerequisite of embryonic hematopoiesis and a critical regulator of normal hematopoietic development, is one of the most frequently mutated genes in human leukemia, involving over 50 chromosome translocations and over 20 partner genes. In the few existing studies investigating AML1 gene expression in childhood leukemias, aberrant upregulation seems to specifically associate with AML1 translocations and amplifications. The aim of this study was to determine whether overexpression also extends to other leukemic subtypes than the ones karyoty
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5

Hurwitz, CA, MR Loken, ML Graham, et al. "Asynchronous antigen expression in B lineage acute lymphoblastic leukemia." Blood 72, no. 1 (1988): 299–307. http://dx.doi.org/10.1182/blood.v72.1.299.299.

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Abstract Cell surface phenotypes of 113 B lineage acute lymphocytic leukemia (ALL) cases, defined by the presence of HLA-DR and at least one B-cell- specific antigen (either CD19, CD20, or CD22), were compared with antigen-defined stages of normal B lymphocyte development. The cases were first evaluated for expression of HLA-DR, CD19, CD34, CD10, CD20, and CD22 by indirect one-color immunofluorescence. Pairwise comparisons of cell surface marker expression were performed for each leukemic sample: no correlations were observed for paired antigen expression on the leukemic samples using antigens
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6

Hurwitz, CA, MR Loken, ML Graham, et al. "Asynchronous antigen expression in B lineage acute lymphoblastic leukemia." Blood 72, no. 1 (1988): 299–307. http://dx.doi.org/10.1182/blood.v72.1.299.bloodjournal721299.

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Cell surface phenotypes of 113 B lineage acute lymphocytic leukemia (ALL) cases, defined by the presence of HLA-DR and at least one B-cell- specific antigen (either CD19, CD20, or CD22), were compared with antigen-defined stages of normal B lymphocyte development. The cases were first evaluated for expression of HLA-DR, CD19, CD34, CD10, CD20, and CD22 by indirect one-color immunofluorescence. Pairwise comparisons of cell surface marker expression were performed for each leukemic sample: no correlations were observed for paired antigen expression on the leukemic samples using antigens expresse
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7

Li, Shiyong, and Glen Lew. "Is B-Lineage Acute Lymphoblastic Leukemia With a Mature Phenotype and L1 Morphology a Precursor B-Lymphoblastic Leukemia/Lymphoma or Burkitt Leukemia/Lymphoma?" Archives of Pathology & Laboratory Medicine 127, no. 10 (2003): 1340–44. http://dx.doi.org/10.5858/2003-127-1340-iballw.

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Abstract Context.—B-lineage acute lymphoblastic leukemia (ALL) with a mature phenotype and L1 morphology is a rare condition that may pose a diagnostic and management challenge. Objective.—To report our experience with 2 such unusual cases of pediatric B-lineage ALL. Design.—Morphologic, immunophenotypic, and cytogenetic features of the leukemic blast cells were reviewed in conjunction with clinical and other laboratory findings. Results.—The leukemic blast cells in both cases were small to medium with scant basophilic cytoplasm and several small inconspicuous nucleoli, characteristic of L1 ly
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8

Buhring, HJ, I. Sures, B. Jallal, et al. "The receptor tyrosine kinase p185HER2 is expressed on a subset of B- lymphoid blasts from patients with acute lymphoblastic leukemia and chronic myelogenous leukemia." Blood 86, no. 5 (1995): 1916–23. http://dx.doi.org/10.1182/blood.v86.5.1916.bloodjournal8651916.

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The class I receptor tyrosine kinase (RTK) HER2 is an oncoprotein that is frequently involved in the pathogenesis of tumors of epithelial origin. Here we report mRNA expression in peripheral blood and bone marrow cells from healthy donors in hematopoietic cell lines and leukemic blasts from patients with acute lymphoblastic leukemia (ALL), acute myeloblastic leukemia (AML), chronic lymphoblastic leukemia (CLL), and chronic myeloid leukemia (CML). However, cell surface expression of HER2 protein (p185HER2) was found exclusively on a subset of leukemic cells of the B-lymphoblastic lineage. p185H
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9

Silva, Alessandra Suelen Jardim, Gustavo Henrique de Medeiros Oliveira, Lenilton Silva DA Silva Júnior, et al. "Clinical Utility of Flow Cytometry Immunophenotyping in Acute Lymphoblastic Leukemia." Blood 136, Supplement 1 (2020): 8. http://dx.doi.org/10.1182/blood-2020-143281.

