Cited by 74

The DOI matches its Crossref record.

MicroRNA-486-5p is an erythroid oncomiR of the myeloid leukemias of Down syndrome.

Shaham, Lital, Vendramini, Elena, Ge, Yubin, Goren, Yaron, Birger, Yehudit, Tijssen, Marloes R., McNulty, Maureen, Geron, Ifat, Schwartzman, Omer, Goldberg, Liat, Chou, Stella T., Pitman, Holly, Weiss, Mitchell J., Michaeli, Shulamit, Sredni, Benjamin, Göttgens, Berthold, Crispino, John D., Taub, Jeffrey W., Izraeli, Shai·2015·Blood

Abstract

Key Points: miR-486-5p, a GATA1 regulated miR, is expressed in ML-DS and enhances their aberrant erythroid phenotype. miR-486-5p cooperates with GATA1s to promote the survival of pre-leukemic and leukemic cells.

Overview

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Integrity signals

Registry

Crossref · 10.1182/blood-2014-06-581892

Cites

Statistics

Verification

Claims the paper makes

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

The self-check needs the paper’s full text.

Citations

Cites

No references could be resolved yet.

Research works printed but not linked: 57

  1. Hasle, 2003, A pediatric approach to the WHO classification of myelodysplastic and myeloproliferative diseases., Leukemia, 17, 277, 10.1038/sj.leu.2402765 · DOI
  2. Langebrake, 2005, Immunophenotype of Down syndrome acute myeloid leukemia and transient myeloproliferative disease differs significantly from other diseases with morphologically identical or similar blasts., Klin Padiatr, 217, 126, 10.1055/s-2005-836510 · DOI
  3. Bourquin, 2006, Identification of distinct molecular phenotypes in acute megakaryoblastic leukemia by gene expression profiling., Proc Natl Acad Sci USA, 103, 3339, 10.1073/pnas.0511150103 · DOI
  4. Ito, 1995, Expression of erythroid-specific genes in acute megakaryoblastic leukaemia and transient myeloproliferative disorder in Down’s syndrome., Br J Haematol, 90, 607, 10.1111/j.1365-2141.1995.tb05591.x · DOI
  5. Caldwell, 2014, Prognosis and management of acute myeloid leukemia in patients with Down syndrome, Expert Rev Hematol, 7, 1, 10.1586/17474086.2014.959923 · DOI
  6. Malinge, 2009, Insights into the manifestations, outcomes, and mechanisms of leukemogenesis in Down syndrome., Blood, 113, 2619, 10.1182/blood-2008-11-163501 · DOI
  7. Hitzler, 2005, Origins of leukaemia in children with Down syndrome., Nat Rev Cancer, 5, 11, 10.1038/nrc1525 · DOI
  8. Roberts, 2014, Haematopoietic development and leukaemia in Down syndrome., Br J Haematol, 167, 587, 10.1111/bjh.13096 · DOI
  9. Gamis, 2011, Natural history of transient myeloproliferative disorder clinically diagnosed in Down syndrome neonates: a report from the Children’s Oncology Group Study A2971., Blood, 118, 6752, 10.1182/blood-2011-04-350017 · DOI
  10. Klusmann, 2008, Treatment and prognostic impact of transient leukemia in neonates with Down syndrome., Blood, 111, 2991, 10.1182/blood-2007-10-118810 · DOI
  11. Rainis, 2003, Mutations in exon 2 of GATA1 are early events in megakaryocytic malignancies associated with trisomy 21., Blood, 102, 981, 10.1182/blood-2002-11-3599 · DOI
  12. Wechsler, 2002, Acquired mutations in GATA1 in the megakaryoblastic leukemia of Down syndrome., Nat Genet, 32, 148, 10.1038/ng955 · DOI
  13. Taub, 2004, Prenatal origin of GATA1 mutations may be an initiating step in the development of megakaryocytic leukemia in Down syndrome., Blood, 104, 1588, 10.1182/blood-2004-04-1563 · DOI
  14. Roberts, 2013, GATA1-mutant clones are frequent and often unsuspected in babies with Down syndrome: identification of a population at risk of leukemia., Blood, 122, 3908, 10.1182/blood-2013-07-515148 · DOI
  15. Crispino, 2005, GATA1 in normal and malignant hematopoiesis., Semin Cell Dev Biol, 16, 137, 10.1016/j.semcdb.2004.11.002 · DOI
  16. Salek-Ardakani, 2009, ERG is a megakaryocytic oncogene., Cancer Res, 69, 4665, 10.1158/0008-5472.CAN-09-0075 · DOI
  17. Klusmann, 2010, Developmental stage-specific interplay of GATA1 and IGF signaling in fetal megakaryopoiesis and leukemogenesis., Genes Dev, 24, 1659, 10.1101/gad.1903410 · DOI
  18. Shaham, 2012, MiR-125 in normal and malignant hematopoiesis., Leukemia, 26, 2011, 10.1038/leu.2012.90 · DOI
  19. O’Connell, 2010, MicroRNAs enriched in hematopoietic stem cells differentially regulate long-term hematopoietic output., Proc Natl Acad Sci USA, 107, 14235, 10.1073/pnas.1009798107 · DOI
  20. Yendamuri, 2009, The role of microRNA in human leukemia: a review., Leukemia, 23, 1257, 10.1038/leu.2008.382 · DOI
  21. Klusmann, 2010, miR-125b-2 is a potential oncomiR on human chromosome 21 in megakaryoblastic leukemia., Genes Dev, 24, 478, 10.1101/gad.1856210 · DOI
  22. Alexander, 2014, MicroRNA-486-dependent modulation of DOCK3/PTEN/AKT signaling pathways improves muscular dystrophy-associated symptoms., J Clin Invest, 124, 2651, 10.1172/JCI73579 · DOI
  23. Aoi, Muscle-enriched microRNA miR-486 decreases in circulation in response to exercise in young men [published online ahead of print April 11, 2013]., Front Physiol
  24. Hitachi, 2014, Myostatin signaling regulates Akt activity via the regulation of miR-486 expression., Int J Biochem Cell Biol, 47, 93, 10.1016/j.biocel.2013.12.003 · DOI
  25. Small, 2010, Regulation of PI3-kinase/Akt signaling by muscle-enriched microRNA-486., Proc Natl Acad Sci USA, 107, 4218, 10.1073/pnas.1000300107 · DOI
  26. Xu, 2012, Transcription factor FoxO1, the dominant mediator of muscle wasting in chronic kidney disease, is inhibited by microRNA-486., Kidney Int, 82, 401, 10.1038/ki.2012.84 · DOI
