Relevant bibliographies by topics / B-acute lymphoblastic leukemia

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  2. Dissertations / Theses
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Academic literature on the topic 'B-acute lymphoblastic leukemia'

Author: Grafiati
Published: 25 May 2024

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Journal articles on the topic "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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Dissertations / Theses on the topic "B-acute lymphoblastic leukemia"

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Oliveira, Tiago M. "The importance of glycosylation in Acute Lymphoblastic Leukemia." Thesis, Griffith University, 2021. http://hdl.handle.net/10072/410463.

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Acute leukemias, such as acute lymphoblastic leukemia (ALL), are aggressive cancers characterized by the rapid proliferation of malignant hematopoietic cells. Throughout the last 60 years, childhood ALL’s long-term survival rates increased from less than 10% to more than 90%. Despite these improvements, certain subtypes remain hard to manage (e.g. mixed lineage leukemia, MLL-r), and even new therapies frequently fail. Therefore, identifying leukemia-cell restricted antigens in these ALL subtypes remains crucial in the quest to develop novel diagnostic tools and specific treatments. Traditionally, ALL research has mostly been focusing on genomics and transcriptomics efforts, mainly due to the limited amounts of patient material, and technical difficulties throughout sample processing. The potential encompassed in the use of other -omics technologies has remained unexplored in the context of ALL. For the work presented in this thesis, I have focused on undertaking the first comprehensive characterisation of glycocalyx alterations that occur in ALL and particularly in MLL-r in primary, patient derived cancer cells. This work supports the concept that the glycocalyx of ALL and MLL-r cells undergoes dramatic alterations that clearly differentiate these cells from healthy precursor B- (pre-B) cells. These findings might open doors towards novel potential diagnostic and therapeutic targets. The studies encompassed in chapters III, IV and V were performed in collaboration with Prof. Eleonora Heisterkamp’s team at the Beckman Research Institute (City of Hope, CA, USA). I have performed the first multi-omics analyses of primary patient MLL-r cells by integrating data from the transcriptome, glycome, and proteome of these cells. These results revealed that MLL-r cells exhibit distinct glycosylation features that differentiate them from healthy pre-B cells, which I was able to correlate with alterations at the transcript level of relevant glycosyltransferases. In depth proteome analyses revealed an overall good correlation between proteomics and transcriptomics findings, but also uncovered numerous examples where significant changes were just found in one but not the other approach. Nevertheless, this integrated approach used for the systematic evaluation of MLL-r allowed to obtain significant data for putative novel diagnostic/therapeutic protein markers and revealed important features of the disease that remained elusive until now. I was also able to apply the developed integrated multi-omics workflow to investigate the protective role of the surrounding microenvironment and its impact in environmentmediated drug resistance (EMDR) of pre-B ALL cells, which remains a major obstacle for the efficacy of chemotherapeutics in patients. To date the relevance of glycoconjugates for the development of EMDR has been largely unexplored. I explored a long-term co-culture system using human pre-B ALL cells and mitotically inactivated supporting murine stromal cells (OP9 cells), where pre-B ALL cells were put under a selective pressure to survive in the presence of vincristine, a widely used chemotherapeutic drug. I have performed a multi-omics analyses to understand the effect vincristine-resistance has on the cells' glycocalyx. These results demonstrated both glycome-wide and glycoprotein site-specific alterations, which could potentially be employed to identify emerging drug-resistance at an earlier stage or possibly serve as treatment targets in pre-B ALL. Throughout these studies, I have observed a significant modulation of the sialylation profile on pre-B ALL cells in patients and during EMDR development. Unsurprisingly, changes in sialylation have frequently been linked with development and progression of many cancer types but remain largely unexplored in the context of pre-B ALL. I investigated the impact of the major sialyltransferase, ST6Gal1, on the glycome of pre-B ALL cells. ST6Gal1 is the transferase known to be largely responsible for attaching sialic acids in an a2-6 linkage onto N-glycans. Surprisingly, these results demonstrated that a ST6GAL1 knockout did not ablate the production of a2-6 sialylated N-glycans, unless these N-glycans carried a core fucose residue. Demonstrating for the first time how core-fucosylation regulates a2-6 sialylation also allowed me to unravel the existence of ST6Gal1 independent, alternative a2-6 sialylation pathways that are specific for non-fucosylated N-glycans. I demonstrated that ST6GalNAc3-6 are capable to produce a2-6 sialylated N-glycans in the absence of core-fucose and that ST6Gal1 is required to introduce a2-6 sialylation on corefucosylated N-glycans. These results challenge long standing dogmas in glycobiology while delivering a novel understanding of hitherto unknown mechanism that regulate protein glycosylation, which will have a significant impact on our understanding of glycosylation changes in health and disease.
Thesis (PhD Doctorate)
Doctor of Philosophy (PhD)
Institute for Glycomics
Griffith Health
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Besada, Rana Hany. "BiTEs and CAR-Ts : immunotherapy in childhood B-cell acute lymphoblastic leukemia." Thesis, Massachusetts Institute of Technology, 2018. http://hdl.handle.net/1721.1/115699.

