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Original Articles

Overexpression of chromatin remodeling and tyrosine kinase genes in iAMP21-positive acute lymphoblastic leukemia

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Pages 604-613 | Received 13 Jun 2019, Accepted 30 Sep 2019, Published online: 22 Oct 2019

References

  • Schmiegelow K, Forestier E, Hellebostad M, et al. Long-term results of NOPHO ALL-92 and ALL-2000 studies of childhood acute lymphoblastic leukemia. Leukemia. 2010;24(2):345–354.
  • Harewood L, Robinson H, Harris R, et al. Amplification of AML1 on a duplicated chromosome 21 in acute lymphoblastic leukemia: a study of 20 cases. Leukemia. 2003;17(3):547–553.
  • Robinson HM, Broadfield ZJ, Cheung KL, et al. Amplification of AML1 in acute lymphoblastic leukemia is associated with a poor outcome. Leukemia. 2003;17(11):2249–2250.
  • Moorman AV, Ensor HM, Richards SM, et al. Prognostic effect of chromosomal abnormalities in childhood B-cell precursor acute lymphoblastic leukaemia: results from the UK Medical Research Council ALL97/99 randomised trial. Lancet Oncol. 2010;11(5):429–438.
  • Moorman AV, Robinson H, Schwab C, et al. Risk-directed treatment intensification significantly reduces the risk of relapse among children and adolescents with acute lymphoblastic leukemia and intrachromosomal amplification of chromosome 21: a comparison of the MRC ALL97/99 and UKALL2003 trials. JCO. 2013;31(27):3389–3396.
  • Heerema NA, Carroll AJ, Devidas M, et al. Intrachromosomal amplification of chromosome 21 is associated with inferior outcomes in children with acute lymphoblastic leukemia treated in contemporary standard-risk children's oncology group studies: a report from the children's oncology group. JCO. 2013;31(27):3397–3402.
  • Harrison CJ, Moorman AV, Schwab C, et al. An international study of intrachromosomal amplification of chromosome 21 (iAMP21): cytogenetic characterization and outcome. Leukemia. 2014;28(5):1015–1021.
  • Toft N, Birgens H, Abrahamsson J, et al. Results of NOPHO ALL2008 treatment for patients aged 1–45 years with acute lymphoblastic leukemia. Leukemia. 2018;32(3):606–615.
  • Robinson HM, Harrison CJ, Moorman AV, et al. Intrachromosomal amplification of chromosome 21 (iAMP21) may arise from a breakage-fusion-bridge cycle. Genes Chromosom Cancer. 2007;46(4):318–326.
  • Kuchinskaya E, Nordgren A, Heyman M, et al. Tiling-resolution array-CGH reveals the pattern of DNA copy number alterations in acute lymphoblastic leukemia with 21q amplification: the result of telomere dysfunction and breakage/fusion/breakage cycles? Leukemia. 2007;21(6):1327–1330.
  • Rand V, Parker H, Russell LJ, et al. Genomic characterization implicates iAMP21 as a likely primary genetic event in childhood B-cell precursor acute lymphoblastic leukemia. Blood. 2011;117(25):6848–6855.
  • Sinclair PB, Parker H, An Q, et al. Analysis of a breakpoint cluster reveals insight into the mechanism of intrachromosomal amplification in a lymphoid malignancy. Hum Mol Genet. 2011;20(13):2591–2602.
  • Li Y, Schwab C, Ryan SL, et al. Constitutional and somatic rearrangement of chromosome 21 in acute lymphoblastic leukaemia. Nature. 2014;508(7494):98–102.
  • Baughn LB, Meredith MM, Oseth L, et al. SH2B3 aberrations enriched in iAMP21 B lymphoblastic leukemia. Cancer Genet. 2018;226–227:30–35.
  • Ivanov Ofverholm I, Tran AN, Olsson L, et al. Detailed gene dose analysis reveals recurrent focal gene deletions in pediatric B-cell precursor acute lymphoblastic leukemia. Leuk Lymphoma. 2016;57:2161–2170.
  • Sinclair PB, Ryan S, Bashton M, et al. SH2B3 inactivation through CN-LOH 12q is uniquely associated with B-cell precursor ALL with iAMP21 or other chromosome 21 gain. Leukemia 2019;33:1881–1894.
