Journal articles: 'B-acute lymphoblastic leukemia'

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Juárez-Avendaño, Gerardo, Nuria Citlalli Luna-Silva, Euler Chargoy-Vivaldo, Laura Alicia Juárez-Martínez, Mayra Noemí Martínez-Rangel, Noemí Zárate-Ortiz, Edith Martínez-Valencia, Briceida López-Martínez, Rosana Pelayo, and Juan Carlos Balandrán. "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 82.5% younger than 14 years and 17.5% adolescents. The median age was 9 years and a main peak of incidence was recorded at age of 4 to 5 years. B-cell acute lymphoblastic leukemia was diagnosed in 70.64% of all cases, acute myeloid leukemia was in 22.48%, T-cell acute lymphoblastic leukemia in 6.42%, and mixed lineage acute leukemia in 0.46% of cases. Overall, chromosomal translocations were positive in 29.82% of cases. While 65.31% of patients with acute myeloid leukemia reported aberrancies, only in 18.83% of B-cell acute lymphoblastic leukemia cases genetic abnormalities were obvious. Surprisingly, most prevalent translocations in B-cell acute lymphoblastic leukemia were t(9;22) in 20.7%, followed by t(4;11) in 17.2% and t(6;11) in 13.8%, whereas patients with acute myeloid leukemia showed t(15;17) in 40.6% and t(8;21) in 21.9%. In contrast, an homogeneous expression of t(3;21) and t(6;11) was recorded for T-cell acute lymphoblastic leukemia and mixed lineage acute leukemia cases, respectively. Except for t(1;19), expressed only by pre-B cells, there was no association of any of the studied translocations with differentiation stages of the B-leukemic developmental pathway. Conclusion: Our findings identify near 50% of patients with acute lymphoblastic leukemia at debut with high-risk translocations and poor prognosis in B-cell acute lymphoblastic leukemia as well as an unexpected increase of acute myeloid leukemia cases in young children, suggesting a molecular shift that support a higher incidence of poor prognosis cases in Oaxaca.

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Sugisaki, Manato, Kenji Imamura, Yukie Terasaki, Hiromasa Iino, Takumi Hoshino, Nahoko Hatsumi, Hiroshi Handa, and Satoru Takada. "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 antigen expression and genetic abnormalities. Notably, the patient demonstrated persistently low white blood cell and neutrophil counts, without evidence of increasing lymphoblast infiltration in the bone marrow during the ensuing 6-month period. Subsequent chemotherapy led to normalization of hematopoiesis and disappearance of lymphoblasts, resulting in complete remission of the disease.

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Loghavi, Sanam, Jeffery L. Kutok, and Jeffrey L. Jorgensen. "B-Acute Lymphoblastic Leukemia/Lymphoblastic Lymphoma." American Journal of Clinical Pathology 144, no. 3 (September 1, 2015): 393–410. http://dx.doi.org/10.1309/ajcpan7bh5dnywzb.

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Hurwitz, CA, MR Loken, ML Graham, JE Karp, MJ Borowitz, DJ Pullen, and CI Civin. "Asynchronous antigen expression in B lineage acute lymphoblastic leukemia." Blood 72, no. 1 (July 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 expressed either early or late during normal B lymphoid development. Complete immunophenotypes of the cases were then compared with normal B-cell developmental stages. Sixteen different complete immunophenotypes were observed on the leukemias that were not found in normal marrow; at least 78% of the cases demonstrated such “asynchronous” combinations of B lymphoid- associated differentiation antigens. Several samples were subsequently studied by two-color immunofluorescence, and the presence of doubly labeled cells with “asynchronous” antigen combinations was confirmed. These results indicate that the majority of B lineage leukemias exhibit “developmental asynchrony,” as compared with normal marrow B cells. The data further suggest that ALL cases do not accurately represent cells arrested at the stage where the leukemogenic event occurred. Rather, ALL appears to be a disease in which there may be maturation of leukemic blasts; but this maturation is “asynchronous” when compared with the normal developmental process.

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Hurwitz, CA, MR Loken, ML Graham, JE Karp, MJ Borowitz, DJ Pullen, and CI Civin. "Asynchronous antigen expression in B lineage acute lymphoblastic leukemia." Blood 72, no. 1 (July 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 expressed either early or late during normal B lymphoid development. Complete immunophenotypes of the cases were then compared with normal B-cell developmental stages. Sixteen different complete immunophenotypes were observed on the leukemias that were not found in normal marrow; at least 78% of the cases demonstrated such “asynchronous” combinations of B lymphoid- associated differentiation antigens. Several samples were subsequently studied by two-color immunofluorescence, and the presence of doubly labeled cells with “asynchronous” antigen combinations was confirmed. These results indicate that the majority of B lineage leukemias exhibit “developmental asynchrony,” as compared with normal marrow B cells. The data further suggest that ALL cases do not accurately represent cells arrested at the stage where the leukemogenic event occurred. Rather, ALL appears to be a disease in which there may be maturation of leukemic blasts; but this maturation is “asynchronous” when compared with the normal developmental process.