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The acute lymphoblastic leukemia (ALL) is a malignant disease of the immune system and hematologic characterized by accumulation of neoplastic B lymphoid precursors or T (lymphoblasts) in the bone marrow and / or peripheral blood. The diagnosis of these leukemias occurs by morphological classification of French-American-British (L1, L2 or L3) associated with features of immunological profile T or B cell malignancies, based on the expression profile of monoclonal antibodies (MoAb) directed against the antigens of cell differentiation by flow cytometry (FC). Several studies have shown that blast
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10

Khabirova, Eleonora, Laura Jardine, Tim H. H. Coorens, et al. "Single-cell transcriptomics reveals a distinct developmental state of KMT2A-rearranged infant B-cell acute lymphoblastic leukemia." Nature Medicine 28, no. 4 (2022): 743–51. http://dx.doi.org/10.1038/s41591-022-01720-7.

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AbstractKMT2A-rearranged infant ALL is an aggressive childhood leukemia with poor prognosis. Here, we investigated the developmental state of KMT2A-rearranged infant B-cell acute lymphoblastic leukemia (B-ALL) using bulk messenger RNA (mRNA) meta-analysis and examination of single lymphoblast transcriptomes against a developing bone marrow reference. KMT2A-rearranged infant B-ALL was uniquely dominated by an early lymphocyte precursor (ELP) state, whereas less adverse NUTM1-rearranged infant ALL demonstrated signals of later developing B cells, in line with most other childhood B-ALLs. We comp
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11

Venugopalan, Radhika K., Neha Singh, Michael L. Anthony, et al. "Leukemia-associated aberrant immunophenotype: A flow cytometry-based experience of 110 cases from a tertiary care center in Northern India." Journal of Cancer Research and Therapeutics 19, no. 5 (2023): 1335–39. http://dx.doi.org/10.4103/jcrt.jcrt_809_21.

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ABSTRACT Background: Leukemic cells express a characteristic set of “cluster of differentiation” (CD) markers, which forms the basis of the current WHO classification. Leukemia-associated aberrant immunophenotype (LAIP) refers to expression of unusual CD markers by leukemic cells, which are not normally expressed by their respective lineage. The incidence of LAIP varies considerably, and its clinical implications, prognostic relevance, and sensitivity to therapy are still debatable. This study was conducted to identify the immunophenotypic aberrancies in newly diagnosed leukemias in our Instit
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12

Schotte, Diana, Jacqueline C. K. Chau, Giselle Sylvester, et al. "Unique MicroRNA Profiles in Childhood Acute Lymphoblastic Leukemia." Blood 108, no. 11 (2006): 615. http://dx.doi.org/10.1182/blood.v108.11.615.615.

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Abstract MicroRNAs (miRNAs), an abundant class of ~22-nt endogenous regulatory RNAs that control gene expression at the posttranscriptional levels, have been implicated to play roles in the normal hematopoiesis and pathogenesis of leukemias. To identify “leukemic miRNAs”--miRNAs that may be oncogenes or tumor suppressors in human leukemias, we systematically cloned miRNAs from the blast cells of childhood acute lymphoblastic leukemia (ALL) patients with either a poor prognostic mixed-lineage leukemia rearrangement phenotype (MLL) or a prognostically more favorable precursor B-cell ALL phenotyp
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13

Homans, AC, EN Forman, and BE Barker. "Use of monoclonal antibodies to identify cerebrospinal fluid lymphoblasts in children with acute lymphoblastic leukemia." Blood 66, no. 6 (1985): 1321–25. http://dx.doi.org/10.1182/blood.v66.6.1321.1321.

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Abstract The identification of small numbers of leukemic cells in the cerebrospinal fluid (CSF) presents a diagnostic problem in the treatment of children with acute lymphoblastic leukemia (ALL). We adapted a latex sphere rosetting technique to allow us to identify simultaneously cell surface markers and cell morphology in 199 CSF samples from 34 patients and 14 control subjects. In patients without leukemic meningitis, the majority of CSF lymphocytes (69%) were found to be mature T cells positive for OKT11. A much smaller number of cells (8%) were found to be B cells positive for la. In these
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14

Homans, AC, EN Forman, and BE Barker. "Use of monoclonal antibodies to identify cerebrospinal fluid lymphoblasts in children with acute lymphoblastic leukemia." Blood 66, no. 6 (1985): 1321–25. http://dx.doi.org/10.1182/blood.v66.6.1321.bloodjournal6661321.