  27. Borjigin, 2012, TLS-CHOP represses miR-486 expression, inducing upregulation of a metastasis regulator PAI-1 in human myxoid liposarcoma., Biochem Biophys Res Commun, 427, 355, 10.1016/j.bbrc.2012.09.063 · DOI
  28. Hu, 2010, Serum microRNA signatures identified in a genome-wide serum microRNA expression profiling predict survival of non-small-cell lung cancer., J Clin Oncol, 28, 1721, 10.1200/JCO.2009.24.9342 · DOI · Paper page
  29. Kim, 2012, miR-486-5p induces replicative senescence of human adipose tissue-derived mesenchymal stem cells and its expression is controlled by high glucose., Stem Cells Dev, 21, 1749, 10.1089/scd.2011.0429 · DOI
  30. Mees, 2009, Involvement of CD40 targeting miR-224 and miR-486 on the progression of pancreatic ductal adenocarcinomas., Ann Surg Oncol, 16, 2339, 10.1245/s10434-009-0531-4 · DOI
  31. Oh, 2011, Genomic loss of miR-486 regulates tumor progression and the OLFM4 antiapoptotic factor in gastric cancer., Clin Cancer Res, 17, 2657, 10.1158/1078-0432.CCR-10-3152 · DOI
  32. Peng, 2013, Insulin growth factor signaling is regulated by microRNA-486, an underexpressed microRNA in lung cancer., Proc Natl Acad Sci USA, 110, 15043, 10.1073/pnas.1307107110 · DOI
  33. Song, 2013, miR-486 sustains NF-κB activity by disrupting multiple NF-κB-negative feedback loops., Cell Res, 23, 274, 10.1038/cr.2012.174 · DOI
  34. Wang, 2014, Downregulation of miR-486-5p contributes to tumor progression and metastasis by targeting protumorigenic ARHGAP5 in lung cancer., Oncogene, 33, 1181, 10.1038/onc.2013.42 · DOI
  35. Stachura, 2006, Early block to erythromegakaryocytic development conferred by loss of transcription factor GATA-1., Blood, 107, 87, 10.1182/blood-2005-07-2740 · DOI
  36. Rosenfeld, 2008, MicroRNAs accurately identify cancer tissue origin., Nat Biotechnol, 26, 462, 10.1038/nbt1392 · DOI · Paper page
  37. Gefen, 2010, Hsa-mir-125b-2 is highly expressed in childhood ETV6/RUNX1 (TEL/AML1) leukemias and confers survival advantage to growth inhibitory signals independent of p53., Leukemia, 24, 89, 10.1038/leu.2009.208 · DOI
  38. Chlon, 2012, Cofactor-mediated restriction of GATA-1 chromatin occupancy coordinates lineage-specific gene expression., Mol Cell, 47, 608, 10.1016/j.molcel.2012.05.051 · DOI
  39. Goldberg, 2013, Genome-scale expression and transcription factor binding profiles reveal therapeutic targets in transgenic ERG myeloid leukemia., Blood, 122, 2694, 10.1182/blood-2013-01-477133 · DOI
  40. Muntean, 2005, Differential requirements for the activation domain and FOG-interaction surface of GATA-1 in megakaryocyte gene expression and development., Blood, 106, 1223, 10.1182/blood-2005-02-0551 · DOI
  41. Czogalla, 2010, Do we already know how spectrin attracts ankyrin?, Cell Mol Life Sci, 67, 2679, 10.1007/s00018-010-0371-1 · DOI
  42. Gallagher, 2005, Hematologically important mutations: ankyrin variants in hereditary spherocytosis., Blood Cells Mol Dis, 35, 345, 10.1016/j.bcmd.2005.08.008 · DOI
  43. Gallagher, 2000, The human ankyrin-1 gene is selectively transcribed in erythroid cell lines despite the presence of a housekeeping-like promoter., Blood, 96, 1136, 10.1182/blood.V96.3.1136.015k48_1136_1143 · DOI
  44. Baskerville, 2005, Microarray profiling of microRNAs reveals frequent coexpression with neighboring miRNAs and host genes., RNA, 11, 241, 10.1261/rna.7240905 · DOI · Paper page
  45. Kim, 2007, Processing of intronic microRNAs., EMBO J, 26, 775, 10.1038/sj.emboj.7601512 · DOI · Paper page
  46. Rodriguez, 2004, Identification of mammalian microRNA host genes and transcription units., Genome Res, 14, 1902, 10.1101/gr.2722704 · DOI · Paper page
  47. Calligaris, 1995, Alternative translation initiation site usage results in two functionally distinct forms of the GATA-1 transcription factor., Proc Natl Acad Sci USA, 92, 11598, 10.1073/pnas.92.25.11598 · DOI
  48. Li, 2005, Developmental stage-selective effect of somatically mutated leukemogenic transcription factor GATA1., Nat Genet, 37, 613, 10.1038/ng1566 · DOI
  49. Edwards, 2009, RUNX1 regulates phosphoinositide 3-kinase/AKT pathway: role in chemotherapy sensitivity in acute megakaryocytic leukemia., Blood, 114, 2744, 10.1182/blood-2008-09-179812 · DOI
  50. Birger, 2013, Perturbation of fetal hematopoiesis in a mouse model of Down syndrome’s transient myeloproliferative disorder., Blood, 122, 988, 10.1182/blood-2012-10-460998 · DOI
  51. Chou, 2008, Trisomy 21 enhances human fetal erythro-megakaryocytic development., Blood, 112, 4503, 10.1182/blood-2008-05-157859 · DOI
  52. Roy, 2012, Perturbation of fetal liver hematopoietic stem and progenitor cell development by trisomy 21., Proc Natl Acad Sci USA, 109, 17579, 10.1073/pnas.1211405109 · DOI
  53. Tunstall-Pedoe, 2008, Abnormalities in the myeloid progenitor compartment in Down syndrome fetal liver precede acquisition of GATA1 mutations., Blood, 112, 4507, 10.1182/blood-2008-04-152967 · DOI
  54. Fu, 2005, Identification of human fetal liver miRNAs by a novel method., FEBS Lett, 579, 3849, 10.1016/j.febslet.2005.05.064 · DOI
  55. Lulli, 2013, MicroRNA-486-3p regulates γ-globin expression in human erythroid cells by directly modulating BCL11A., PLoS ONE, 8, e60436, 10.1371/journal.pone.0060436 · DOI
  56. Wang, 2015, MicroRNA-486 regulates normal erythropoiesis and enhances growth and modulates drug response in CML progenitors., Blood
  57. Ghaffari, 2006, AKT induces erythroid-cell maturation of JAK2-deficient fetal liver progenitor cells and is required for Epo regulation of erythroid-cell differentiation., Blood, 107, 1888, 10.1182/blood-2005-06-2304 · DOI

