D myelodysplastic syndrome results in an NUP98-TOP1 fusion. Blood 1999, 94:3258-3261 Hussey DJ, Nicola M,

D myelodysplastic syndrome results in an NUP98-TOP1 fusion. Blood 1999, 94:3258-3261 Hussey DJ, Nicola M, Moore S, Peters GB, Dobrovic A: The t(4;11)q21;p15) translocation fuses the NUP98 and RAP1GDS1 genes and is recurrent in Necrostatin-1MedChemExpress Necrostatin-1 T-cell acute lymphocytic leukemia. Blood 1999, 94:2072-2079 Jaju RJ, Fidler C, Haas OA, et al: A novel gene, NSD1, is fused to NUP98 in the t(5;11)(q35;p15.5) in de novo childhood acute myeloid leukemia. Blood 2001, 98:1264-1267 Melo JV, Gordon DE, Cross NC, Goldman JM: The ABL-BCR fusion gene is expressed in chronic myeloid leukemia. Blood 1993, 81:158-165 Kasper LH, Brindle PK, Schnabel CA, et al: CREB binding protein interacts with nucleoporin-specific FG repeats that activate transcription and mediate NUP98-HOX9 oncogenicity. Mol Cell Biol 1999, 19:764-776 Ge H, Si Y, Roeder RG: Isolation of cDNAs encoding novel transcription coactivators p52 and p75 reveals an alternate regulatory mechanism of transcriptional activation. EMBO J 1998, 17:6723-6729 Stec I, Nagl SB, van Ommen GJ, den Dunnen JT: The PWWP domain: a potential protein-protein interaction domain in nuclear proteins influencing differentiation? FEBS Lett 2000, 473:1-5 Ahuja HG, Felix CA, PubMed ID:https://www.ncbi.nlm.nih.gov/pubmed/25636517 Aplan PD: Potential role for DNA topoisomerase II poisons in the generation of t(11;20)(p15;q11) translocations. Genes Chromosomes Cancer 2000, 29:96-105 Singh DP, Kimura A, Chylack LT Jr, Shinohara T: Lens epitheliumderived growth factor (LEDGF/p75) and p52 are derived from a single gene by alternative splicing. Gene 2000, 242:AcknowledgementsWe thank Professor LC Chan for fixed cells and information on patient 1 and Marilyn Slovak for supplying further information on patient 2. We thank John Norman and Professor RE Sage of the Haematology-Oncology Department of the Queen Elizabeth Hospital for their support and information on patient 3. This work is supported by a National Health Medical Research Council grant to AD.
O’Donnell and Burns Mobile DNA 2010, 1:21 http://www.mobilednajournal.com/content/1/1/REVIEWOpen AccessMobilizing diversity: transposable element insertions in genetic variation and diseaseKathryn A O’Donnell1,2*, Kathleen H Burns3,Abstract Transposable elements (TEs) comprise a large fraction of mammalian genomes. A number of these elements are actively jumping in our genomes today. As a consequence, these insertions provide a source of genetic variation and, in rare cases, these events cause mutations that lead to disease. Yet, the extent to which these elements impact their host genomes is not completely understood. This review will summarize our current understanding of the mechanisms underlying transposon regulation and the contribution of TE insertions to genetic diversity in the germline and in somatic cells. Finally, traditional methods and emerging technologies for identifying transposon insertions will be considered. Introduction In the 60 years since Barbara McClintock first discovered transposable elements (TEs), it has become increasingly recognized that these mobile sequences are important components of mammalian genomes and not merely `junk DNA’. We now appreciate that these elements modify gene structure and alter gene expression. Through their mobilization, transposons reshuffle sequences, promote ectopic rearrangements and create novel genes. In rare cases, TE insertions which cause mutations and lead to diseases both in humans and in mice have also been documented. However, we are at the very earliest stages of understanding how mobi.