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Thesis: S.M., Massachusetts Institute of Technology, Department of Biology, 2018.
Cataloged from PDF version of thesis.
Includes bibliographical references (pages 18-21).
B-cell acute lymphoblastic leukemia is the most common pediatric cancer, responsible for the most cancer-related deaths in children. Advances in chemotherapy over the past half-century have steadily increased the remission and survival of children with B-cell acute lymphoblastic leukemia to nearly 90%. However, the problems of minimal residual disease and relapsed and refractory disease persist. Personalized, targeted therapies have improved outcomes among the minority of patients for whom chemotherapy is ineffective. Immunotherapy, specifically bispecific T-cell engaging antibody therapy and chimeric antigen receptor T-cell therapy, has proven an effective treatment for relapsed and refractory B-cell acute lymphoblastic leukemia in children. These new modalities, however, have also introduced new adverse side effects to the treatment regimen. Though immunotherapy has increased remission and survival, more work must be done to reduce adverse effects and eliminate relapsed and refractory disease.
by Rana Hany Besada.
S.M.
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Morisot, Sebastien. "Détermination of the frequency of leukemia stem cells in childhood precursor B cell acute lymphoblastic leukemias." Paris 11, 2009. http://www.theses.fr/2009PA11T022.

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Soto-Feliciano, Yadira M. (Yadira Marie). "PHF6 is a novel regulator of B-cell identity in acute lymphoblastic leukemia." Thesis, Massachusetts Institute of Technology, 2016. http://hdl.handle.net/1721.1/103165.