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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 (March 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 karyotypically involving AML1. We use quantitative real-time polymerase chain reaction methodology to investigate gene expression in 100 children with acute leukemias and compare them to those of healthy controls. We show that in childhood acute lymphoblastic leukemia, AML1 gene overexpression is associated with a variety of leukemic subtypes, both immunophenotypically and cytogenetically. Statistically significantly higher transcripts of the gene were detected in the acute lymphoblastic leukemia group as compared to the acute myeloid leukemia group, where AML1 overexpression appeared to associate with cytogenetic abnormalities additional to those that engage the AML1 gene, or that are reported as showing a “normal” karyotype. Collectively, our study shows that AML1 gene overexpression characterizes a broader range of leukemic subtypes than previously thought, including various maturation stages of B-cell acute lymphoblastic leukemia and cytogenetic types additional to those involving the AML1 gene.

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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 (October 1, 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 lymphoblasts. Immunophenotypically, they were positive for CD19, CD22, and low-density CD20, with expression of surface immunoglobulin λ light chain. They were negative for immature (CD34 and terminal deoxynucleotidyl transferase), myeloid, and T-cell–associated markers. Conventional cytogenetic and fluorescent in situ hybridization studies failed to demonstrate chromosomal translocations involving the c-myc gene. Both patients were treated with Children's Cancer Group ALL protocols and had good responses. Conclusions.—B-lineage ALL with a mature phenotype, L1 morphology, and absent chromosomal translocations involving the c-myc gene is best classified and managed as precursor B-lymphoblastic leukemia/lymphoma instead of Burkitt leukemia/lymphoma.

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Silva, Alessandra Suelen Jardim, Gustavo Henrique de Medeiros Oliveira, Lenilton Silva DA Silva Júnior, Hugo Henrique de Freitas Ferreira, Maria das Graças Pereira Araujo, Victor lima Soares, Rodrigo Villar Freitas, et al. "Clinical Utility of Flow Cytometry Immunophenotyping in Acute Lymphoblastic Leukemia." Blood 136, Supplement 1 (November 5, 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 cell immunophenotypes of cases of acute lymphoblastic leukemia does not always exhibit characteristics of lymphoid differentiation normal but exhibit aberrant immunophenotypes. Thus, blasts some cases of acute lymphoblastic leukemia of B lineage may show myeloid or T antigens. Also blasts of cases of acute lymphoblastic leukemia T cell determinants may possess B or myeloid cells.Objective:To determine the immunophenotypic profile by FC in 88 patients with ALL (B or T lineage) diagnosed in the Laboratory of Flow Cytometry Blood Center of Dalton Cunha - HEMONORTE, from State of Rio Grande do Norte, Brazil.Methods:All samples from peripheral blood and / or bone marrow were subjected to FC immunophenotyping using a panel of MoAb specific for diagnosis of acute leukemia (AL) directly conjugated to fluorochromes as fluorescein isothiocyanate (FITC), phycoerythrin (PE), peridinin-chlorophyll protein (PerCP) and allophycocyanin (APC).Results:The patients' age range was between 1 month and 84 years old, with an average of 20.3 years, with 62.5% of the patients being male. The most frequently observed strain was B and the most evident subtype was the Common Pre-B ALL. Among the cell markers evaluated, the most expressed in lineage B were CD19, CD10, HLADR and cCD79a and the antigens most frequently expressed in lineage T were cytoplasmic CD3 (cCD3) and membrane (mCD3), CD7, CD5 and CD2. A small percentage (6.8%) were doubly positive T cells.Conclusion:It is concluded that individuals with ALL in this study have demographic, clinical and immunophenotypic characteristics similar to those observed in other studies, demonstrating that CF immunophenotyping is an essential methodology in the diagnosis of follow-up of these leukemias. Disclosures No relevant conflicts of interest to declare.