  • Ryan SL, Matheson E, Grossmann V, et al. The role of the RAS pathway in iAMP21-ALL. Leukemia. 2016;30(9):1824–1831.
  • Nordlund J, Backlin CL, Wahlberg P, et al. Genome-wide signatures of differential DNA methylation in pediatric acute lymphoblastic leukemia. Genome Biol. 2013;14(9):r105.
  • Marincevic-Zuniga Y, Dahlberg J, Nilsson S, et al. Transcriptome sequencing in pediatric acute lymphoblastic leukemia identifies fusion genes associated with distinct DNA methylation profiles. J Hematol Oncol. 2017;10(1):148.
  • Venkatraman ES, Olshen AB. A faster circular binary segmentation algorithm for the analysis of array CGH data. Bioinformatics. 2007;23(6):657–663.
  • Rasmussen M, Sundström M, Kultima H, et al. Allele-specific copy number analysis of tumor samples with aneuploidy and tumor heterogeneity. Genome Biol. 2011;12(10):R108.
  • Neph S, Kuehn MS, Reynolds AP, et al. BEDOPS: high-performance genomic feature operations. Bioinformatics. 2012;28(14):1919–1920.
  • Thorvaldsdottir H, Robinson JT, Mesirov JP. Integrative Genomics Viewer (IGV): high-performance genomics data visualization and exploration. Brief Bioinform. 2013;14(2):178–192.
  • Tran AN, Taylan F, Zachariadis V, et al. High-resolution detection of chromosomal rearrangements in leukemias through mate pair whole genome sequencing. PLoS One. 2018;13(3):e0193928.
  • Eisfeldt J, Vezzi F, Olason P, et al. TIDDIT, an efficient and comprehensive structural variant caller for massive parallel sequencing data. F1000Res. 2017;6:664.
  • Dobin A, Davis CA, Schlesinger F, et al. STAR: ultrafast universal RNA-seq aligner. Bioinformatics. 2013;29(1):15–21.
  • Robinson MD, Oshlack A. A scaling normalization method for differential expression analysis of RNA-seq data. Genome Biol. 2010;11(3):R25.
  • Law CW, Chen Y, Shi W, et al. Voom: precision weights unlock linear model analysis tools for RNA-seq read counts. Genome Biol. 2014;15(2):R29.
  • Ritchie ME, Phipson B, Wu D, et al. Limma powers differential expression analyses for RNA-sequencing and microarray studies. Nucleic Acids Res. 2015;43(7):e47.
  • Robinson JT, Thorvaldsdottir H, Winckler W, et al. Integrative genomics viewer. Nat Biotechnol. 2011;29(1):24–26.
  • Untergasser A, Nijveen H, Rao X, et al. Primer3Plus, an enhanced web interface to Primer3. Nucleic Acids Res. 2007;35(Web Server):W71–74.
  • Nordlund J, Backlin CL, Zachariadis V, et al. DNA methylation-based subtype prediction for pediatric acute lymphoblastic leukemia. Clin Epigenet. 2015;7(1):11.
  • Bignell GR, Santarius T, Pole JC, et al. Architectures of somatic genomic rearrangement in human cancer amplicons at sequence-level resolution. Genome Res. 2007;17(9):1296–1303.
  • Gu Z, Churchman M, Roberts K, et al. Genomic analyses identify recurrent MEF2D fusions in acute lymphoblastic leukaemia. Nat Commun. 2016;7(1):13331.
  • Gingeras TR. Implications of chimaeric non-co-linear transcripts. Nature. 2009;461(7261):206–211.
  • Strefford JC, van Delft FW, Robinson HM, et al. Complex genomic alterations and gene expression in acute lymphoblastic leukemia with intrachromosomal amplification of chromosome 21. Proc Natl Acad Sci U S A. 2006;103(21):8167–8172.
  • Zhou X, Edmonson MN, Wilkinson MR, et al. Exploring genomic alteration in pediatric cancer using ProteinPaint. Nat Genet. 2016;48(1):4–6.