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Thesis: Ph. D., Massachusetts Institute of Technology, Department of Biology, 2016.
This electronic version was submitted by the student author. The certified thesis is available in the Institute Archives and Special Collections.
Cataloged from student-submitted PDF version of thesis. Vita.
Includes bibliographical references.
Mutations in the zinc finger gene PHF6 are seen in approximately 20% of adult T-cell acute lymphoblastic leukemias and 3% of adult acute myeloid leukemias. The notable absence of PHF6 mutations in B-cell lineage malignancies has led to the hypothesis that PHF6 may act as a lineage-specific tumor suppressor gene. Recent work from our group described a role for PHF6 as a positive regulator of growth in B-cell acute lymphoblastic leukemia (B-ALL). To identify the mechanisms by which PHF6 acts to promote B-ALL growth in vivo, we utilized CRISPR-Cas9 to delete Phf6 in murine B-ALL cells. Transplantation of Phf6 knockout cells (Phf6KO) into immunocompetent recipients significantly extended disease latency and survival. Strikingly, these mice developed lymphomas, characterized by significantly enlarged lymph nodes, decreased disease burden in the spleen and increased expression of the canonical T-cell marker CD4, suggesting that Phf6KO B-ALL cells adopt alternate lineage programs in vivo. To dissect the molecular mechanisms by which Phf6 regulates this lineage decision, we carried out a combination of RNA and chromatin immunoprecipitation (ChIP-Seq) sequencing analyses in Phf6WT and Phf6KO cells. RNA sequencing analysis revealed many differentially expressed genes in Phf6KO B-ALL cells. Notably, genes and gene sets that were significantly down-regulated in Phf6KO cells included those involved in pathways important for B-cell development and function. ChIP-Seq analysis of PHF6 and several histone marks revealed that PHF6 and H3K27ac signals co-localize close to the transcription start site and enhancer regions of a significant proportion of differentially expressed genes. Transcription factor binding motif analysis revealed significant enrichment for several well-described transcriptional regulators of B-cell development. Importantly, we demonstrated that the transcription factors TCF12 and NF-kB co-immunoprecipitated with PHF6 in Phf6WT B-ALL cells. These findings discovered a novel role for PHF6 in the maintenance of B-cell identity in B-ALL, by activating genes that are crucial for B-cell lineage maintenance. Collectively, these results indicate that loss-of-function of Phf6 in B-ALL leads to an unstable cell identity state, in which cells need to acquire alternate developmental programs in order to survive. These findings could potentially explain the absence of PHF6 mutations in human B-cell lineage malignancies.
by Yadira M. Soto-Feliciano.
Ph. D.
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James, Alva Rani [Verfasser]. "LncRNAs signature defining major subtypes of B-cell acute lymphoblastic leukemia / Alva Rani James." Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2019. http://d-nb.info/1189140330/34.

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Nicoletti, Simon. "Natural Killer Cells and Pre-B Acute Lymphoblastic Leukemia : Evidence for an Unconventional Cytotoxicity Pathway." Thesis, Université Paris-Saclay (ComUE), 2017. http://www.theses.fr/2017SACLS383.

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Les cellules Natural Killer (NK) représentent une population de cellules innées lymphoïdes aux fonctions anti-infectieuses et antitumorales. Les leucémies aiguës lymphoblastiques pré-B (LAL pré-B) constituent le cancer de l’enfant le plus fréquent et ont été décrites comme résistantes à la cytotoxicité médiée par les NK bien que les bases moléculaires demeurent inconnues.L’objectif de ces travaux a été de caractériser cette résistance. En développant un essai de cytotoxicité par cytométrie en flux et en utilisant des cellules effectrices activées in vitro, nous avons établi la sensibilité retardée des LAL pré-B à la cytotoxicité NK : initialement résistantes après 4h d’incubation, elles sont fortement tuées après 25h.Cette cytotoxicité est contact-dépendante mais ni la voie de l’exocytose des granules cytotoxiques ni celle des récepteurs de mort n’y contribuent. La mort cellulaire des cibles est de profil apoptotique mais indépendante des caspases ; la signalisation mitochondriale l’amplifie partiellement. Interférer avec les dérivés de l’oxygène par un antioxydant diminue la cytotoxicité. Nous montrons que les cellules NK de patients atteints de granulomatose septique chronique liée à l’X présentent un défaut de cette nouvelle cytotoxicité. Nous démontrons l’expression par les NK des composants clefs d’une NADPH oxydase distincte du complexe utilisé par les phagocytes. Nos travaux établissent l’existence d’une voie de cytotoxicité non conventionnelle et en définissent les principaux prérequis moléculaires
Natural Killer (NK) cells are innate lymphoid cells with anti-infectious and anti-tumoral activities. Among neoplasia, pre-B acute lymphoblastic leukemias (pre-B ALL) represent the most common form of cancer in childhood and were shown to be resistant to NK cell mediated cytotoxicity although the mechanisms explaining this phenomenon are incompletely understood.In the present work, we investigated the relative immune resistance of pediatric pre-B ALL targets to activated NK cells. We developed a flow cytometry based cytotoxicity assay to assess the NK activity and the involvement of long term cytotoxic pathways. Although pre-B ALL blasts were strongly resistant at 4h, we found a considerable delayed NK killing at 25h.Further investigations revealed that cell contact was mandatory for efficient killing but also that neither the granule exocytosis nor the death receptor pathway were involved. Target cell death was caspase independent but mitochondria signaling amplified it. We then showed that NK cells from patients with X-linked chronic granulomatous disease could not kill efficiently ALL blasts and that NK cells expressed key components of a NADPH oxidase complex that was distinct from the phagocyte type. Our work reveals an uncharacterized effector pathway among cytotoxic lymphocytes and establishes key molecular requirements for this unconventional pathway
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Ueno, Hiroo. "Landscape of driver mutations and their clinical impacts in pediatric B-cell precursor acute lymphoblastic leukemia." Doctoral thesis, Kyoto University, 2021. http://hdl.handle.net/2433/263562.