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Buhring, HJ, I. Sures, B. Jallal, FU Weiss, FW Busch, WD Ludwig, R. Handgretinger, HD Waller, and A. Ullrich. "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 (September 1, 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. p185HER2 expression was found on blasts in 2 of 15 samples from infants, 9 of 19 samples from adult patients with C-ALL (CD19+CD10+), and 1 of 2 samples from patients with pro-B ALL (CD19+CD10-), whereas none of the leukemic cells from patients with AML (0/30), T-ALL (0/7), CLL (0/5) (CD19+CD5+), or CML in chronic and accelerated phase (0/5) or in blast crisis with myeloid differentiation (0/14) were positive for p185HER2. However, cells from 3 of 4 patients with CML in B-lymphoid blast crisis (CD19+CD10+) expressed high levels of p185HER2, which was also found on the surface of the CML-derived B-cell lines BV-173 and Nalm-1. Our study shows p185HER2 expression on malignant cells of hematopoietic origin for the first time. Aberrant expression of this oncogenic receptor tyrosine kinase in hematopoietic cell types may be an oncogenic event contributing to the development of a subset of B- lymphoblastic leukemias.

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Khabirova, Eleonora, Laura Jardine, Tim H. H. Coorens, Simone Webb, Taryn D. Treger, Justin Engelbert, Tarryn Porter, et al. "Single-cell transcriptomics reveals a distinct developmental state of KMT2A-rearranged infant B-cell acute lymphoblastic leukemia." Nature Medicine 28, no. 4 (March 14, 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 compared infant lymphoblasts with ELP cells and revealed that the cancer harbored hybrid myeloid–lymphoid features, including nonphysiological antigen combinations potentially targetable to achieve cancer specificity. We validated surface coexpression of exemplar combinations by flow cytometry. Through analysis of shared mutations in separate leukemias from a child with infant KMT2A-rearranged B-ALL relapsing as AML, we established that KMT2A rearrangement occurred in very early development, before hematopoietic specification, emphasizing that cell of origin cannot be inferred from the transcriptional state.

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

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

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Maslak, P. "Precusor B-cell Acute Lymphoblastic Leukemia." ASH Image Bank 2002, no. 1028 (October 28, 2002): 100526. http://dx.doi.org/10.1182/ashimagebank-2002-100526.

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Schotte, Diana, Jacqueline C. K. Chau, Giselle Sylvester, Gwen Liu, Susan T. C. J. M. Peters, Rob Pieters, Monique L. Den Boer, and Chang-Zheng Chen. "Unique MicroRNA Profiles in Childhood Acute Lymphoblastic Leukemia." Blood 108, no. 11 (November 16, 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 phenotype (B-ALL). We have identified 87 known and 43 new human mature miRNAs, which potentially encoded by 101 known and 94 new human miRNA genes, respectively. Many newly identified miRNAs are not conserved in mouse, suggesting that systematic miRNA cloning analysis can facilitate the discovery of many novel human leukemia specific miRNAs. Interestingly, quantification of miRNA expression by real-time PCR analyses revealed that miRNAs are generally expressed at higher levels in MLL and B-ALL leukemia cells when compared to that in normal CD34+ bone marrow cells. We selected 21 highly differentially expression miRNA candidates and determined their expression in a larger group of 14 MLL patients and 16 B-ALL patients. We found that 9 miRNAs, including 4 newly identified miRNAs, were significantly differentially expressed (p < 0.05) between MLL and B-ALL subtypes. These findings demonstrate that the expression of both known and newly identified miRNA genes differs in genetically and prognostically different subgroups of ALL and normal CD34+ progenitor cells, suggesting that systematic miRNA cloning analyses and subsequent expression profiling analysis may facilitate the identification of specific signatures for leukemia classification and tumor suppressors or oncogenes that contribute to the pathogenesis of MLL and B-ALL.

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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 treatments are poly-chemotherapy, radiation therapy, hematopoietic stem cell transplantation. Case report. We presented a 20-year-old patient. On his first visit, he complained of neck pain. He was treated by a physiotherapist. After he finished with physical therapy we noticed pancytopenia in his lab work. His general practitioner (GP) referred him to a hematologist where further medical examinations were performed and ALL diagnosis was made. The treatment started with a chemotherapy regimen. An allogeneic hematopoietic stem cell transplantation was performed afterward. In the follow-up, regular haematologic assessments were done, as well as, the assessment of MRD (Minimal Residual Disease). Complete morphologic remission was maintained the whole time but with positive MRD findings. He received an antiCD22 monoclonal antibody therapy and the therapeutic response was good. Eight months later B-ALL relapse was confirmed. The patient's general condition got worse and in spite of an intensive therapy the patient died. Conclusion. Acute lymphoblastic leukemia is a disease whose outcome depends on many a factor. Due to atypical symptoms, it should be taken into consideration to shorten the time to diagnosis, provide timely treatment and thus influence the disease outcome.

