ArticleLeukemia2015
Evolutionary trajectories of hyperdiploid ALL in monozygotic twins.
Article in Leukemia, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
29 citing papers in PubMed, 59 citations in OpenAlex.
- Trial
- Space-time clustering of childhood high hyperdiploid B-cell precursor acute lymphoblastic leukemia: a nationwide Swedish study.European journal of epidemiology · 2026Article
- The Eμ-Ret mouse is a novel model of hyperdiploid B-cell acute lymphoblastic leukemia.Leukemia · 2024Article
- Cross-individual cancer transmission to children during the gestational and perinatal periods.Cancer science · 2024Review
- In Utero Origins of Acute Leukemia in Children.Biomedicines · 2024Review
- PersonALL: a genetic scoring guide for personalized risk assessment in pediatric B-cell precursor acute lymphoblastic leukemia.British journal of cancer · 2023Article
- Clonal origin and development of high hyperdiploidy in childhood acute lymphoblastic leukaemia.Nature communications · 2023Article
- Oncogenic lesions and molecular subtypes in adults with B-cell acute lymphoblastic leukemia.Cancer science · 2023Review
- Hyperdiploidy: the longest known, most prevalent, and most enigmatic form of acute lymphoblastic leukemia in children.Leukemia · 2022Review
- Uncovering novel mutational signatures byCell genomics · 2022Article
- Childhood B-Cell Preleukemia Mouse Modeling.International journal of molecular sciences · 2022Review
- An alternative CYB5A transcript is expressed in aneuploid ALL and enriched in relapse.BMC genomic data · 2022Article
- A somatic UBA2 variant preceded ETV6-RUNX1 in the concordant BCP-ALL of monozygotic twins.Blood advances · 2022Article
- Sister chromatid cohesion defects are associated with chromosomal copy number heterogeneity in high hyperdiploid childhood acute lymphoblastic leukemia.Genes, chromosomes & cancer · 2021Article
- Proteogenomics and Hi-C reveal transcriptional dysregulation in high hyperdiploid childhood acute lymphoblastic leukemia.Nature communications · 2019Article
- Epigenetic Priming in Childhood Acute Lymphoblastic Leukemia.Frontiers in cell and developmental biology · 2019Review
- Interactions Between Gut Microbiota and Acute Childhood Leukemia.Frontiers in microbiology · 2019Review
- A causal mechanism for childhood acute lymphoblastic leukaemia.Nature reviews. Cancer · 2018Review
- Global efforts toward the cure of childhood acute lymphoblastic leukaemia.The Lancet. Child & adolescent health · 2018Review
- Whole-transcriptome sequencing identifies a distinct subtype of acute lymphoblastic leukemia with predominant genomic abnormalities of EP300 and CREBBP.Genome research · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Identical twins have provided unique insights on timing or sequence of genetic events in acute lymphoblastic leukaemia (ALL). To date, this has mainly focused on ALL with MLL or ETV6-RUNX1 fusions, with hyperdiploid ALL remaining less well characterised. We examined three pairs of monozygotic twins, two concordant and one discordant for hyperdiploid ALL, for single-nucleotide polymorphism (SNP)-defined copy number alterations (CNAs), IGH/L plus TCR gene rearrangements and mutations in NRAS, KRAS, FLT3 and PTPN11 genes. We performed whole exome sequencing in one concordant twin pair. Potential 'driver' CNAs were low, 0-3 per case, and all were different within a pair. One patient had an NRAS mutation that was lacking from leukaemic cells of the twin sibling. By exome sequencing, there were 12 nonsynonymous mutations found in one twin and 5 in the other, one of which in SCL44A2 was shared or identical. Concordant pairs had some identical IGH/L and TCR rearrangements. In the twin pair with discordant hyperdiploid ALL, the healthy co-twin had persistent low level hyperdiploid CD19+ cells that lacked a CNA present in the ALL cells of her sibling. From these data, we propose that hyperdiploid ALL arises in a pre-B cell in utero and mutational changes necessary for clinical ALL accumulate subclonally and postnatally.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.