ReviewCancer metastasis reviews2020
Insights into the prenatal origin of childhood acute lymphoblastic leukemia.
Review in Cancer metastasis reviews, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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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.
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Who cites it
42 citing papers in PubMed, 68 citations in OpenAlex.
- Modulation of theInternational journal of molecular sciences · 2025Trial
- A genomic and epigenomic lens into the biology of acute lymphoblastic leukaemia.Nature reviews. Cancer · 2026Review
- Cancer-associated fusion transcripts: mechanisms, functional roles, and clinical implications.Clinical and experimental medicine · 2026Review
- Article
- RAG-mediated structural variation and its impact on relapse risk in acute lymphoblastic leukemia.medRxiv : the preprint server for health sciences · 2026Article
- Detection of AdenoviralInternational journal of molecular sciences · 2026Article
- Pediatric leukemia: origins, pathogenesis, the role of microenvironment and immunological modulation.Frontiers in immunology · 2026Review
- Ambient Fine Particulate Matter, Residential Greenness, and Childhood Cancer Risk by Trimester of Exposure in Minnesota 2000 to 2014: A Case-Control Study.Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology · 2025Article
- Ontogeny-specific induction of the KMT2A::AFF1-fusion drives development of a distinct CD24 positive pre-leukemic state.Leukemia · 2025Article
- Immune-aging at diagnosis determines T-cell recovery in childhood leukemia survivors.npj aging · 2025Article
- Exploring Biochemical Characteristics of Pediatric Hyperdiploid Acute Lymphoblastic Leukemia by Raman Spectroscopy.Analytical chemistry · 2025Article
- Genetic instability in HSPC subpopulations of umbilical cord blood from patients with childhood acute lymphoblastic leukemia.Scientific reports · 2025Article
- T cell exhaustion in pediatric B-ALL: current knowledge and future perspectives.Frontiers in immunology · 2025Review
- Article
- PROteolysis-Targeting Chimeras (PROTACs) in leukemia: overview and future perspectives.MedComm · 2024Review
- Article
- In Utero Origins of Acute Leukemia in Children.Biomedicines · 2024Review
- Article
- The dark side of stemness - the role of hematopoietic stem cells in development of blood malignancies.Frontiers in oncology · 2024Review
- Comprehensive genetic analyses of childhood acute leukemia in Iraq using next-generation sequencing.Translational pediatrics · 2023Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Pediatric acute lymphoblastic leukemia (ALL) is defined by recurrent chromosomal aberrations including hyperdiploidy and chromosomal translocations. Many of these aberrations originate in utero and the cells transform in early childhood through acquired secondary mutations. In this review, we will discuss the most common prenatal lesions that can lead to childhood ALL, with a special emphasis on the most common translocation in childhood ALL, t(12;21), which results in the ETV6-RUNX1 gene fusion. The ETV6-RUNX1 fusion arises prenatally and at a 500-fold higher frequency than the corresponding ALL. Even though the findings regarding the frequency of ETV6-RUNX1 were originally challenged, newer studies have confirmed the higher frequency. The prenatal origin has also been proven for other gene fusions, including KMT2A, the translocations t(1;19) and t(9;22) leading to TCF3-PBX1 and BCR-ABL1, respectively, as well as high hyperdiploidy. For most of these aberrations, there is evidence for more frequent occurrence than the corresponding leukemia incidences. We will briefly discuss what is known about the cells of origin, the mechanisms of leukemic transformation through lack of immunosurveillance, and why only a part of the carriers develops ALL.
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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.