Expression profiling of EWS/FLI identifies NKX2.2 as a critical target gene in Ewing's sarcoma.

[1]  J. Navas‐Palacios,et al.  On the histogenesis of Ewing's sarcoma: An ultrastructural, immunohistochemical, and cytochemical study , 1984, Cancer.

[2]  T. Triche,et al.  Experimental evidence for a neural origin of Ewing's sarcoma of bone. , 1987, The American journal of pathology.

[3]  M. Nirenberg,et al.  Drosophila NK-homeobox genes. , 1989, Proceedings of the National Academy of Sciences of the United States of America.

[4]  H Kovar,et al.  MIC2 is a specific marker for ewing's sarcoma and peripheral primitive neuroectodermal tumors. Evidence for a common histogenesis of ewing's sarcoma and peripheral primitive neuroectodermal tumors from MIC2 expression and specific chromosome aberration , 1991, Cancer.

[5]  D. Duboule,et al.  Regional expression of the homeobox gene Nkx-2.2 in the developing mammalian forebrain , 1992, Neuron.

[6]  G. Thomas,et al.  Gene fusion with an ETS DNA-binding domain caused by chromosome translocation in human tumours , 1992, Nature.

[7]  C. Denny,et al.  Ewing sarcoma 11;22 translocation produces a chimeric transcription factor that requires the DNA-binding domain encoded by FLI1 for transformation. , 1993, Proceedings of the National Academy of Sciences of the United States of America.

[8]  C. Denny,et al.  The Ewing's sarcoma EWS/FLI-1 fusion gene encodes a more potent transcriptional activator and is a more powerful transforming gene than FLI-1 , 1993, Molecular and cellular biology.

[9]  P. Ambros,et al.  Flow cytometric assessment of human MIC2 expression in bone marrow, thymus, and peripheral blood. , 1994, Blood.

[10]  M. Roussel,et al.  DNA-binding and transcriptional activation properties of the EWS-FLI-1 fusion protein resulting from the t(11;22) translocation in Ewing sarcoma , 1994, Molecular and cellular biology.

[11]  C. Denny,et al.  Identification of target genes for the Ewing's sarcoma EWS/FLI fusion protein by representational difference analysis , 1995, Molecular and cellular biology.

[12]  C. Denny,et al.  Multiple domains mediate transformation by the Ewing's sarcoma EWS/FLI-1 fusion gene. , 1995, Oncogene.

[13]  C. Denny,et al.  EAT-2 is a novel SH2 domain containing protein that is up regulated by Ewing's sarcoma EWS/FLI1 fusion gene. , 1996, Oncogene.

[14]  Marcienne M Wright,et al.  EWS/FLI1-induced manic fringe renders NIH 3T3 cells tumorigenic , 1997, Nature Genetics.

[15]  P. Roach,et al.  Glycogenin-2, a Novel Self-glucosylating Protein Involved in Liver Glycogen Biosynthesis* , 1997, The Journal of Biological Chemistry.

[16]  S. Welford,et al.  EWS/FLI1 up regulates mE2-C, a cyclin-selective ubiquitin conjugating enzyme involved in cyclin B destruction , 1998, Oncogene.

[17]  X. Matías-Guiu,et al.  Müllerian inhibiting substance, alpha-inhibin, and CD99 expression in sex cord-stromal tumors and endometrioid ovarian carcinomas resembling sex cord-stromal tumors. , 1998, Human pathology.

[18]  M. Roussel,et al.  Transforming activity of EWS/FLI is not strictly dependent upon DNA-binding activity , 1999, Oncogene.

[19]  P. Sorensen,et al.  EWS/ETS fusion genes induce epithelial and neuroectodermal differentiation in NIH 3T3 fibroblasts. , 1999, Laboratory investigation; a journal of technical methods and pathology.

[20]  J. Rubenstein,et al.  Homeobox gene Nkx2.2 and specification of neuronal identity by graded Sonic hedgehog signalling , 1999, Nature.

[21]  P. Sorensen,et al.  Delayed early embryonic lethality following disruption of the murine cyclin A2 gene , 1999, Nature Genetics.

[22]  C. Denny,et al.  Divergent Ewing's sarcoma EWS/ETS fusions confer a common tumorigenic phenotype on NIH3T3 cells , 1999, Oncogene.

[23]  A. McMahon.  Neural patterning: the role of Nkx genes in the ventral spinal cord. , 2000, Genes & Development.