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The identification of small numbers of leukemic cells in the cerebrospinal fluid (CSF) presents a diagnostic problem in the treatment of children with acute lymphoblastic leukemia (ALL). We adapted a latex sphere rosetting technique to allow us to identify simultaneously cell surface markers and cell morphology in 199 CSF samples from 34 patients and 14 control subjects. In patients without leukemic meningitis, the majority of CSF lymphocytes (69%) were found to be mature T cells positive for OKT11. A much smaller number of cells (8%) were found to be B cells positive for la. In these children
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15

Dunphy, Cherie H., Laura J. Gardner, H. Lance Evans, and Nader Javadi. "CD15+ Acute Lymphoblastic Leukemia and Subsequent Monoblastic Leukemia." Archives of Pathology & Laboratory Medicine 125, no. 9 (2001): 1227–30. http://dx.doi.org/10.5858/2001-125-1227-callas.

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Abstract The abnormality in the translocation of chromosomes 4 and 11 (t[4;11]) has been characteristically associated with calla-negative CD15+ acute lymphoblastic leukemia (ALL) of early pre–B-cell origin. Transformation of a lymphoblastoid to a monoblastoid morphologic structure has rarely been described at relapse in these cases; however, these cases have lacked flow cytometric immunophenotyping (FCI) and genotypic studies (GS) to define the immunophenotype of and the presence of a B-cell gene rearrangement in the monoblastoid component. We report a case of CD15+, CD10− ALL of early pre–B-
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16

Costinean, Stefan, Sukhinder K. Sandhu, Irene M. Pedersen та ін. "Src homology 2 domain–containing inositol-5-phosphatase and CCAAT enhancer-binding protein β are targeted by miR-155 in B cells of Eμ-MiR-155 transgenic mice". Blood 114, № 7 (2009): 1374–82. http://dx.doi.org/10.1182/blood-2009-05-220814.

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AbstractWe showed that Eμ-MiR-155 transgenic mice develop acute lymphoblastic leukemia/high-grade lymphoma. Most of these leukemias start at approximately 9 months irrespective of the mouse strain. They are preceded by a polyclonal pre–B-cell proliferation, have variable clinical presentation, are transplantable, and develop oligo/monoclonal expansion. In this study, we show that in these transgenic mice the B-cell precursors have the highest MiR-155 transgene expression and are at the origin of the leukemias. We determine that Src homology 2 domain–containing inositol-5-phosphatase (SHIP) and
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17

Brissot, Éolia, and Patrice Chevallier. "Immunotherapy for B acute lymphoblastic leukemia." Hématologie 22, no. 1 (2016): 39–48. http://dx.doi.org/10.1684/hma.2016.1086.

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18

Francis, Jasmine H., Anton Orlin, and Eytan M. Stein. "Intraocular B-cell Acute Lymphoblastic Leukemia." Ophthalmology Retina 2, no. 8 (2018): 826. http://dx.doi.org/10.1016/j.oret.2018.03.002.

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19

Maslak, P. "Precusor B-cell Acute Lymphoblastic Leukemia." ASH Image Bank 2002, no. 1028 (2002): 100526. http://dx.doi.org/10.1182/ashimagebank-2002-100526.

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20

Cardoso, Angelo A., J. Pedro Veiga, Paolo Ghia, et al. "Adoptive T-Cell Therapy for B-Cell Acute Lymphoblastic Leukemia: Preclinical Studies." Blood 94, no. 10 (1999): 3531–40. http://dx.doi.org/10.1182/blood.v94.10.3531.422k14_3531_3540.

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We have previously shown that leukemia-specific cytotoxic T cells (CTL) can be generated from the bone marrow of most patients with B-cell precursor acute leukemias. If these antileukemia CTL are to be used for adoptive immunotherapy, they must have the capability to circulate, migrate through endothelium, home to the bone marrow, and, most importantly, lyse the leukemic cells in a leukemia-permissive bone marrow microenvironment. We demonstrate here that such antileukemia T-cell lines are overwhelmingly CD8+ and exhibit an activated phenotype. Using a transendothelial chemotaxis assay with hu
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21

Toljić, Branka, and Snežana Stojanović-Ristić. "Acute lymphoblastic leukemia." Opsta medicina 29, no. 1-2 (2023): 27–32. http://dx.doi.org/10.5937/opmed29-43121.

