Hyperdiploid B cells have been found in autoimmune NZB mice as they age. The hyperdiploid cells were found to be clonal both on the basis of cytogenetic analysis and studies of immunoglobulin gene rearrangements at the DNA level. Studies of the inheritance of the hyperdiploid traits in both F1 and backcrosses, as well as NZB recombinant inbred strains, revealed that the presence of hyperdiploid B cells was an inherited recessive trait linked to autoimmune hyperactivity. In addition, hyperdiploid B cells were found to possess a unique chromosome pair which lacked terminal C-bands. This observation allowed analysis of the fate of transferred NZB hyperdiploid B cells into unirradiated recipients. The hyperdiploid B cells were found to expand in recipients and become the dominant population in several lymphoid organs. Spontaneously occurring hyperdiploid B cells were not observed in NZB-xid mice possessing the CBA/N X chromosome, which confers abnormal B cell maturation and results in decreased autoimmunity in NZB-xid mice. Following the discovery that CD5+ B cells were elevated in certain autoimmune states, hyperdiploid B cells were examined and found to be CD5+ B cells as well. The malignant cell in chronic lymphocytic leukemia is also a CD5+ B cell. The hyperdiploid B cells of NZB mice appear to have many of the features of autoimmune B cells, as well as malignant cells.
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Zhongguo Shi Yan Xue Ye Xue Za Zhi
December 2024
Shaanxi Institute for Pediatric Diseases, Shaanxi Provincial Key Laboratory of Children's Health and Diseases, Xi'an Children's Hospital, Shaanxi Province, China.
Objective: To analyze the expression of B-cell development-related genes in acute B lymphoblastic leukemia (B-ALL), and to explore the relationship between B-cell development-related genes and the prognosis of B-ALL patients.
Methods: The GEO and TARGET databases were integrated to analyze the differential expression of B-cell development-related genes between the healthy persons and B-ALL patients and their differential expression in the B-ALL relapse and non-relapse groups. Cox single factor regression and Lasso regression were used to constructe a B-ALL specific prognosis model of B-cell development-related genes.
Sci Rep
November 2024
Department of Clinical and Molecular Medicine, Norwegian University of Science and Technology (NTNU), Trondheim, Norway.
Zhongguo Dang Dai Er Ke Za Zhi
July 2024
Department of Hematology and Oncology, Kunming Children's Hospital/Children's Hospital Affiliated to Kunming Medical University, Kunming 650228, China.
Objectives: To investigate the expression of CD123 in children with acute lymphoblastic leukemia (ALL) and its effect on the clinical characteristics and prognosis of children with B-lineage acute lymphoblastic leukemia (B-ALL).
Methods: A retrospective analysis was conducted on the clinical data of 251 children with ALL who were admitted to the Department of Hematology and Oncology, Children's Hospital of Kunming Medical University, from December 2019 to June 2022. According to the expression of CD123 at initial diagnosis, the children were divided into CD123 group and CD123 group, and the two groups were compared in terms of clinical characteristics and treatment outcome.
Blood
September 2024
Division of Clinical Genetics, Department of Laboratory Medicine, Lund University, Lund, Sweden.
B-cell progenitor acute lymphoblastic leukemia (BCP-ALL) is the most common childhood malignancy and is driven by multiple genetic alterations that cause maturation arrest and accumulation of abnormal progenitor B cells. Current treatment protocols with chemotherapy have led to favorable outcomes but are associated with significant toxicity and risk of side effects, highlighting the necessity for highly effective, less toxic, targeted drugs, even in subtypes with a favorable outcome. Here, we used multimodal single-cell sequencing to delineate the transcriptional, epigenetic, and immunophenotypic characteristics of 23 childhood BCP-ALLs belonging to the BCR::ABL1+, ETV6::RUNX1+, high hyperdiploid, and recently discovered DUX4-rearranged (DUX4-r) subtypes.
View Article and Find Full Text PDFGenome Biol
June 2024
Computational Genomics and Bioinformatics Branch, Center for Biomedical Informatics and Information Technology (CBIIT), National Cancer Institute, Rockville, MD, USA.
Background: Copy number variation (CNV) is a key genetic characteristic for cancer diagnostics and can be used as a biomarker for the selection of therapeutic treatments. Using data sets established in our previous study, we benchmark the performance of cancer CNV calling by six most recent and commonly used software tools on their detection accuracy, sensitivity, and reproducibility. In comparison to other orthogonal methods, such as microarray and Bionano, we also explore the consistency of CNV calling across different technologies on a challenging genome.
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