[24]  S. Welford,et al.  The COOH-terminal domain of FLI-1 is necessary for full tumorigenesis and transcriptional modulation by EWS/FLI-1. , 2001, Cancer research.

[25]  S. Welford,et al.  DNA Binding Domain-independent Pathways Are Involved in EWS/FLI1-mediated Oncogenesis* , 2001, The Journal of Biological Chemistry.

[26]  J. Rubenstein,et al.  Control of oligodendrocyte differentiation by the Nkx2.2 homeodomain transcription factor. , 2001, Development.

[27]  M. Ringnér,et al.  Classification and diagnostic prediction of cancers using gene expression profiling and artificial neural networks , 2001, Nature Medicine.

[28]  Y. Suh,et al.  CD99 Immunoreactivity in Ependymoma , 2001, Applied immunohistochemistry & molecular morphology : AIMM.

[29]  O. Delattre,et al.  Analysis of the expression of cell cycle regulators in Ewing cell lines: EWS-FLI-1 modulates p57KIP2 and c-Myc expression , 2001, Oncogene.

[30]  W. May,et al.  PDGF-C is an EWS/FLI induced transforming growth factor in Ewing family tumors , 2001, Oncogene.

[31]  C. Denny,et al.  Loss of p16 pathways stabilizes EWS/FLI1 expression and complements EWS/FLI1 mediated transformation , 2001, Oncogene.

[32]  T. Golub,et al.  Supplemental Information for , 2002 .

[33]  W. Muller,et al.  CD99 plays a major role in the migration of monocytes through endothelial junctions , 2002, Nature Immunology.

[34]  Kenneth Chu,et al.  Sustained Loss of a Neoplastic Phenotype by Brief Inactivation of MYC , 2002, Science.

[35]  B. Li,et al.  Expression profiling reveals off-target gene regulation by RNAi , 2003, Nature Biotechnology.

[36]  Andrew L Kung,et al.  A small-molecule antagonist of CXCR4 inhibits intracranial growth of primary brain tumors , 2003, Proceedings of the National Academy of Sciences of the United States of America.

[37]  M. Daly,et al.  PGC-1α-responsive genes involved in oxidative phosphorylation are coordinately downregulated in human diabetes , 2003, Nature Genetics.

[38]  C. Denny,et al.  Functional analysis of the EWS/ETS target gene uridine phosphorylase. , 2003, Cancer research.

[39]  P. Navarria,et al.  Evidence of Neural Differentiation in a Case of Post-therapy Primitive Neuroectodermal Tumor/Ewing Sarcoma of Bone , 2003, The American journal of surgical pathology.

[40]  Akihiro Umezawa,et al.  Upregulation of Id2, an oncogenic helix-loop-helix protein, is mediated by the chimeric EWS/ets protein in Ewing sarcoma , 2003, Oncogene.

[41]  W. Hahn,et al.  Telomerase Maintains Telomere Structure in Normal Human Cells , 2003, Cell.

[42]  Stanley N Cohen,et al.  Disparate effects of telomere attrition on gene expression during replicative senescence of human mammary epithelial cells cultured under different conditions , 2004, Oncogene.

[43]  DNA Microarrays Reveal Relationship of Ewing Family Tumors to Both Endothelial and Fetal Neural Crest-Derived Cells and Define Novel Targets , 2004, Cancer Research.

[44]  O. Delattre,et al.  EWS/FLI-1 Silencing and Gene Profiling of Ewing Cells Reveal Downstream Oncogenic Pathways and a Crucial Role for Repression of Insulin-Like Growth Factor Binding Protein 3 , 2004, Molecular and Cellular Biology.

[45]  P. Meltzer,et al.  Gene expression profiling of human sarcomas: insights into sarcoma biology. , 2005, Cancer research.

[46]  T. Triche,et al.  EWS-FLI1 fusion protein up-regulates critical genes in neural crest development and is responsible for the observed phenotype of Ewing's family of tumors. , 2005, Cancer research.

[47]  N. Caplen,et al.  Defining and assaying RNAi in mammalian cells. , 2005, Molecular cell.

[48]  Mark E. Davis,et al.  Sequence-specific knockdown of EWS-FLI1 by targeted, nonviral delivery of small interfering RNA inhibits tumor growth in a murine model of metastatic Ewing's sarcoma. , 2005, Cancer research.