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Introduction. Acute lymphoblastic leukemia (ALL) is a heterogeneous disease distinguished by clonal replication and piling of immature lymphoid cells in the bone marrow and lymph organs. The etiology is unknown but radiation and some chemical exposure, as well as genetics, might play a role. The disease onset is abrupt. Clinical presentation is characterized by a variety of general symptoms: fatigue, malaise, night sweats, weight loss, fever. The diagnosis is based on a patient's history, physical examination, blood tests, bone marrow biopsy, cytogenetic, and immunohistochemical tests. Core tr
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22

Austin, Publishing Group. "Isolated Intra-Oral Relapsed B-Acute Lymphoblastic Leukemia (B-ALL): A Case Report." Annals of Hematology & Oncology 10, no. 1 (2023): 1414. https://doi.org/10.26420/annhematoloncol.2023.1414.

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Abstract B-Lymphoblastic Leukemia (B-ALL) is the second most common acute leukemia in adults. Its clinical manifestations include leukocytosis or leukopenia, anemia, and thrombocytopenia with an overall poor prognosis in elderly patients. If relapse occurs, it commonly involves the bone marrow but can also involve Extramedullary (EM) sites such as the brain, testis, liver, spleen and lymph nodes. Isolated extramedullary involvement of the oral cavity in relapse B-ALL is extremely rare with only a few reposted cases in the literature in pediatrics and Adolescent-and-Young-Adult (AYA) population
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23

Langabeer, Stephen E., Karl Haslam, David O’Brien, et al. "Acute Lymphoblastic Leukemia Arising inCALRMutated Essential Thrombocythemia." Case Reports in Hematology 2016 (2016): 1–5. http://dx.doi.org/10.1155/2016/6545861.

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The development of acute lymphoblastic leukemia in an existing myeloproliferative neoplasm is rare with historical cases unable to differentiate between concomitant malignancies or leukemic transformation. Molecular studies of coexistingJAK2V617F-positive myeloproliferative neoplasms and mature B cell malignancies indicate distinct disease entities arising in myeloid and lymphoid committed hematopoietic progenitor cells, respectively. Mutations ofCALRin essential thrombocythemia appear to be associated with a distinct phenotype and a lower risk of thrombosis yet their impact on disease progres
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24

Whitehead, VM, DS Rosenblatt, MJ Vuchich, JJ Shuster, A. Witte, and D. Beaulieu. "Accumulation of methotrexate and methotrexate polyglutamates in lymphoblasts at diagnosis of childhood acute lymphoblastic leukemia: a pilot prognostic factor analysis." Blood 76, no. 1 (1990): 44–49. http://dx.doi.org/10.1182/blood.v76.1.44.44.

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Abstract Lymphoblasts in bone marrow samples, obtained from 43 children with acute lymphoblastic leukemia at diagnosis, were incubated with 1.0 mumols/L [3H] methotrexate for 24 hours in vitro. Nonexchangeable methotrexate and methotrexate polyglutamates were separated and quantitated. Event-free survival at 5 years was 38% +/- 9% for all 43 patients (27 failures), and 44% +/- 10% for the 35 with non-T, non-B- cell acute lymphoblastic leukemia (20 failures). Of these 35 children, those whose lymphoblasts accumulated more than 100 pmol methotrexate and 500 pmol methotrexate polyglutamates per b
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25

Whitehead, VM, DS Rosenblatt, MJ Vuchich, JJ Shuster, A. Witte, and D. Beaulieu. "Accumulation of methotrexate and methotrexate polyglutamates in lymphoblasts at diagnosis of childhood acute lymphoblastic leukemia: a pilot prognostic factor analysis." Blood 76, no. 1 (1990): 44–49. http://dx.doi.org/10.1182/blood.v76.1.44.bloodjournal76144.

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Lymphoblasts in bone marrow samples, obtained from 43 children with acute lymphoblastic leukemia at diagnosis, were incubated with 1.0 mumols/L [3H] methotrexate for 24 hours in vitro. Nonexchangeable methotrexate and methotrexate polyglutamates were separated and quantitated. Event-free survival at 5 years was 38% +/- 9% for all 43 patients (27 failures), and 44% +/- 10% for the 35 with non-T, non-B- cell acute lymphoblastic leukemia (20 failures). Of these 35 children, those whose lymphoblasts accumulated more than 100 pmol methotrexate and 500 pmol methotrexate polyglutamates per billion ce
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26

Sykes, David B., and Mark P. Kamps. "E2a/Pbx1 Induces the Rapid Proliferation of Stem Cell Factor-Dependent Murine Pro-T Cells That Cause Acute T-Lymphoid or Myeloid Leukemias in Mice." Molecular and Cellular Biology 24, no. 3 (2004): 1256–69. http://dx.doi.org/10.1128/mcb.24.3.1256-1269.2004.