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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 (September 1, 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-cell origin defined by morphologic testing and FCI with the t(4;11) abnormality. At relapse, the morphologic testing, enzyme cytochemistry, and FCI data were characteristic of monoblastic leukemia. The t(4;11) abnormality persisted with associated additional chromosomal abnormalities, and the monoblasts contained a B-cell gene rearrangement by GS. These findings support the concept that both processes arose from a multipotential progenitor cell.

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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 (December 1, 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 children, only 3% of CSF lymphoid cells expressed the common acute lymphoblastic leukemia antigen (CALLA). Similar results were found in the control subjects. By contrast, 28 CSF samples from nine children with varying numbers of CSF lymphoblasts had much greater proportions of CALLA- and la-positive CSF cells (24% to 96%). Leukemic meningitis was present in one of these patients and later developed in four others. However, three patients with small numbers of lymphoblasts present but with low proportions of CALLA-positive CSF cells (less than 5%) subsequently had normal CSF examinations. We found the use of this rosetting technique valuable in providing information complementary to that obtained from cell morphology alone about the possible malignant nature of small numbers of lymphoblast-like CSF cells seen on cytocentrifuge preparations in children with ALL.

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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 (December 1, 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, only 3% of CSF lymphoid cells expressed the common acute lymphoblastic leukemia antigen (CALLA). Similar results were found in the control subjects. By contrast, 28 CSF samples from nine children with varying numbers of CSF lymphoblasts had much greater proportions of CALLA- and la-positive CSF cells (24% to 96%). Leukemic meningitis was present in one of these patients and later developed in four others. However, three patients with small numbers of lymphoblasts present but with low proportions of CALLA-positive CSF cells (less than 5%) subsequently had normal CSF examinations. We found the use of this rosetting technique valuable in providing information complementary to that obtained from cell morphology alone about the possible malignant nature of small numbers of lymphoblast-like CSF cells seen on cytocentrifuge preparations in children with ALL.

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Venugopalan, Radhika K., Neha Singh, Michael L. Anthony, Arathi Kunnumbrath, Arvind K. Gupta, Uttam K. Nath, Nilotpal Chowdhury, and Harish Chandra. "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 Institute. Method: This was an observational study, which included newly diagnosed leukemias on flow cytometry. Aberrant immunophenotypic expressions were recorded whenever present and were correlated with prognostic factors like age, gender, and total leucocyte count (TLC). Results: The study included 110 newly diagnosed cases of leukemias (85 acute and 25 chronic) over 1.5 years. Immunophenotypic aberrancies were detected in 40.4% of the cases. The highest incidence of aberrations was detected in acute myeloid leukemia (60.7%). LAIPs were detected in 50% of T-acute lymphoblastic leukemia and 25% cases of in B-cell acute lymphoblastic leukemia (B-ALL). Aberrant CD33 and CD56 expression in B-ALL correlated with poor prognostic factors like higher age and higher TLC, respectively. Immunophenotypic aberrancies were present in 28% cases of chronic lymphocytic leukemia. Conclusion: The results of this study have generated valuable baseline data on the incidence of LAIPs in this region. This information is vital because establishing LAIPs at the time of diagnosis is crucial for disease monitoring. Some LAIPs are associated with underlying cytogenetic abnormalities and hence impact the management and prognosis.

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Cardoso, Angelo A., J. Pedro Veiga, Paolo Ghia, Hernani M. Afonso, W. Nicholas Haining, Stephen E. Sallan, and Lee M. Nadler. "Adoptive T-Cell Therapy for B-Cell Acute Lymphoblastic Leukemia: Preclinical Studies." Blood 94, no. 10 (November 15, 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 human endothelial cells, we observed that these T cells can be recruited and transmigrate through vascular and bone marrow endothelium and that these transmigrated cells preserve their capacity to lyse leukemic cells. Additionally, these antileukemia T-cell lines are capable of adhering to autologous stromal cell layers. Finally, autologous antileukemia CTL specifically lyse leukemic cells even in the presence of autologous marrow stroma. Importantly, these antileukemia T-cell lines do not lyse autologous stromal cells. Thus, the capacity to generate anti–leukemia-specific T-cell lines coupled with the present findings that such cells can migrate, adhere, and function in the presence of the marrow microenvironment enable the development of clinical studies of adoptive transfer of antileukemia CTL for the treatment of ALL.

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Langabeer, Stephen E., Karl Haslam, David O’Brien, Johanna Kelly, Claire Andrews, Ciara Ryan, Richard Flavin, Patrick J. Hayden, and Christopher L. Bacon. "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 progression is less well defined. The as yet undescribed scenario of pro-B cell acute lymphoblastic leukemia arising inCALRmutated essential thrombocythemia is presented. Intensive treatment for the leukemia allowed for expansion of the originalCALRmutated clone. WhetherCALRmutations in myeloproliferative neoplasms predispose to the acquisition of additional malignancies, particularly lymphoproliferative disorders, is not yet known.