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Sartor, Chiara <1988&gt. "Research of predictive biomarkers to anti-CD22 antibody-drug conjugate treatment in B-cell acute lymphoblastic leukemia." Doctoral thesis, Alma Mater Studiorum - Università di Bologna, 2022. http://amsdottorato.unibo.it/10252/1/PhD%20thesis_Chiara%20Sartor_XXXIV%20ciclo.pdf.

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Background: The treatment of B-cell acute lymphoblastic leukemia (B-ALL) has been enriched by novel agents targeting surface markers CD19 and CD22. Inotuzumab ozogamicin (INO) is a CD22-calicheamicin conjugated monoclonal antibody approved in the setting of relapse/refractory (R/R) B-ALL able to induce a high rate of deep responses, not durable over time. Aims: This study aims to identify predictive biomarkers to INO treatment in B- ALL by flow cytometric analysis of CD22 expression and gene expression profile. Materials and methods: Firstly, the impact on patient outcome in 30 R/R B-ALL patients of baseline CD22 expression in terms of CD22 blast percentage and CD22 fluorescent intensity (CD22-FI) was explored. Secondly, baseline gene expression profile of 18 R/R B-ALL patient samples was analyzed. For statistical analysis of differentially expressed genes (DEGs) patients were divided in non-responders (NR), defined as either INO-refractory or with duration of response (DoR) < 3 months, and responders (R). Gene expression results were analyzed with Ingenuity pathway analysis (IPA). Results: In our patient set higher CD22-FI, defined as higher quartiles (Q2-Q4), correlated with better patient outcome in terms of CR rate, OS and DoR, compared to lower CD22-FI (Q1). CD22 blast percentage was less able to discriminate patients’ outcome, although a trend for better outcome in patients with CD22 ≥ 90% could be appreciated. Concerning gene expression profile, 32 genes with corrected p value <0.05 and absolute FC ≥2 were differentially expressed in NR as compared to R. IPA upstream regulator and regulator effect analysis individuated the inhibition of tumor suppressor HIPK2 as causal upstream condition of the downregulation of 6 DEGs. Conclusions: CD22-FI integrates CD22-percentage on leukemic blasts for a more comprehensive target pre-treatment evaluation. Moreover, a unique pattern of gene expression signature based on HIPK2 downregulation was identified, providing important insights in mechanisms of resistance to INO.
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Auer, Franziska [Verfasser], Arndt [Gutachter] Borkhardt, and Hermann [Gutachter] Aberle. "Paired Box 5 (PAX5) in B cell precursor acute lymphoblastic leukemia / Franziska Auer ; Gutachter: Arndt Borkhardt, Hermann Aberle." Düsseldorf : Universitäts- und Landesbibliothek der Heinrich-Heine-Universität Düsseldorf, 2017. http://d-nb.info/1123197628/34.