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ABSTRACT Oncoprotein E2a/Pbx1 is produced by the t(1;19) chromosomal translocation of human pre-B acute lymphoblastic leukemia. E2a/Pbx1 blocks differentiation of primary myeloid progenitors but, paradoxically, induces apoptosis in established pre-B-cell lines, and no transforming function of E2a/Pbx1 has been reported in cultured lymphoid progenitors. Here, we demonstrate that E2a/Pbx1 induces immortal proliferation of stem cell factor (SCF)-dependent pro-T thymocytes by a mechanism dependent upon both its transactivation and DNA-binding functions. E2a-Pbx1 cooperated with cytokines or activa
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27

Oevermann, Lena, Sebastian U. Michaelis, Markus Mezger, et al. "KIR B haplotype donors confer a reduced risk for relapse after haploidentical transplantation in children with ALL." Blood 124, no. 17 (2014): 2744–47. http://dx.doi.org/10.1182/blood-2014-03-565069.

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Key Points KIR haplotype B donors and high KIR B content score confer better protection against relapse after HLA-haploidentical transplantation in pediatric acute lymphoblastic leukemia. Haploidentical donor selection criteria for childhood acute lymphoblastic leukemia should include KIR haplotype and KIR B-content score.
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28

Besalduch, J., N. Matamoros, J. Sanchis, et al. "Pre-B Acute Lymphoblastic Leukemia During a Complete Remission in T-Acute Lymphoblastic Leukemia." Leukemia & Lymphoma 3, no. 5-6 (1991): 443–45. http://dx.doi.org/10.3109/10428199109070291.

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29

Movchan, L. V., and T. V. Shman. "ANALYSIS OF THE NUMBER OF CELLS WITH CD34+CD38- AND CD34+CD38-CD19+ PHENOTYPES AS POTENTIAL LEUKEMIC STEM CELLS IN ACUTE LYMPHOBLASTIC LEUKEMIA IN CHILDREN." Health and Ecology Issues, no. 2S (December 28, 2011): 66–69. http://dx.doi.org/10.51523/2708-6011.2011-8-2s-22.

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The number of the supposed leukemic stem cells in marrow samples of 54 patients with primary B-linear acute lymphoblastic leukemia was detected by the method of multiparametric flow cytofluorimetry in leukemia diagnosis (zero day). The level of minimal residual disease was estimated on zero and on the fifteenth days of induction therapy. In the course of the research it was found out that leukemic B-cell precursors with СD34+СD38-CD19+ phenotype prevailed among the cells with СD34+СD38-phenotype. The high percentage of both СD34+СD38-, СD34+СD38-, and СD34+СD38-CD19+ among the general populati
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30

Suwandari, Ni Luh Ayu, Anak Agung Wiradewi Lestari, I. Nyoman Wande, Ida Ayu Putri Wirawati, and I. Putu Yuda Prabawa. "Acute Lymphoblastic Leukemia (ALL)-L2 in an adult woman: a case report." Bali Medical Journal 12, no. 1 (2023): 669–74. http://dx.doi.org/10.15562/bmj.v12i1.3934.

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Background: Acute lymphoblastic leukemia (ALL) is a malignant disease of the bone marrow in which early lymphoid precursors proliferate and replace normal hematopoietic cells without developing into normal B and T cells. Acute lymphoblastic leukemia (ALL) is the most common leukemia in pediatric patients, accounting for up to 80% of cases in children and less frequently in adults. Case Presentation: A 47-year-old woman complained of fever, feeling weak and dizzy, and also complained that if she spits, there has been blood since 7 days ago. A complete blood count showed leukocytosis, anemia, an
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31

Bipesh Kumar Shah, Rachna Seth, Aditi Sinha, Aditya Kumar Gupta, and Jagdish Prasad Meena. "Acute Kidney Injury in Methotrexate treated Leukemia." Journal of BP Koirala Institute of Health Sciences 6, no. 2 (2023): 23–28. http://dx.doi.org/10.3126/jbpkihs.v6i2.55836.

