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The T-Lineage-affiliated CD2 Gene Lies within an Open Chromatin Environment in Acute Promyelocytic Leukemia Cells¹

Division of Medical and Molecular Genetics, Guy’s, King’s and St. Thomas’ School of Medicine, London SE1 9RT [D. G., R. F., E. S.]; Department of Biology, Imperial College of Science Technology and Medicine, London SW7 2AZ [S. V. O.]; Department of Academic Haematology, Royal Marsden Hospital, London SW3 6JJ [R. M.]; Department of Haematology, University of Birmingham, Birmingham B15 2TH [C. F. C.]; and Department of Haematology, University College London Medical School, London WC1E 6M2C, [D. G., S. J. I., A. R. P., D. C. L.], United Kingdom

The nature of hemopoietic progenitors subject to leukemic transformation in acute myeloid leukemia (AML) has not been clearly defined. To address this issue, we have used DNase I hypersensitivity assays to study the chromatin structure surrounding the T-lineage-affiliated CD2 gene in the acute promyelocytic subtype of AML (APL). Upstream and downstream flanking regions of CD2 were found to be hypersensitive to DNase I in primary APL blasts, with an identical pattern of hypersensitive sites to those detected in cells of T-lineage. All of the sites were confirmed to be inaccessible to DNase I in B-lineage leukemia cells. The demonstration of T-cell-associated chromatin features in primary APL blasts has implications for the origin of APL that may arise in more primitive progenitors than previously considered to be the case.

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