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Search: WFRF:(Boggs J.) > (2015-2019)

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  • Kristo, Michael J., et al. (author)
  • The application of radiochronometry during the 4th collaborative materials exercise of the nuclear forensics international technical working group (ITWG)
  • 2018
  • In: Journal of Radioanalytical and Nuclear Chemistry. - : Springer Science and Business Media LLC. - 0236-5731 .- 1588-2780. ; 315:2, s. 425-434
  • Journal article (peer-reviewed)abstract
    • In a recent international exercise, 10 international nuclear forensics laboratories successfully performed radiochronometry on three low enriched uranium oxide samples, providing 12 analytical results using three different parent-daughter pairs serving as independent chronometers. The vast majority of the results were consistent with one another and consistent with the known processing history of the materials. In general, for these particular samples, mass spectrometry gave more accurate and more precise analytical results than decay counting measurements. In addition, the concordance of the U-235-Pa-231 and U-234-Th-230 chronometers confirmed the validity of the age dating assumptions, increasing confidence in the resulting conclusions.
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3.
  • Faber, Zachary J, et al. (author)
  • The genomic landscape of core-binding factor acute myeloid leukemias
  • 2016
  • In: Nature Genetics. - : Springer Science and Business Media LLC. - 1546-1718 .- 1061-4036. ; 48, s. 1551-1556
  • Journal article (peer-reviewed)abstract
    • Acute myeloid leukemia (AML) comprises a heterogeneous group of leukemias frequently defined by recurrent cytogenetic abnormalities, including rearrangements involving the core-binding factor (CBF) transcriptional complex. To better understand the genomic landscape of CBF-AMLs, we analyzed both pediatric (n = 87) and adult (n = 78) samples, including cases with RUNX1-RUNX1T1 (n = 85) or CBFB-MYH11 (n = 80) rearrangements, by whole-genome or whole-exome sequencing. In addition to known mutations in the Ras pathway, we identified recurrent stabilizing mutations in CCND2, suggesting a previously unappreciated cooperating pathway in CBF-AML. Outside of signaling alterations, RUNX1-RUNX1T1 and CBFB-MYH11 AMLs demonstrated remarkably different spectra of cooperating mutations, as RUNX1-RUNX1T1 cases harbored recurrent mutations in DHX15 and ZBTB7A, as well as an enrichment of mutations in epigenetic regulators, including ASXL2 and the cohesin complex. This detailed analysis provides insights into the pathogenesis and development of CBF-AML, while highlighting dramatic differences in the landscapes of cooperating mutations for these related AML subtypes.
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