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Background: The study was performed to know the incidence of acute kidney injury within 48 hours following High dose Methotrexate administration in children with high-risk B cell Acute Lymphoblastic Leukemia along with its risk factors and toxicities. Most studies have been conducted in adults and have included non-Hodgkin lymphoma along with leukemia. There is a paucity of data regarding the burden of Acute kidney injury with Methotrexate use in the pediatric age group with B cell Acute Lymphoblastic Leukemia. Methods: It was a prospective observational study conducted at the pediatric ward o
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32

Terek, M. C., E. Ozkinay, O. Zekioglu, et al. "Acute leukemia in pregnancy with ovarian metastasis: a case report and review of the literature." International Journal of Gynecologic Cancer 13, no. 6 (2003): 904–8. http://dx.doi.org/10.1136/ijgc-00009577-200311000-00027.

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Acute leukemias tend to affect a younger population and are much more common in pregnant patients than chronic leukemias are. We report a case of acute lymphoblastic leukemia diagnosed during the third trimester presenting with organomegaly and thrombocytopenia. Delivery of the fetus by cesarean section was decided because of the fulminant nature of the acute leukemia within days of admission. Bone marrow biopsy revealed acute lymphocytic leukemia, French American-British L2 subtype B cell immunotype. A left ovarian mass was identified during the cesarean section which later proved to be lymph
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33

Bapat, Kalyani, Dia Mansukhani, Shanaz Khodaiji, and Sachin Almel. "Acute Lymphoblastic Leukemia With Surface Light Chain Expression." Annals of Pathology and Laboratory Medicine 10, no. 5 (2023): C37–43. http://dx.doi.org/10.21276/apalm.3214.

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Acute Lymphoblastic leukemias (ALL) are a heterogeneous group of neoplasms which can either be having precursor B cell immunophenotype or mature B cell immunophenotype. Surface immunoglobulin light chain restriction is usually a feature of mature B cell neoplasms. A precursor B cell lymphoblastic leukemia (pre-B-ALL) with surface immunoglobulin light chain expression is a rare immunophenotype . We report a case of a 4 year old female with L1 type of blast morphology yet showing surface light chain restriction. Recognizing this rare immunophenotype and arriving at a correct diagnosis has therap
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34

Conserva, Maria Rosa, Immacolata Redavid, Luisa Anelli, et al. "IKAROS in Acute Leukemia: A Positive Influencer or a Mean Hater?" International Journal of Molecular Sciences 24, no. 4 (2023): 3282. http://dx.doi.org/10.3390/ijms24043282.

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One key process that controls leukemogenesis is the regulation of oncogenic gene expression by transcription factors acting as tumor suppressors. Understanding this intricate mechanism is crucial to elucidating leukemia pathophysiology and discovering new targeted treatments. In this review, we make a brief overview of the physiological role of IKAROS and the molecular pathway that contributes to acute leukemia pathogenesis through IKZF1 gene lesions. IKAROS is a zinc finger transcription factor of the Krüppel family that acts as the main character during hematopoiesis and leukemogenesis. It c
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35

Taneja, Vipul, Goud Raghvendra, and Kusum Mahajan. "Association of Acute Lymphoblastic Leukemia with Unilateral Facial Palsy: A Rare Presentation." International Journal of Health Sciences and Research 11, no. 8 (2021): 79–80. http://dx.doi.org/10.52403/ijhsr.20210811.

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Acute lymphoblastic leukemia (ALL) is the most common pediatric cancer. Survival probability of pediatric ALL had been 10-20%, but the most recent clinical trials with multiagent chemotherapy have achieved overall survival probability of better than 80%. This is achieved because of better supportive care, treatment stratification based on relapse risk, and the biological features of leukemic cells. Diagnosis of ALL was based principally on morphological identification of leukemic blasts in bone marrow, and immunophenotype assessment by flow cytometry is necessary, and most pediatric ALL cases
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36

Mohammed, Dnya Jaza, Sana Dlawar Jalal, Ahmed Khudair Yassin, and Ali Ibrahim Mohammed. "Pattern, clinical and laboratory features from of adult acute lymphoblastic leukemia patients from Kurdistan-Iraq." Advanced Medical Journal 5, no. 2 (2019): 55–59. http://dx.doi.org/10.56056/amj.2019.101.