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

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Costinean, Stefan, Sukhinder K. Sandhu, Irene M. Pedersen, Esmerina Tili, Rossana Trotta, Danilo Perrotti, David Ciarlariello, et al. "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, no. 7 (August 13, 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 CCAAT enhancer-binding protein β (C/EBPβ), 2 important regulators of the interleukin-6 signaling pathway, are direct targets of MiR-155 and become gradually more down-regulated in the leukemic than in the preleukemic mice. We hypothesize that miR-155, by down-modulating Ship and C/EBPβ, initiates a chain of events that leads to the accumulation of large pre-B cells and acute lymphoblastic leukemia/high-grade lymphoma.

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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 (July 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 billion cells experienced better 5-year event-free survival than those whose lymphoblasts did not (65% +/- 12% v 22% +/- 9%, P = .010). This difference characterized “good-risk” patients who were female (P = .014), less than age 7 at diagnosis (P = .005), or had low initial white blood cell counts (less than 20 X 10(9)/L, P = .018). Findings were similar for the 43 children with acute lymphoblastic leukemia and for the “good-risk” children in this total group. Thus, the ability of lymphoblasts to accumulate methotrexate and form methotrexate polyglutamates may be important to the curative properties of current therapy of acute lymphoblastic leukemia in children, particularly for “good-risk” patients. In such patients, inherent rather than acquired drug resistance may be the initial event leading to treatment failure.

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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 (July 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 cells experienced better 5-year event-free survival than those whose lymphoblasts did not (65% +/- 12% v 22% +/- 9%, P = .010). This difference characterized “good-risk” patients who were female (P = .014), less than age 7 at diagnosis (P = .005), or had low initial white blood cell counts (less than 20 X 10(9)/L, P = .018). Findings were similar for the 43 children with acute lymphoblastic leukemia and for the “good-risk” children in this total group. Thus, the ability of lymphoblasts to accumulate methotrexate and form methotrexate polyglutamates may be important to the curative properties of current therapy of acute lymphoblastic leukemia in children, particularly for “good-risk” patients. In such patients, inherent rather than acquired drug resistance may be the initial event leading to treatment failure.

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26

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 (December 31, 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 of All India Institute of Medical Sciences, New Delhi between 2019 September to 2021 June. Children between 1 to 18 years with high-risk B lineage Acute Lymphoblastic Leukemia planned for high-dose Methotrexate at 3gm/m² were enrolled. The measurement of serum creatinine was done at baseline, 24 and 42 hours while serum methotrexate at 24 and 42 hours, adverse reactions were assessed till day 14 of methotrexate administration. Results: The incidence of Acute Kidney Injury and severe Acute Kidney Injury (stages 2 and 3) at 42 hours of High dose Methotrexate infusion was 24.3% and 12.8% respectively. Low serum albumin was associated with an increased risk of Acute Kidney Injury (p=0.004). Transaminitis and thrombocytopenia were common toxicities. Conclusions: Acute Kidney Injury is common following High dose Methotrexate administration in B cell Acute Leukemic Leukemia. Low serum albumin level increases renal toxicity following methotrexate infusion. The measures to prevent renal toxicity should be instituted promptly in high-risk groups.

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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 (August 27, 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 therapeutic implications as treatment regimens differ for precursor B ALL as compared to mature B cell neoplasms.

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28

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 (July 18, 2015): 251–52. http://dx.doi.org/10.1007/s12185-015-1842-9.

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

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30

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 (February 1, 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 activated signaling oncoproteins to induce cell division, as inactivation of conditional E2a/Pbx1 in either factor-dependent pro-T cells or pro-T cells made factor independent by expression of Bcr/Abl resulted in pro-T-cell quiescence, while reactivation of E2a/Pbx1 restored cell division. Infusion of E2a/Pbx1 pro-T cells in mice caused T lymphoblastic leukemia and, unexpectedly, acute myeloid leukemia. The acute lymphoblastic leukemia did not evidence further maturation, suggesting that E2a/Pbx1 establishes an early block in pro-T-cell development that cannot be overcome by marrow or thymic microenvironments. In an E2a/Pbx1 pro-T thymocyte clone that induced only pro-T acute lymphoblastic leukemia, coexpression of Bcr/Abl expanded its leukemic phenotype to include acute myeloid leukemia, suggesting that unique functions of cooperating signaling oncoproteins can influence the lymphoid versus myeloid character of E2a/Pbx1 leukemia and may cooperate with E2a/Pbx1 to dictate the pre-B-cell phenotype of human leukemia containing t(1;19).