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Groeneveld-Krentz, Stefanie [Verfasser]. "The clinical relevance of aneuploidy in relapses of pediatric B-cell precursor acute lymphoblastic leukemia / Stefanie Groeneveld-Krentz." Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2020. http://d-nb.info/1223927180/34.

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Books on the topic "B-acute lymphoblastic leukemia"

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St-Denis, Emily Jean. The progression of precursor B cell acute lymphoblastic leukemia in murine models. 2005.

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Book chapters on the topic "B-acute lymphoblastic leukemia"

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Fukano, Reiji. "Mature B-Cell Acute Lymphoblastic Leukemia." In Pediatric Acute Lymphoblastic Leukemia, 73–80. Singapore: Springer Singapore, 2019. http://dx.doi.org/10.1007/978-981-15-0548-5_8.

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Gastier-Foster, Julie M. "Precursor B-Cell Acute Lymphoblastic Leukemia." In Molecular Pathology Library, 287–307. Boston, MA: Springer US, 2010. http://dx.doi.org/10.1007/978-1-4419-5698-9_24.

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Gorczyca, Wojciech. "B-Cell Acute Lymphoblastic Leukemia/Lymphoma." In Flow Cytometry in Neoplastic Hematology, 495–516. 4th ed. Boca Raton: CRC Press, 2022. http://dx.doi.org/10.1201/9781003197935-17.

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Ghanem, Hady, Hagop Kantarjian, Nitin Jain, and Elias Jabbour. "Management of B-Cell Acute Lymphoblastic Leukemia." In Cancer Consult: Expertise for Clinical Practice, 22–28. Oxford, UK: John Wiley & Sons, Ltd, 2014. http://dx.doi.org/10.1002/9781118589199.ch3.

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Hogan, Laura E., Luke D. Maese, Keith J. August, and Jennifer L. McNeer. "Treatment of Pediatric B- and T-Cell Acute Lymphoblastic Leukemia." In Clinical Management of Acute Lymphoblastic Leukemia, 75–104. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-030-85147-7_4.

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Roberts, Kathryn G., and Charles G. Mullighan. "Molecular Pathways and Targets in B-Cell Progenitor Acute Lymphoblastic Leukemia." In Clinical Management of Acute Lymphoblastic Leukemia, 3–32. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-030-85147-7_1.

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Gorczyca, Wojciech. "B-Cell Acute Lymphoblastic Leukemia/Lymphoma (B-ALL/LBL)." In Atlas of Differential Diagnosis in Neoplastic Hematopathology, 663–78. 4th ed. Boca Raton: CRC Press, 2021. http://dx.doi.org/10.1201/9781003120445-40.

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Molina, John C., and Nirali N. Shah. "Monoclonal Antibody-Based Treatment and Other New Agents for B-Lineage Acute Lymphoblastic Leukemia." In Clinical Management of Acute Lymphoblastic Leukemia, 295–328. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-030-85147-7_13.

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Larson, R. A., C. D. Bloomfield, and C. A. Schiffer. "Cancer and Leukemia Group B Studies in Acute Lymphoblastic Leukemia." In Haematology and Blood Transfusion / Hämatologie und Bluttransfusion, 420–26. Berlin, Heidelberg: Springer Berlin Heidelberg, 1994. http://dx.doi.org/10.1007/978-3-642-78350-0_75.

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Kulhalli, Rahul, Chinmay Savadikar, and Bhushan Garware. "Toward Automated Classification of B-Acute Lymphoblastic Leukemia." In Lecture Notes in Bioengineering, 63–72. Singapore: Springer Singapore, 2019. http://dx.doi.org/10.1007/978-981-15-0798-4_7.

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Conference papers on the topic "B-acute lymphoblastic leukemia"

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Ain, N. U., A. Kainat, A. Hurera, and J. Bierenbaum. "Acute Adult B-lymphoblastic Leukemia Presenting as Hypercalcemia." In American Thoracic Society 2024 International Conference, May 17-22, 2024 - San Diego, CA. American Thoracic Society, 2024. http://dx.doi.org/10.1164/ajrccm-conference.2024.209.1_meetingabstracts.a3389.

