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1. |
NPM-ALK kinase has a role in the regulation of responsiveness of tumor cells with cdk dysregulation |
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2. |
NPM1 exon 12 mutations occur with a considerable percentage in AML patients with normal karyotype, and are associated with higher peripheral white cell count and lower expression of CD34 and CD117. |
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3. |
Minimal residual disease levels assessed by NPM1 mutation-specific RQ-PCR provide important prognostic information in AML. |
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4. |
The NPM/ALK alteration affects diverse cellular pathways, and provide novel insights into NPM/ALK-positive anaplastic large cell lymphoma pathobiology. |
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5. |
study reports on 20 cases with acute myeloid leukemia (AML) with limited differentiation; all of these cases were shown to carry an NPM1 type A mutation |
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6. |
Acetylated NPM1 transcriptionally regulates genes involved in cell survival and proliferation during carcinogenesis. |
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7. |
NPM knockdown reduces heat-induced inhibition of DNA DSB repair. |
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8. |
Folding and unfolding kinetics of the C-terminal domain. This small helical domain folds via a compact denatured state, displaying a malleable residual structure. |
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9. |
identified novel reciprocal functional interactions between IGF-IR and NPM-ALK |
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10. |
2 novel NPM1 mutants in de novo AML add new insights into the heterogeneity of genomic insertions at exon 12. |
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11. |
In (NK) AML patients, complete remission rates and percentage of patients with adequate in vivo blast cell reduction 1 week after the end of the first induction cycle were significantly higher in NPM1(+) patients, but were unaffected by FLT3-ITD status. |
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12. |
NPM-ALK-induced activation of the PI3-kinase and Jun N-terminal kinase and stress-activated protein kinase proteins, with a role for these in the regulation of p53 activity in an intricate signaling system |
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13. |
nucleophosmin is a candidate of independent prognostic marker for Ewing's sarcoma patients |
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14. |
limiting the usefulness of the NPM1 mutation A mutation as a molecular marker in patients with minimal residual disease in acute myeloid leukaemia |
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15. |
nucleophosmin as a positive post-translational regulator of p21. |
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16. |
nucleophosmin is consistently cytoplasmic in NPMc(+) AML (because of the presence of NPM1 mutations), whilst it is nucleus-restricted (predictive of a germline NPM1 gene) in blastic plasmacytoid dendritic cell neoplasm |
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17. |
ATIC associated with nucleophosmin-ALK, and its phosphorylation required ALK activity. ALK-mediated ATIC phosphorylation enhanced its enzymatic activity. |
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18. |
NPM1 gene mutations are associated with acute myeloid leukemia. |
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19. |
Association of nucleophosmin with bladder cancer recurrence based on immunohistochemical assessment is reported. |
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20. |
NPM is essential for cell viability, these data suggest that targeting of NPM by granzyme M may contribute to tumor cell eradication by abolishing NPM function. |
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21. |
The 2 physiological nuclear export signal motifs mediated NPM1 homo/heterodimerization, influencing subcellular distribution of NPM1wt, mutated NPM1 and p14(ARF) in a 'dose-dependent tug of war' fashion. This event is critical for leukaemogenesis. |
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22. |
A novel interaction between nucleophosmin (NPM1) and APE1 was characterized. |
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23. |
Observational study of gene-disease association and genetic testing. (HuGE Navigator) |
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24. |
NPM1 mutations confer a favorable prognosis in childhood AML and in cytogenetically normal AML in particular. |
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25. |
Nucleophosmin is a binding partner of nucleostemin in human osteosarcoma cells |
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26. |
NPM1 expression levels of mRNA and protein in myelodysplastic syndromes were not related to chromosome 5 abnormalities and were almost the same as those in normal bone marrow and acute myeloid leukemia cells |
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27. |
The ribosomal protein L23 is a negative regulator of Miz1-dependent transactivation. |
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28. |
detailed cytogenetic analysis of acute myeloid leukaemia with mutated NPM1 in a father and daughter, with different NPM1 mutations |
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29. |
NPM1 mutants coexisted mainly with FLT3 mutants |
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30. |
38.9% (14/36) patients with NPM1 mutations simultaneously exhibited internal tandem duplications in the FLT3 gene |
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31. |
Clinical trial of gene-disease association, gene-environment interaction, and pharmacogenomic / toxicogenomic. (HuGE Navigator) |
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32. |
These findings indicate that nucleophosmin is essential for mitotic progression and cell proliferation. |
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33. |