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31

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 (February 9, 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, and thrombocytopenia. Bone marrow appearance corresponds to Acute Lymphoblastic Leukemia (ALL-L2) with 60% lymphoblast infiltration and heterogeneous size into the bone marrow. The immunophenotyping results showed a population of blasts expressing CD79a positive, CD19 positive, and CD34 positive with an ALL-B Lineage effect. During treatment, the patient experienced a worsening and was declared dead. Conclusion: We report a case of an adult woman with a diagnosis of ALL L2. The diagnosis is based on clinical symptoms, laboratory examination, peripheral blood smear, bone marrow aspiration, and immunophenotyping examination.

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32

De Braekeleer, Etienne, Nathalie Douet-Guilbert, Frédéric Morel, Marie-Josée Le Bris, Christian Berthou, Claude Férec, and Marc De Braekeleer. "RUNX1amplification in B-cell acute lymphoblastic leukemia." Leukemia & Lymphoma 51, no. 2 (December 9, 2009): 329–32. http://dx.doi.org/10.3109/10428190903456967.

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33

Peterson, Michael R., Kyle J. Noskoviak, and Robert Newbury. "CD5-Positive B-Cell Acute Lymphoblastic Leukemia." Pediatric and Developmental Pathology 10, no. 1 (January 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 (February 1998): 193–95. http://dx.doi.org/10.1016/s0145-2126(97)00155-0.

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35

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

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36

Maslak, P. "Relapsed Precursor B Cell Acute Lymphoblastic Leukemia." ASH Image Bank 2003, no. 0508 (May 8, 2003): 100706. http://dx.doi.org/10.1182/ashimagebank-2003-100706.

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37

Shobhanaa, P. S., and Naveen Kakkar. "Cannibalism in Relapsed B-acute Lymphoblastic Leukemia." Indian Journal of Hematology and Blood Transfusion 34, no. 3 (February 27, 2018): 544–45. http://dx.doi.org/10.1007/s12288-018-0936-y.

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38

Helman, Sarah R., and Zeba N. Singh. "B-acute lymphoblastic leukemia with eosinophilic inclusions." Blood 141, no. 13 (March 30, 2023): 1645. http://dx.doi.org/10.1182/blood.2022018796.

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39

Suppipat, Koramit, Evelyn Zhu, and Daniel Lacorazza. "Targeting AKT Signaling in Pediatric Acute Lymphoblastic Leukemia with Sulforaphane." Blood 118, no. 21 (November 18, 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 (pre-B ALL) (approximately 30% of ALL patients). Thus, drugs able to inhibit AKT signaling are potential candidates for ALL treatment. Sulforaphane (SF) is a dietary compound found in cruciferous vegetables with well-known chemopreventive and chemotherapeutic function in solid tumors by inducing apoptosis and inhibiting survival and cell division. However, the anti-leukemic capacity of SF in hematologic malignancies has not been extensively investigated. In this study, we found increased cleavage of PARP, caspase-3, caspase-8 and caspase-9 by immunoblots in pre-B and T-ALL cell lines treated with SF (5–10 μM) for 24 –48 hours. In addition, we detected increased expression of p21 and cyclin B that correlated with a G2/M block and DNA damage observed in SF treated cells by analysis of DNA content and H2AXγ expression. Noteworthy, SF-treated pre-B and T-ALL cell lines exhibit lower levels of total and phosphorylated AKT in addition to decreased levels of total and phosphorylated mTOR, which was independent of p53 and PTEN activities. Lower survival signals upon SF treatment correlated with a dose- and time-dependent cytotoxicity in pre-B ALL cell lines (Nalm-6, REH and RS-4) and T-ALL cell lines (Jurkat, RPMI, DND-41 and KOPTK1) compared to EBV-transformed lymphoblasts used as a control. Interestingly, SF showed a synergistic effect with vincristine in pre-B and T-ALL cell lines, suggesting a potential use of SF in adjunctive therapy. Aiming to support future clinical trials, we confirmed that SF is effective in lymphoblasts from pediatric patients suffering with ALL, both pre-B and T, in a time- and dose-dependent manner (95% confidence interval IC50: pre-B ALL = 9.9 – 12.13 μM, T-ALL = 8.3 –11.00 μM). To investigate whether SF is effective in vivo in a xenograft mouse model, we injected nonobese diabetic/severe combined immunodeficient (NOD/SCID) mice with Nalm-6 cells transduced with GFP-FFluc for bioluminescent imaging detection. SF treatment (2 mg i.p. daily) significantly reduced tumor burden compared to the control group (injected with vehicle). Collectively, our data show that SF has anti-leukemic properties in ALL, both in primary samples from patients and cell lines, by inducing cell death selectively in leukemic cells likely by inhibiting AKT-dependent survival signals. Disclosures: No relevant conflicts of interest to declare.

