ArticleVirchows Archiv : an international journal of pathology2009
RABGAP1L gene rearrangement resulting from a der(Y)t(Y;1)(q12;q25) in acute myeloid leukemia arising in a child with Klinefelter syndrome.
Article in Virchows Archiv : an international journal of pathology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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9 citing papers in PubMed, 16 citations in OpenAlex.
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- DNA methylation 101: what is important to know about DNA methylation and its role in SLE risk and disease heterogeneity.Lupus science & medicine · 2018Article
- A Graph Based Framework to Model Virus Integration Sites.Computational and structural biotechnology journal · 2016Article
- Genome-Wide Assessment of Differential DNA Methylation Associated with Autoantibody Production in Systemic Lupus Erythematosus.PloS one · 2015Article
- Acute myeloid leukemia in a patient with constitutional 47,XXY karyotype.Leukemia research reports · 2015Article
- Molecular analysis of diffuse intrinsic brainstem gliomas in adults.Journal of neuro-oncology · 2014Article
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Abstract
In this study, we report the molecular cytogenetic characterization of an acute myeloid leukemia with a der(Y)t(Y;1)(q12;q25) in bone marrow cells in a child with Klinefelter syndrome. Conventional cytogenetics demonstrated the unbalanced translocation, i.e., a trisomic 1q25-qter juxtaposed to Yq12 replaced the terminal segment of chromosome Y was acquired and present only on bone marrow cells. Fluorescence in situ hybridization showed that the breakpoint at 1q25 disrupted RABGAP1L, a strongly expressed gene in CFU-GEMM, erythroid cells, and megakaryocytes, while the Yq12 breakpoint fell within the heterochromatic region. As der(Y)t(Y;1)(q12;q25) was an isolated cytogenetic change, RABGAP1L rearrangement as well as gene(s) dosage effects correlated to 1q25-qter trisomy, and Yq12-qter loss may make a major contribution to leukemogenesis and/or disease progression.
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