Cited by

Sorted by citations

Metadata

Authors
Shaham, L., Vendramini, E., Ge, Y., Goren, Y., Birger, Y., Tijssen, M. R., McNulty, M., Geron, I., Schwartzman, O., Goldberg, L., Chou, S. T., Pitman, H., Weiss, M. J., Michaeli, S., Sredni, B., Göttgens, B., Crispino, J. D., Taub, J. W., & Izraeli, S.
Affiliations
  • Childhood Leukemia Research Institute, Cancer Research Center, Sheba Medical Center, Ramat-Gan, Israel;
  • Department of Oncology, Molecular Therapeutics Program, Barbara Ann Karmanos Cancer Institute, Wayne State University School of Medicine, Detroit, MI;
  • Rosetta Genomics Ltd, Rehovot, Israel;
  • Department of Haematology, Cambridge Institute for Medical Research and Wellcome Trust and MRC Cambridge Stem Cell Institute, University of Cambridge, Cambridge, United Kingdom;
  • Division of Hematology/Oncology, Northwestern University, Chicago, IL;
  • Division of Hematology, The Children’s Hospital of Philadelphia, Philadelphia, PA;
  • Department of Life Sciences, Bar-Ilan University, Ramat-Gan, Israel;
Venue
Blood
Published
2015-02-19
Volume
125
Issue
8
Pages
1292-1301
ISSN
  • 0006-4971
  • 1528-0020
Cited by
74
References
0
Language
en
Update notices
erratum (2016-04-21)

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review