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Background and objectives: Acute lymphoblastic leukemia is a heterogeneous group of neoplasm resulting from clonal proliferation and tissue infiltration by leukemic lymphoblasts. Adult acute lymphoblastic leukemia is character- ized by distinctive clinical and genetic features in comparison to childhood leukemia. This study aimed to outline the clinco-hematological features of adult Iraqi patients newly diagnosed with acute lymphoblastic leukemia in Kurdis- tan-Iraq. Methods:This study was conducted at Hiwa Cancer Hospital in Sulaimani City and Nanakali Hospital in Erbil City, Kurdistan, Iraq.
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37

Suppipat, Koramit, Evelyn Zhu, and Daniel Lacorazza. "Targeting AKT Signaling in Pediatric Acute Lymphoblastic Leukemia with Sulforaphane." Blood 118, no. 21 (2011): 1521. http://dx.doi.org/10.1182/blood.v118.21.1521.1521.

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Abstract Abstract 1521 Refractory and relapse acute lymphoblastic leukemia (ALL) is one of the leading causes of cancer-related death in children. Novel agents are still in need as a frontline therapy in high risk patients and salvage agent in relapse patients. Leukemic cells acquire a survival advantage over normal blood cells by losing control of the cell cycle and activating pro-survival signals. There are emerging evidences showing that the PI3K/AKT/mTOR pathway is frequently activated in both T cell acute lymphoblastic leukemia (T-ALL) and precursor B cell acute lymphoblastic leukemia (pr
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38

Algarni, Ayed A., Mojtaba Akhtari, and Kai Fu. "Myelodysplastic Syndrome with Myelofibrosis Transformed to a Precursor B-Cell Acute Lymphoblastic Leukemia: A Case Report with Review of the Literature." Case Reports in Hematology 2012 (2012): 1–6. http://dx.doi.org/10.1155/2012/207537.

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Myelodysplastic syndromes (MDS) comprise a group of heterogeneous clonal hematopoietic cell disorders characterized by cytopenias, bone marrow hypercellularity, and increased risk of transformation to acute leukemias. MDS usually transformed to acute myeloid leukemia, and transformation to acute lymphoblastic leukemia (ALL) is rare. Herein, we report a unique patient who presented with MDS with myelofibrosis. Two months after the initial diagnosis, she progressed to a precursor B-cell acute lymphoblastic leukemia. She was treated with induction therapy followed by allogenic stem cell transplan
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39

Hsieh, Yao-Te, Eun Ji Gang, Huimin Geng, et al. "Integrin alpha4 blockade sensitizes drug resistant pre-B acute lymphoblastic leukemia to chemotherapy." Blood 121, no. 10 (2013): 1814–18. http://dx.doi.org/10.1182/blood-2012-01-406272.

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Key Points We evaluated interference with integrin alpha4–mediated stromal adhesion as a new acute lymphoblastic leukemia treatment. Integrin alpha4 blockade using natalizumab in combination with chemotherapy sensitizes pre-B acute lymphoblastic leukemia to chemotherapy.
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40

Hirzel, Alicia C., Aaron Cotrell, Robert Gasparini, and Vathany Sriganeshan. "Precursor B-Cell Acute Lymphoblastic Leukemia/Lymphoma with L3 Morphology, Philadelphia Chromosome, MYC Gene Translocation, and Coexpression of TdT and Surface Light Chains: A Case Report." Case Reports in Pathology 2013 (2013): 1–4. http://dx.doi.org/10.1155/2013/679892.

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Acute lymphoblastic leukemia is predominantly found in children. It is a neoplasm of precursor cells or lymphoblasts committed to either a B- or T-cell lineage. The immature cells in B-acute lymphoblastic leukemia/lymphoma can be small or medium sized with scant or moderate cytoplasm and typically express B-cell markers such as CD19, cytoplasmic CD79a, and TdT without surface light chains. These markers, along with cytogenetic studies, are vital to the diagnosis, classification, and treatment of these neoplasms. We present an unusual case of a precursor B-cell ALL, in an 82-year-old woman, who
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41

Song, Joo Y., Elham Vali Khojeini, Denis M. Dwyre, and Brian A. Jonas. "B lymphoblastic leukemia with granules mimicking acute myeloid leukemia." International Journal of Hematology 102, no. 3 (2015): 251–52. http://dx.doi.org/10.1007/s12185-015-1842-9.