NPM is an essential protein not only for the formation of normal nucleolar structure, but also for the maintenance of regular nuclear shape in HeLa cells. |
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34. |
The NPM1-mutated is specific of leukemic cells and shows higher levels at MRD in AML patients presentation. |
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35. |
Nucleolar protein B23/nucleophosmin regulates the vertebrate SUMO pathway through SENP3 and SENP5 proteases. |
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36. |
Model fits with the hypothesis that acute myeloid leukemia arises from an NPM1 mutation with haploinsufficiency of the wild-type NPM1 allele. |
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37. |
structural analysis of nucleophosmin mutations in acute myeloid leukemia |
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38. |
NPMc(+) acute myeloid leukemia represents a primary event rather than a transformation stage of NPMc(-) acute myeloid leukemia |
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39. |
NPM1-mutated acute myeloid leukaemia occurring in JAK2-V617F+ primary myelofibrosis. |
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40. |
SMT3IP1 desumoylates nucleophosmin and might controls its physiological functions at both the nucleolus and other subcellular compartments. |
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41. |
findings point to DR negativity as another phenotypic feature of AML with NPM1 mutation |
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42. |
NPM1 mutations were observed in 7 of 51 patients presenting as overt therapy-related acute myeloid leukemia as compared to only 3 of 89 patients presenting as therapy-related myelodysplasia |
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43. |
The present investigations demonstrate the importance of exposure of the C-terminus of Bax for its interaction with nucleophosmin. These protein-protein interaction assays provide a technical approach for the study of Bax-interacting proteins. |
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44. |
B23 selectively stores, and protects ribosomal protein S9 in nucleoli and therefore could facilitate ribosome biogenesis. |
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45. |
p53-Driven apoptosis limits centrosome amplification and genomic instability downstream of NPM1 phosphorylation |
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46. |
study confirms in 2562 patients with acute myeloid leukemia the previous observation that NPM1 mutations and cytoplasmic nucleophosmin are mutually exclusive of recurrent genetic abnormalities |
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47. |
The leukemia-associated NPMc+ is an in vitro oncogene under the appropriate genetic context |
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48. |
correlation of PTPN11 mutations with NPM1 mutations and FLT3/ITD among adult AML patients |
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49. |
NPM1 mutation is a unique genetic event that is specific to Acute myeloid leukemia |
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50. |
Increase sensitivity to chemotherapeutical agents and cytoplasmatic interaction between NPM leukemic mutant and NF-kappaB is associated with acute myeloid leukemia carrying NPM1 mutations |
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51. |
review of mutations of NPM1 associated with AML and the implications for prognosis |
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52. |
Could regulate androgen receptor (AR) functions by promoting assembly of AR-containing regulatory complexes; high levels might alter AR functions in prostate cancer. |
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53. |
Fusion protein nucleophosmin (NPM)-ALK activates GTPase Rac1 via phosphatidylkinase 3-kinase (PI3K) and protein-tyrosine kinase c-src (Src) in anaplastic large cell lymphoma patients. |
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54. |
B23 was found to be associated with the rRNA gene chromatin. Small-interfering-RNA-mediated down-regulation of the B23 expression level resulted in reduction of the transcription rate of the rRNA gene. |
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55. |
NPM binds to HEXIM1 in vitro and in vivo, and functions as a negative regulator of HEXIM1. |
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56. |
These results define SENP3 as an essential factor for ribosome biogenesis and suggest that deconjugation of SUMO2 from NPM1 by SENP3 is critically involved in 28S rRNA maturation. |
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57. |
nucleolar localization determines the stability of ARF but not its primary function |
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58. |
There was a highly significant trend for worsening in relapse risk (RR) and overall survival (OS) with increasing FLT3/ITD (internal tandem duplication) mutant level. |
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59. |
a molecular mechanism of B23 in the mitotic inhibition of GCN5-mediated histone acetylation and transactivation. |
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60. |
c-Jun translocates B23 and ARF from the nucleolus after JNK activation by means of protein interactions |
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61. |
These results identify a unique miRNA signature associated with Acute myeloid leukemia (AML) carrying NPM1 mutations and cytoplasmic nucleophosmin (NPMc+ AML) and provide evidence that support a role for miRNAs in the regulation of HOX genes. |
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62. |
NPM1 mutations were not detected in the 28 patients with myelodysplastic syndrome and acute myeloid leukemia with chromosome 5 abnormalities. |
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63. |
AML cells are a major source of Ang-1 in leukemic bone marrow, especially in patients with NPM1 mutations |
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64. |
