Cytoplasmic nucleophosmin in acute myelogenous leukemia with a normal karyotype.
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Paola Fazi | Marco Vignetti | Natalia Meani | Myriam Alcalay | Brunangelo Falini | Roberto Rosati | Giuseppe Saglio | Laura Pasqualucci | Enrico Tiacci | Arcangelo Liso | L. Pasqualucci | M. Vignetti | F. Mandelli | B. Falini | F. Lo‐Coco | P. Pelicci | C. Mecucci | M. Martelli | G. Saglio | R. Rosati | M. Alcalay | E. Colombo | R. la Starza | P. Fazi | A. Santucci | E. Tiacci | Roberta La Starza | Massimo F Martelli | Cristina Mecucci | Francesco Lo-Coco | A. Liso | Franco Mandelli | D. Diverio | Roberta Pacini | Barbara Bigerna | Alessandra Pucciarini | N. Meani | B. Bigerna | R. Pacini | A. Pucciarini | V. Pettirossi | Antonella Santucci | Valentina Pettirossi | Daniela Diverio | Pier-Giuseppe Pelicci | Emanuela Colombo | Natalia Meani
[1] J. Weber,et al. ARF Impedes NPM/B23 Shuttling in an Mdm2-Sensitive Tumor Suppressor Pathway , 2004, Molecular and Cellular Biology.
[2] Leena Latonen,et al. Nucleolar protein NPM interacts with HDM2 and protects tumor suppressor protein p53 from HDM2-mediated degradation. , 2004, Cancer cell.
[3] R. Tibshirani,et al. Use of gene-expression profiling to identify prognostic subclasses in adult acute myeloid leukemia. , 2004, The New England journal of medicine.
[4] R. Verhaak,et al. Prognostically useful gene-expression profiles in acute myeloid leukemia. , 2004, The New England journal of medicine.
[5] Charles J. Sherr,et al. Physical and Functional Interactions of the Arf Tumor Suppressor Protein with Nucleophosmin/B23 , 2004, Molecular and Cellular Biology.
[6] Pamela A. Silver,et al. Nuclear transport and cancer: from mechanism to intervention , 2004, Nature Reviews Cancer.
[7] A. Aventín,et al. FLT3 mutations are associated with other molecular lesions in AML. , 2004, Leukemia research.
[8] E. Jaffe. Pathology and Genetics: Tumours of Haematopoietic and Lymphoid Tissues , 2003 .
[9] G. Ehninger,et al. Comparative analysis of MLL partial tandem duplication and FLT3 internal tandem duplication mutations in 956 adult patients with acute myeloid leukemia , 2003, Genes, chromosomes & cancer.
[10] Axel Benner,et al. Prognostic significance of activating FLT3 mutations in younger adults (16 to 60 years) with acute myeloid leukemia and normal cytogenetics: a study of the AML Study Group Ulm. , 2002, Blood.
[11] F. Mandelli,et al. Alterations of the FLT3 gene in acute promyelocytic leukemia: association with diagnostic characteristics and analysis of clinical outcome in patients treated with the Italian AIDA protocol , 2002, Leukemia.
[12] C. Bloomfield,et al. Pretreatment cytogenetic abnormalities are predictive of induction success, cumulative incidence of relapse, and overall survival in adult patients with de novo acute myeloid leukemia: results from Cancer and Leukemia Group B (CALGB 8461). , 2002, Blood.
[13] Martin Dugas,et al. Analysis of FLT3 length mutations in 1003 patients with acute myeloid leukemia: correlation to cytogenetics, FAB subtype, and prognosis in the AMLCG study and usefulness as a marker for the detection of minimal residual disease. , 2002 .
[14] Pier Giuseppe Pelicci,et al. Nucleophosmin regulates the stability and transcriptional activity of p53 , 2002, Nature Cell Biology.
[15] B. Falini,et al. Proteins encoded by genes involved in chromosomal alterations in lymphoma and leukemia: clinical value of their detection by immunocytochemistry. , 2002, Blood.
[16] H. Umekawa,et al. Tryptophans 286 and 288 in the C-terminal Region of Protein B23.1 are Important for Its Nucleolar Localization , 2002, Bioscience, biotechnology, and biochemistry.
[17] D. Christiansen,et al. Internal tandem duplications of the FLT3 and MLL genes are mainly observed in atypical cases of therapy-related acute myeloid leukemia with a normal karyotype and are unrelated to type of previous therapy , 2001, Leukemia.