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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 population leukemic cells was associated with a worse response to the therapy. Therefore, the initial number of such cells can be considered as a prognostic marker in acute lymphoblastic leukemia in children.

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41

Oevermann, Lena, Sebastian U. Michaelis, Markus Mezger, Peter Lang, Jacek Toporski, Alice Bertaina, Marco Zecca, Lorenzo Moretta, Franco Locatelli, and Rupert Handgretinger. "KIR B haplotype donors confer a reduced risk for relapse after haploidentical transplantation in children with ALL." Blood 124, no. 17 (October 23, 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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42

Raetz, Elizabeth A., and David T. Teachey. "T-cell acute lymphoblastic leukemia." Hematology 2016, no. 1 (December 2, 2016): 580–88. http://dx.doi.org/10.1182/asheducation-2016.1.580.

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Abstract T-cell acute lymphoblastic leukemia (T-ALL) is biologically distinct from its B lymphoblastic (B-ALL) counterpart and shows different kinetic patterns of disease response. Although very similar regimens are used to treat T-ALL and B-ALL, distinctions in response to different elements of therapy have been observed. Similar to B-ALL, the key prognostic determinant in T-ALL is minimal residual disease (MRD) response. Unlike B-ALL, other factors including age, white blood cell count at diagnosis, and genetics of the ALL blasts are not independently prognostic when MRD response is included. Recent insights into T-ALL biology, using modern genomic techniques, have identified a number of recurrent lesions that can be grouped into several targetable pathways, including Notch, Jak/Stat, PI3K/Akt/mTOR, and MAPK. With contemporary chemotherapy, outcomes for de novo T-ALL have steadily improved and now approach those observed in B-ALL, with approximately 85% 5-year event-free survival. Unfortunately, salvage has remained poor, with less than 25% event-free and overall survival rates for relapsed disease. Thus, current efforts are focused on preventing relapse by augmenting therapy for high-risk patients, sparing toxicity in favorable subsets and developing new approaches for the treatment of recurrent disease.

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43

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 (August 6, 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 are clinically classified as B-cell precursor, T-cell ALL, or mature B-cell types. Key words: Acute Lymphoblastic Leukemia, ALL, Unilateral Facial palsy, pediatric ALL.

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44

Terek, M. C., E. Ozkinay, O. Zekioglu, Y. Erhan, S. Cagirgan, M. Pehlivan, and L. Mgoyi. "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 lymphoblastic infiltration. The patient was started on induction chemotherapy consisting of vincristine, daunorubicin, prednisolone, and L-asparaginase immediately after the diagnosis. The patient died of Acinetobacter septicemia 18 days after the first admission.

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Conserva, Maria Rosa, Immacolata Redavid, Luisa Anelli, Antonella Zagaria, Francesco Tarantini, Cosimo Cumbo, Giuseppina Tota, et al. "IKAROS in Acute Leukemia: A Positive Influencer or a Mean Hater?" International Journal of Molecular Sciences 24, no. 4 (February 7, 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 can activate or repress tumor suppressors or oncogenes, regulating the survival and proliferation of leukemic cells. More than 70% of Ph+ and Ph-like cases of acute lymphoblastic leukemia exhibit IKZF1 gene variants, which are linked to worse treatment outcomes in both childhood and adult B-cell precursor acute lymphoblastic leukemia. In the last few years, much evidence supporting IKAROS involvement in myeloid differentiation has been reported, suggesting that loss of IKZF1 might also be a determinant of oncogenesis in acute myeloid leukemia. Considering the complicated “social” network that IKAROS manages in hematopoietic cells, we aim to focus on its involvement and the numerous alterations of molecular pathways it can support in acute leukemias.

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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 (December 1, 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. A total of 109 patients of newly diagnosed acute lymphoblastic leukemia aged >15 years were included. Clinical history, physical examination, complete blood counts, with peripheral smear, bone marrow aspira- tion and immunophenotypic data (using flow cytometry) and genetic study were collected for all the enrolled cases. Results: The median age at diagnosis was 24 years with male to female ratio of 1.7:1. B- lineage was predominant at (76.1%), while T -lineage was less frequent, at 23.9%. Mean hemoglobin level was 9.1 g/dl (+2.3) with a range of (4-15.2) g/dl, white blood cells count had a range of (0.4-300) ×109/L, with a mean of 47.5 ×109/L (+62.5). The mean platelet count was 79×109/L (+83), and a range of (3-490) ×109/L. Fifty eight patients (53.2%) presented with lymphadenopathy, and seventy eight patients (71.6%) had organomegaly. Philadelphia chromosome was detected in 9.5% of cases. Fifty seven (52.3%) patients stra tified into high risk group. Conclusions: Patients from our locality have some distinct disease characters from that were reported elsewhere.