mutated NPM peptides can be presented by HLA molecules, suggesting that AML cells carrying cytoplasmic mutated NPM could induce an anti-leukaemic T-cell response |
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65. |
In this general and unselected AML patient population, NPM1 mutation was not a prognostic indicator of a favorable outcome. |
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66. |
Observational study of genotype prevalence and gene-disease association. (HuGE Navigator) |
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67. |
Observational study of gene-disease association. (HuGE Navigator) |
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68. |
Observational study of gene-disease association and gene-gene interaction. (HuGE Navigator) |
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69. |
Observational study of genetic testing. (HuGE Navigator) |
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70. |
Observational study of genotype prevalence. (HuGE Navigator) |
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71. |
NPM1 mutations is associated with absence of nucleophosmin leukemic mutants in B and T cells from AML |
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72. |
Elderly (range 60-85 yr) but medically fit patients with acute myeloid leukemia (AML) carrying NPM1 mutations demonstrate a higher rate of complete remission compared to NPM1 wildtype AML patients. |
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73. |
B23 distinctively binds Ebp1 isoforms and regulates cell proliferation and survival through p42 and p48, respectively. |
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74. |
Oncogenic NPM1-ALK contains the NPM1 oligomerization motif plus ALK catalytic domain and mediates malignant cell transformation by epigenetic silencing of signal transducer and activator of transcription STAT5A in T-cell anaplastic large cell lymphomas. |
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75. |
NPM1 mutations are associated with residual disease of acute myeloid leukemia |
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76. |
Sustained expression of nucleophosmin (NPM1) mutation at late relapse presenting as isolated myeloid sarcoma in a patient with acute myeloid leukemia. |
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77. |
B23 sumoylation regulates its subcellular localization, cell proliferation, and survival activities. |
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78. |
JunB is a critical target of mTOR and is translationally regulated in NPM-ALK-positive lymphomas. |
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79. |
This study provides evidence for a novel role for NPM as a negative regulator of CXCR4 signaling induced by CXCL12 that may be relevant to the biology of acute myelogenous leukemia. |
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80. |
crystal structure of human NPM-core (Met9-Asp122) |
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81. |
NPM1 mutations were significantly associated with old age, high peripheral white blood cell count, and the subtypes of French-American-British categories M1/M5, but negatively associated with expression of CD34 and CD117 in a Chinese population. |
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82. |
identify splicing factor as a novel NPM/anaplastic lymphoma kinase-binding protein and substrate |
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83. |
B23 functions as a chaperone in the viral chromatin assembly process in infected cells. |
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84. |
NPM1 mutations in acute myeloid leukemia act to achieve maximum nuclear export and cytoplasmic accumulation of NPM1 |
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85. |
mutated NPM1 leads to dysregulated HOX expression via a different mechanism than MLL rearrangement |
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86. |
In pediatric patients, NPM1 mutations are less common than in adults and tend to affect older patients. |
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87. |
A new type of NPM mutation was found, and NPM mutations in MDS patients were demonstrated foe the first time. The results provides new hints for NPM gene mutations in the pathogenesis of AML and MDS. |
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88. |
Frameshift mutations in exon 12 of the nucleophosmin gene (NPM1) result in aberrant cytoplasmic localization of the NPM protein (NPMc(+); NPMc(+) is relatively rare in childhood AML, particularly in younger children |
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89. |
Nuclear matrix proteins such as mutant Pyst1 and nucleophosmin 1 were downregulated, whereas eIF6 and beta-tubulin were upregulated during cell differentiation in hepatocarcinoma cells. |
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90. |
Ddetermination of mutations and promoter methylation status of NPM1 using pyrosequencing in 199 samples of myeloid neoplasia including myeloproliferative disorders (MPD). |
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91. |
NPM1 exon 12 mutations is associated with acute myeloid leukemia |
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92. |
This study unveils a hitherto unrecognized transcriptional corepressor function of the NPM protein, and highlights a novel mechanism by which NPM regulates cell growth and differentiation. |
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93. |
Results reveal a molecular mechanism of ARF in regulating ribosome biogenesis and cell proliferation via inhibiting B23. |
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94. |
Often mutation in acute myeloid leukemia. |
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95. |
These results provide evidence that phosphorylation at specific sites reduces the affinity of B23 for nucleolar components and might be a factor in regulating its location during the cell cycle. |
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96. |
nucleophosmin 1 mutations may cause cells to develop along the myelomonocytic lineage |