[18] S. Usui,et al. The carboxyl terminal sequence of nucleolar protein B23.1 is important in its DNA polymerase alpha-stimulatory activity. , 2001, Journal of biochemistry.
[19] Pu Zhang,et al. Dominant-negative mutations of CEBPA, encoding CCAAT/enhancer binding protein-α (C/EBPα), in acute myeloid leukemia , 2001, Nature Genetics.
[20] M. Slovak,et al. Karyotypic analysis predicts outcome of preremission and postremission therapy in adult acute myeloid leukemia: a Southwest Oncology Group/Eastern Cooperative Oncology Group study , 2000 .
[21] H. F. Horn,et al. Nucleophosmin/B23 Is a Target of CDK2/Cyclin E in Centrosome Duplication , 2000, Cell.
[22] M. Olson,et al. Mapping the Functional Domains of Nucleolar Protein B23* , 2000, The Journal of Biological Chemistry.
[23] C. Mecucci,et al. Interphase FISH for Y chromosome, VNTR polymorphisms, and RT-PCR for BCR-ABL in the monitoring of HLA-matched and mismatched transplants. , 2000, Cancer genetics and cytogenetics.
[24] E. Macintyre,et al. Standardized RT-PCR analysis of fusion gene transcripts from chromosome aberrations in acute leukemia for detection of minimal residual disease , 1999, Leukemia.
[25] E. Campo,et al. Lymphomas expressing ALK fusion protein(s) other than NPM-ALK. , 1999, Blood.
[26] S. Pileri,et al. ALK+ lymphoma: clinico-pathological findings and outcome. , 1999, Blood.
[27] B Falini,et al. Detection of normal and chimeric nucleophosmin in human cells. , 1999, Blood.
[28] K Wheatley,et al. The importance of diagnostic cytogenetics on outcome in AML: analysis of 1,612 patients entered into the MRC AML 10 trial. The Medical Research Council Adult and Children's Leukaemia Working Parties. , 1998, Blood.
[29] M. Wu,et al. Evidence for the ability of nucleophosmin/B23 to bind ATP. , 1998, The Biochemical journal.
[30] R. Johnson,et al. Dye efflux studies suggest that hematopoietic stem cells expressing low or undetectable levels of CD34 antigen exist in multiple species , 1997, Nature Medicine.
[31] K. Pulford,et al. Role of the nucleophosmin (NPM) portion of the non-Hodgkin's lymphoma-associated NPM-anaplastic lymphoma kinase fusion protein in oncogenesis , 1997, Molecular and cellular biology.
[32] S. Corey,et al. The t(5;17) variant of acute promyelocytic leukemia expresses a nucleophosmin-retinoic acid receptor fusion. , 1996, Blood.
[33] S. Raimondi,et al. The t(3;5)(q25.1;q34) of myelodysplastic syndrome and acute myeloid leukemia produces a novel fusion gene, NPM-MLF1. , 1996, Oncogene.
[34] F. Mitelman. ISCN 1995 : an international system for human cytogenetic nomenclature (1995) : recommendations of the International Standing Committee on Human Cytogenetic Nomenclature : Memphis, Tennessee, USA, October 9-13, 1994 , 1995 .
[35] C. Croce,et al. ALL-1 gene rearrangements in acute myeloid leukemia: association with M4-M5 French-American-British classification subtypes and young age. , 1995, Cancer research.
[36] D N Shapiro,et al. Fusion of a kinase gene, ALK, to a nucleolar protein gene, NPM, in non-Hodgkin's lymphoma. , 1994, Science.
[37] A. Hagemeijer,et al. The translocation (6;9) (p23;q34) shows consistent rearrangement of two genes and defines a myeloproliferative disorder with specific clinical features , 1992 .
[38] M. Olson,et al. Interaction of nucleolar phosphoprotein B23 with nucleic acids. , 1989, Biochemistry.
[39] C. Lehner,et al. Major nucleolar proteins shuttle between nucleus and cytoplasm , 1989, Cell.
[40] H Stein,et al. Immunoenzymatic labeling of monoclonal antibodies using immune complexes of alkaline phosphatase and monoclonal anti-alkaline phosphatase (APAAP complexes). , 1984, The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society.
[41] Iscn. International System for Human Cytogenetic Nomenclature , 1978 .