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Wei, E., V. Bellamkonda, and J. Polski. "Primary Chronic Myelogenous Leukemia Blast Crisis with Precursor B Lymphoblastic Leukemia, a Case Report." American Journal of Clinical Pathology 158, Supplement_1 (November 1, 2022): S108. http://dx.doi.org/10.1093/ajcp/aqac126.228.

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Abstract Introduction/Objective Primary chronic myelogenous leukemia (CML) blast crisis at the initial disease presentation is rare. Most CML blast crisis cases present with increased myeloblasts with a minority of patients showing lymphoblastic leukemia. Differentiating primary CML lymphoblast crisis from de novo acute lymphoblastic leukemia may represent a diagnostic challenge to both pathologists and treating clinicians. This distinction is important as it has significant implications on patient management. Methods/Case Report A 15-year-old male patient was admitted to our University Hospital for hyperleukocytosis. Patient reportedly had weight loss with occasional sweats and cervical lymphadenopathy. She was found to have massive splenomegaly. Peripheral blood showed hyperleukocytosis with predominance of granulocytes at all maturation stages ranging from blast to segmented neutrophils with increased blasts. Subsequent bone marrow findings were consistent with extensive involvement by B-lymphoblastic leukemia. Ten-color Flow cytometry showed approximately 30% blasts with rare lymphocytes and monocytes. The blasts revealed precursor B-lymphoblastic immunophenotypic expression of CD45, CD10, CD19, CD20, CD22, CD34, CD38, CD200, HLA-DR and TdT expression. The results were similar to that of peripheral blood. Granulocytes showed abnormal maturation pattern with increased immature precursors and partial expression of CD4 and CD56 with no abnormalities detected in lymphocytes. In this case, while the bone marrow findings are consistent with B-lymphoblastic leukemia, the peripheral blood findings are consistent with blast phase of chronic myeloid leukemia. Further evaluation by cytogenetic and molecular studies confirmed the presence of Philadelphia chromosome, p210 transcripts, and rearrangement of BCR-ABL1, which supported the impression of precursor B-lymphoblastic leukemia in primary blast phase of CML. The patient was treated with tyrosine kinase inhibitor combined chemotherapy and went into remission. She has been followed up without significant complications for a year. Results (if a Case Study enter NA) NA. Conclusion The diagnosis of CML in primary lymphoblastic crisis is rare and needs to be systemically excluded before giving the diagnosis of de novo BCR-ABL1-positive acute lymphoblastic leukemia. If the patient does not have splenomegaly or previous leukocytosis, it needs cytological examination and extensive molecular analyses.

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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 transplantation. She was alive and doing well upon last followup. We have also reviewed the literature and discussed the clinicopathologic features of 36 MDS patients who progressed to ALL reported in the literature.

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Ilhan, Burak, Fatma Sen, Rustu Turkay, and Hasan Karanlik. "Acute B-Cell Lymphoblastic Leukemia/Acute B-Cell Lymphoblastic Lymphoma Presenting as Bilateral Breast Masses." British Journal of Medicine and Medical Research 10, no. 11 (January 10, 2015): 1–5. http://dx.doi.org/10.9734/bjmmr/2015/20637.

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50

Bousquet, Marina, Marian Harris, Beiyan Zhou, Mark D. Fleming, and Harvey Lodish. "MicroRNA Mir-125b Causes Leukemia." Blood 116, no. 21 (November 19, 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 showed an increase in white blood cell count, in particular in neutrophils and monocytes, associated with a macrocytic anemia. Among these mice, half of them died of B-cell acute lymphoblastic leukemia, T-cell acute lymphoblastic leukemia, or a myeloproliferative disorder, suggesting an important role of miR-125b in myeloid and lymphoid lineages. Co-expression of miR-125b and the BCR-ABL fusion gene in transplanted cells accelerated the development of leukemia in mice, compared to control mice expressing only BCR-ABL, suggesting that miR-125b confers a proliferative advantage to the leukemic cells. Thus we showed that the overexpression of miR-125b is sufficient to induce leukemia in vivo and decrease the latency of BCR-ABL -induced leukemia. Disclosures: No relevant conflicts of interest to declare.

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

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