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Dobson, Stephanie M., Robert Vanner, Esmé Waanders, Jessica McLeod, Olga I. Gan, Zhaohui Gu, Debbie Payne-Turner, et al. "Abstract A25: Evolving functional heterogeneity in B-acute lymphoblastic leukemia." In Abstracts: Fourth AACR International Conference on Frontiers in Basic Cancer Research; October 23-26, 2015; Philadelphia, PA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.fbcr15-a25.

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Dobson, Stephanie M., Robert Vanner, Esmé Waanders, Olga I. Gan, Jessica McLeod, Ildiko Grandal, Debbie Payne-Turner, et al. "Abstract LB-341: Evolving functional heterogeneity in B-acute lymphoblastic leukemia." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-lb-341.

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Kane, Shriya, Yali Ding, Chandrika Gowda, Jonathon Lee Payne, Soumya Iyer, Pavan K. Dhanyamraju, Chunhua Song, et al. "Abstract 2927: Targeted combination treatment for B-cell acute lymphoblastic leukemia." In Proceedings: AACR Annual Meeting 2020; April 27-28, 2020 and June 22-24, 2020; Philadelphia, PA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.am2020-2927.

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Spinella, Jean-François, Virginie Saillour, Chantal Richer, Manon Ouimet, Pauline Cassart, Jasmine Healy, Eric Bareke, et al. "Abstract 4335: The genomic landscape of childhood pre-B acute lymphoblastic leukemia." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-4335.

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Zanetti, SR, T. Velazco-Hernandez, F. Gutierrez-Agüera, H. Roca-Ho, D. Sánchez-Martínez, P. Petazzi, R. Torres, et al. "CD19 and CD22-directed biespecific CAR for B-cell Acute Lymphoblastic Leukemia." In 32. Jahrestagung der Kind-Philipp-Stiftung für pädiatrisch onkologische Forschung. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-1687121.

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Schröder, C. F., Ž. Antić, U. zur Stadt, M. Tang, M. Zimmermann, C. Eckert, B. Fedders, M. Stanulla, G. Cario, and A. K. Bergmann. "Comprehensive molecular and clinical characterization of DUX4-rearranged B-acute lymphoblastic leukemia." In 34. Jahrestagung der Kind-Philipp-Stiftung für pädiatrisch onkologische Forschung. Georg Thieme Verlag, 2023. http://dx.doi.org/10.1055/s-0043-1768545.

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Liu, S., Q. Sun, K. M. Debatin, and L. H. Meyer. "Effective targeting of Wnt Signaling in B Cell Precursor Acute Lymphoblastic Leukemia." In 34. Jahrestagung der Kind-Philipp-Stiftung für pädiatrisch onkologische Forschung. Georg Thieme Verlag, 2023. http://dx.doi.org/10.1055/s-0043-1768528.

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Lenk, L., M. Carlet, A. Cousins, G. Cario, C. Halsey, I. Jeremias, E. Hobeika, H. Jumaa, A. Alsadeq, and DM Schewe. "CD79a/CD79b Promote CNS-Involvement and Leukemic Engraftment in Pediatric B-cell Precursor Acute Lymphoblastic Leukemia." In 33. Jahrestagung der Kind-Philipp-Stiftung für pädiatr. onkolog. Forschung. © Georg Thieme Verlag KG, 2020. http://dx.doi.org/10.1055/s-0040-1709765.

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Chen, Zhengshan, Seyedmehdi Shojaee, Maike Buchner, Huimin Geng, Jae Woong Lee, Lars Klemm, Eugene Park, et al. "Abstract 2075: Signaling thresholds and negative B cell selection in acute lymphoblastic leukemia." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-2075.

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