ArticleLeukemia2001
Molecular characterization of genomic AML1-ETO fusions in childhood leukemia.
Article in Leukemia, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT00015587 (Chemical Exposures and Leukemia Risks and Childhood Leukemia and Environmental Exposure), which is not on this map. Cited by 15 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.
Chemical Exposures and Leukemia Risks and Childhood Leukemia and Environmental Exposure
Who cites it
15 citing papers in PubMed, 48 citations in OpenAlex.
- Functional analysis of structural variants in single cells using Strand-seq.Nature biotechnology · 2023Article
- Breaking down RET breakpoints in lung adenocarcinoma.Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer · 2014Article
- Amplification and thrifty single-molecule sequencing of recurrent somatic structural variations.Genome research · 2014Article
- Targeted next-generation sequencing at copy-number breakpoints for personalized analysis of rearranged ends in solid tumors.PloS one · 2014Article
- The genetic basis of phenotypic heterogeneity in myelodysplastic syndromes.Nature reviews. Cancer · 2012Review
- Identification of a new translocation that disrupts the RUNX1 gene in a patient with de novo acute myeloid leukemia.Medical oncology (Northwood, London, England) · 2012Article
- T(1;21;8)(p34;q22;q22): a novel variant of t(8;21) in acute myeloblastic leukemia with maturation.Medical oncology (Northwood, London, England) · 2011Article
- Rapid high-resolution mapping of balanced chromosomal rearrangements on tiling CGH arrays.The Journal of molecular diagnostics : JMD · 2011Article
- Characterization of a t(5;8)(q31;q21) translocation in a patient with mental retardation and congenital heart disease: implications for involvement of RUNX1T1 in human brain and heart development.European journal of human genetics : EJHG · 2009Article
- The molecular anatomy of the FIP1L1-PDGFRA fusion gene.Leukemia · 2009Article
- Genetic susceptibility to childhood leukaemia.Radiation protection dosimetry · 2008Review
- The 8;21 translocation in leukemogenesis.Oncogene · 2004Review
- Site-specific translocation and evidence of postnatal origin of the t(1;19) E2A-PBX1 fusion in childhood acute lymphoblastic leukemia.Proceedings of the National Academy of Sciences of the United States of America · 2002Article
- Chromosome translocations and covert leukemic clones are generated during normal fetal development.Proceedings of the National Academy of Sciences of the United States of America · 2002Article
- Genomic DNA breakpoints in AML1/RUNX1 and ETO cluster with topoisomerase II DNA cleavage and DNase I hypersensitive sites in t(8;21) leukemia.Proceedings of the National Academy of Sciences of the United States of America · 2002Article
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
Abstract
T(8;21) AML1(CBFA2)-ETO(MTG8) is the most common chromosomal translocation in acute myeloid leukemia (AML) in both children and adults. We sought to understand the structure and gain insight into the fusion process between AML1 and ETO by sequencing genomic fusions in 17 primary childhood AMLs and two cell lines with t(8;21). Reciprocal translocations were sequenced for seven of the 19 samples. We assumed a null hypothesis that the translocation breakpoints would be evenly distributed along the intronic breakpoint cluster regions. Testing for multimodality via smoothed bootstrap statistical methods suggested, however, the presence of two separate cluster regions within both the AML1 and ETO breakpoint cluster regions. ETObreakpoints were predominantly located in intron 1B in a defined cluster 5' of exon 1A (scan statistic P value = 0.00001). All patients with available RNA expressed an AML1-ETO mRNA fusion between exon 5 of AML1 and exon 2 of ETO. Since the structural restraints for the fusion protein of AML1-ETO exclude exon 1A, we reason that ETO intron 1B harbors a structural feature with propensity for breakage and/or recombination. Chromosomal breakpoints displayed evidence of fusion by a non-homologous end joining process, with microhomologies and nontemplate nucleotides at some fusion junctions. Breakpoints in general displayed similar complexity of duplications, deletions, and insertions to other common pediatric leukemia translocations (TEL-AML1, MLL-AF4, PML-RARA, CBFB-MYH11) that we and others have analyzed.
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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.