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42

Cimmino, Luisa, and Iannis Aifantis. "Fingerprinting Acute Leukemia: DNA Methylation Profiling of B-Acute Lymphoblastic Leukemia." Cancer Discovery 2, no. 11 (2012): 976–78. http://dx.doi.org/10.1158/2159-8290.cd-12-0435.

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43

Pushel, Irina, Byunggil Yoo, Daniel Louiselle, et al. "Single-Cell RNA Sequencing Facilitates Study of Cancer Mechanisms across Pediatric Leukemias." Blood 142, Supplement 1 (2023): 1614. http://dx.doi.org/10.1182/blood-2023-187340.

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Leukemia is the most common pediatric cancer, diagnosed in over 3,000 children annually in the US. While the prognosis for many pediatric leukemias has significantly improved with the addition of DNA sequencing to the diagnosis and treatment selection process, the molecular mechanisms driving some cases remain inscrutable. In this study, we performed single-cell RNA sequencing on a cohort of pediatric leukemia samples (n = 72) to explore intra- and inter-patient heterogeneity across multiple types of malignancies: acute megakaryoblastic leukemia (AMKL, n = 1), acute myeloid leukemia (AML, n =
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44

Bousquet, Marina, Marian Harris, Beiyan Zhou, Mark D. Fleming, and Harvey Lodish. "MicroRNA Mir-125b Causes Leukemia." Blood 116, no. 21 (2010): 3158. http://dx.doi.org/10.1182/blood.v116.21.3158.3158.

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Abstract Abstract 3158 MicroRNA miR-125b has been shown to be involved in different kind of leukemia. Indeed, the chromosomal translocation t(2;11)(p21;q23) found in patients with myelodysplasia and acute myeloid leukemia leads to an overexpression of miR-125b up to 90 fold. Moreover, miR-125b is also upregulated in patients with B-cell acute lymphoblastic leukemia carrying the t(11;14)(q24;q32) translocation. To decipher the presumed oncogenic mechanism of miR-125b, we used transplantation experiments in mice. All of the mice transplanted with fetal liver cells ectopically expressing miR-125b
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Gluzman, D. F., L. M. Sklyarenko, M. P. Zavelevich, S. V. Koval, and T. S. Ivanivskaya. "LEUKEMIC BLAST CELLS AND CONTROVERSIES IN MODELS OF HEMATOPOIESIS." Experimental Oncology 37, no. 1 (2015): 2–4. http://dx.doi.org/10.31768/2312-8852.2015.37(1):2-4.

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Classical and up-to-date models of hematopoietic lineage determination are briefly reviewed with the focus on myeloid-based models challenging the existence of the common progenitor for T cells, B cells and NK cells. The analysis of immunophenotype of leukemic blast cells seems to be a promising approach for interpreting some controversies in the schemes of normal hematopoiesis. The liter ature data as well as our own findings in the patients with various types of acute leukemias are in favor of the concept postulating that common myeloid-lymphoid progenitors giving rise to T and B cell branch
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De Braekeleer, Etienne, Nathalie Douet-Guilbert, Frédéric Morel, et al. "RUNX1amplification in B-cell acute lymphoblastic leukemia." Leukemia & Lymphoma 51, no. 2 (2009): 329–32. http://dx.doi.org/10.3109/10428190903456967.

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Peterson, Michael R., Kyle J. Noskoviak, and Robert Newbury. "CD5-Positive B-Cell Acute Lymphoblastic Leukemia." Pediatric and Developmental Pathology 10, no. 1 (2007): 41–45. http://dx.doi.org/10.2350/06-03-0057.1.

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Goyal, Shama, Suresh K. Pai, Rohini Kelkar, and Suresh H. Advani. "Hepatitis B vaccination in acute lymphoblastic leukemia." Leukemia Research 22, no. 2 (1998): 193–95. http://dx.doi.org/10.1016/s0145-2126(97)00155-0.

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Mohammadi, Seyedeh Momeneh, Daryosh Mohammad Nejad, and Hojjatollah Nozad Charoudeh. "Genetic alterations in B-acute lymphoblastic leukemia." Acta Haematologica Polonica 48, no. 1 (2017): 10–17. http://dx.doi.org/10.1016/j.achaem.2016.11.002.

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50

Maslak, P. "Relapsed Precursor B Cell Acute Lymphoblastic Leukemia." ASH Image Bank 2003, no. 0508 (2003): 100706. http://dx.doi.org/10.1182/ashimagebank-2003-100706.

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