ReviewLeukemia2022
Hyperdiploidy: the longest known, most prevalent, and most enigmatic form of acute lymphoblastic leukemia in children.
Review in Leukemia, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed.
- Identification of favorable subgroups of pediatric high-hyperdiploid acute lymphoblastic leukemia-A retrospective multinational study.HemaSphere · 2026Article
- Personalized reference genome-based pipeline reveals comprehensive haplotype-resolved views of cancer genomes.bioRxiv : the preprint server for biology · 2026Article
- IntegrateALL: An end-to-end RNA-seq analysis pipeline for multilevel data extraction and interpretable subtype classification in B-precursor ALL.HemaSphere · 2026Article
- Single Nucleotide Polymorphism Microarray Analysis Unveils Copy-Number Abnormalities and Genetic Heterogeneity in Malaysian Childhood B-Cell Precursor Acute Lymphoblastic Leukemia.Molecular genetics & genomic medicine · 2026Article
- Article
- Pediatric leukemia: origins, pathogenesis, the role of microenvironment and immunological modulation.Frontiers in immunology · 2026Review
- Diagnostic performance of DNA index for detection of high hyperdiploidy in childhood B-cell acute lymphoblastic leukemia.PloS one · 2026Article
- CanID: A Robust and Accurate RNA-seq Expression-based Diagnostic Classification Scheme for Pediatric Malignancies.Genomics, proteomics & bioinformatics · 2025Article
- Cytogenetic landscape aberrations in paediatric acute lymphoblastic leukaemia - a polish paediatric population treated according to ALL-IC BFM 2009 protocol.Scientific reports · 2025Article
- Exploring Biochemical Characteristics of Pediatric Hyperdiploid Acute Lymphoblastic Leukemia by Raman Spectroscopy.Analytical chemistry · 2025Article
- Single-cell DNA and surface protein characterization of high hyperdiploid acute lymphoblastic leukemia at diagnosis and during treatment.HemaSphere · 2025Article
- The Molecular Pathology of Blood Cancer: A Comprehensive Review of Chromosome and Genetic Abnormalities and Their Clinical Utility.British journal of biomedical science · 2025Review
- Clinical characteristics and prognostic analysis of different fusion gene abnormalities in childhood acute lymphoblastic leukaemia.Frontiers in oncology · 2025Article
- Clinical Risk Factors for High-Dose Methotrexate-Induced Oral Mucositis Following Individualized Dosing.Cancer medicine · 2024Article
- The Eμ-Ret mouse is a novel model of hyperdiploid B-cell acute lymphoblastic leukemia.Leukemia · 2024Article
- Review
- Overexpression of Nrf2 in bone marrow mesenchymal stem cells promotes B-cell acute lymphoblastic leukemia cells invasion and extramedullary organ infiltration through stimulation of the SDF-1/CXCR4 axis.Frontiers in pharmacology · 2024Article
- Hyperdiploid acute lymphoblastic leukemia in children withHemaSphere · 2024Article
- Chromosomal instability in aneuploid acute lymphoblastic leukemia associates with disease progression.EMBO molecular medicine · 2024Article
- Comprehensive genomic characterization of hematologic malignancies at a pediatric tertiary care center.Frontiers in oncology · 2024Article
Corrections and comments
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2 authors.
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Abstract
Hyperdiploidy is the largest genetic entity B-cell precursor acute lymphoblastic leukemia in children. The diagnostic hallmark of its two variants that will be discussed in detail herein is a chromosome count between 52 and 67, respectively. The classical HD form consists of heterozygous di-, tri-, and tetrasomies, whereas the nonclassical one (usually viewed as "duplicated hyperhaploid") contains only disomies and tetrasomies. Despite their apparently different clinical behavior, we show that these two sub-forms can in principle be produced by the same chromosomal maldistribution mechanism. Moreover, their respective array, gene expression, and mutation patterns also indicate that they are biologically more similar than hitherto appreciated. Even though in-depth analyses of the genomic intricacies of classical HD leukemias are indispensable for the elucidation of the disease process, the ensuing results play at present surprisingly little role in treatment stratification, a fact that can be attributed to the overall good prognoses and low relapse rates of the concerned patients and, consequently, their excellent treatment outcome. Irrespective of this underutilization, however, the detailed genetic characterization of HD leukemias may, especially in planned treatment reduction trials, eventually become important for further treatment stratification, patient management, and the clinical elucidation of outcome data. It should therefore become an integral part of all upcoming treatment studies.
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