  • Birger Y, Izraeli S. DYRK1A in down syndrome: an oncogene or tumor suppressor? J Clin Invest. 2012;122(3):807–810.
  • Abbassi R, Johns TG, Kassiou M, et al. DYRK1A in neurodegeneration and cancer: molecular basis and clinical implications. Pharmacol Ther. 2015;151:87–98.
  • Roberts KG, Li Y, Payne-Turner D, et al. Targetable kinase-activating lesions in Ph-like acute lymphoblastic leukemia. N Engl J Med. 2014;371(11):1005–1015.
  • Lee P, Bhansali R, Izraeli S, et al. The biology, pathogenesis and clinical aspects of acute lymphoblastic leukemia in children with Down syndrome. Leukemia. 2016;30(9):1816–1823.
  • Letourneau A, Santoni FA, Bonilla X, et al. Domains of genome-wide gene expression dysregulation in Down's syndrome. Nature. 2014;508(7496):345–350.
  • Malinge S, Bliss-Moreau M, Kirsammer G, et al. Increased dosage of the chromosome 21 ortholog Dyrk1a promotes megakaryoblastic leukemia in a murine model of Down syndrome. J Clin Invest. 2012;122(3):948–962.
  • Pozo N, Zahonero C, Fernandez P, et al. Inhibition of DYRK1A destabilizes EGFR and reduces EGFR-dependent glioblastoma growth. J Clin Invest. 2013;123(6):2475–2487.
  • Thompson BJ, Bhansali R, Diebold L, et al. DYRK1A controls the transition from proliferation to quiescence during lymphoid development by destabilizing Cyclin D3. J Exp Med. 2015;212(6):953–970.
  • Boichuk S, Parry JA, Makielski KR, et al. The DREAM complex mediates GIST cell quiescence and is a novel therapeutic target to enhance imatinib-induced apoptosis. Cancer Res. 2013;73(16):5120–5129.
  • Mjelle R, Hegre SA, Aas PA, et al. Cell cycle regulation of human DNA repair and chromatin remodeling genes. DNA Repair (Amst). 2015;30:53–67.
  • de Tayrac M, Saikali S, Aubry M, et al. Prognostic significance of EDN/RB, HJURP, p60/CAF-1 and PDLI4, four new markers in high-grade gliomas. PLoS One. 2013;8(9):e73332.
  • Staibano S, Mascolo M, Mancini FP, et al. Overexpression of chromatin assembly factor-1 (CAF-1) p60 is predictive of adverse behaviour of prostatic cancer. Histopathology. 2009;54(5):580–589.
  • Staibano S, Mascolo M, Rocco A, et al. The proliferation marker Chromatin Assembly Factor-1 is of clinical value in predicting the biological behaviour of salivary gland tumours. Oncol Rep. 2011;25(1):13–22.
  • Polo SE, Theocharis SE, Grandin L, et al. Clinical significance and prognostic value of chromatin assembly factor-1 overexpression in human solid tumours. Histopathology. 2010;57(5):716–724.
  • Polo SE, Theocharis SE, Klijanienko J, et al. Chromatin assembly factor-1, a marker of clinical value to distinguish quiescent from proliferating cells. Cancer Res. 2004;64(7):2371–2381.
  • Volk A, Liang K, Suraneni P, et al. A CHAF1B-dependent molecular switch in hematopoiesis and leukemia pathogenesis. Cancer Cell. 2018;34(5):707.e7–723.e7.
  • Li Y, Luo H, Liu T, et al. The ets transcription factor Fli-1 in development, cancer and disease. Oncogene. 2015;34(16):2022–2031.
  • Kim JH, Baddoo MC, Park EY, et al. SON and Its alternatively spliced isoforms control MLL complex-mediated H3K4me3 and transcription of leukemia-associated genes. Mol Cell. 2016;61(6):859–873.
  • Ahn EE, Higashi T, Yan M, et al. SON protein regulates GATA-2 through transcriptional control of the microRNA 23a∼27a∼24-2 cluster. J Biol Chem. 2013;288(8):5381–5388.
  • Aranda S, Laguna A, de la Luna S. DYRK family of protein kinases: evolutionary relationships, biochemical properties, and functional roles. FASEB J. 2011;25(2):449–462.