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97. |
the functional integrity of the B23 core motif is required for stability, efficient nucleolar localization as well as ARF binding |
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98. |
Ras and c-Myc play important roles in the up-regulation of nucleophosmin/B23 during proliferation of cells associated with a high degree of malignancy, thus outlining a signaling cascade involving these factors in the cancer cells. |
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99. |
base sequences are given for NPM1 mutated childhood AML patients; consistent deletion/insertion features are presented |
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100. |
Review. NPM1 is translocated or mutated in various lymphomas & leukemias, forming fusion proteins or NPM mutant products. The structural, functional, biological, clinical & pathological features of normal & mutant NPM1 & its malignancies are reviewed. |
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101. |
NPM inhibits ionizing irradiation-induced p53 transactivation, and interacts with p53 in hematopoietic cells. |
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102. |
Aloe-emodin caused increase in the amount of proform and fragment of nucleophosmin in cytoplasm may be one of the important events for aloe-emodin-induced H460 cell apoptosis pf mpm-small cell lung cancer. |
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103. |
involvement of NPM/B23 in the acute response of mammalian cells to environmental stress, such as UV rays |
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104. |
both alterations are crucial for acute myeloid leukemia NPM mutant export from nucleus to cytoplasm; NPM leukemic mutants in turn recruit the wild-type NPM from nucleoli to nucleoplasm and cytoplasm |
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105. |
unique B23 conformation in hepatoma |
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106. |
NPM inhibits ARF's p53-dependent activity by targeting it to nucleoli and impairing ARF-Mdm2 association. |
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107. |
NPM is a crucial regulator of p53 |
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108. |
the NPM1 mutation is not necessarily an early event during leukemogenesis; the NPM1 mutation was a favorable factor for achieving complete remission but was associated with a high relapse rate |
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109. |
new exon-12 NPM mutations in acute myeloid leukemia |
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110. |
While complex formation between ARF and NPM retains ARF in the nucleolus and prevents ARF from activating p53, DNA damaging treatments promote a transient subnuclear redistribution of ARF to the nucleoplasm, where promotes p53 activation. |
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111. |
COOH-terminal nuclear export signals of different strength ensure cytoplasmic accumulation of nucleophosmin leukemic mutants |
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112. |
CDK2-BRCA1-NPM pathway coordinately functions in cell growth and tumor progression pathways. |
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113. |
FRGY2a and YB1 disassemble nucleoli by sequestering B23, which is associated with pre-ribosomes and other structurally important nucleolar components |
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114. |
A novel mechanism of nucleophosmin (NPM) tumorigenesis establishes NPM as a crucial inhibitor of oncogene-induced apoptosis and senescence. |
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115. |
Src-kinases, particularly pp60(c-src), associate with and are activated by NPM-ALK expression in various cells, and in cell lines established from patients with large cell lymphoma |
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116. |
These data suggest that nucleophosmin is an early responder to DNA damage that prevents premature activation of p53. |
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117. |
results indicate that HCV core can recruit B23 and p300 to relieve the repression effect of YY1 on B23 promoter activity |
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118. |
identification of Ser-4 in B23 as a major physiological substrate of Polo-like kinase 1 |
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119. |
cleavage of B23 by granzyme b in intact vascular smooth muscle cells is dependent upon both cell type and phenotype |
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120. |
polyamine depletion increased expression of the NPM gene and enhances NPM nuclear translocation and increased NPM interacts with and stabilizes p53, leading to inhibition of IEC-6 cell proliferation |
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121. |
marker of proliferation activity of human peripheral lymphocytes |
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122. |
The molecular signature of cytoplasmic NPM+ AML includes up-regulation of several genes putatively involved in the maintenance of a stem-cell phenotype, suggesting that cytoplasmic NPM+ AML may derive from a multipotent hematopoietic progenitor. |
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123. |
Enforced expression of an NPM cytoplasmic mutant acutely attenuates p53-dependent and -independent functions of Arf tumor suppressor protein, and also affects endogenous NPM localization. |
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124. |
These findings indicate the involvement of nucleophosmin in the regulation of pre-mRNA processing, and its activity is controlled by CDK2-mediated phosphorylation on Thr(199). |
|
125. |
These results demonstrate a novel mechanism for transcriptional regulation of E2F1 and identify the functional role of nucleophosmin/B23 in modulating the binding of NF-kappaB, E2F1 and pRB to activate E2F1 promoter. |
|
126. |
data indicate that NPM1 exon 12 is mutated in acute myelogenous leukemias but not in other common human cancers, and suggest that the NPM1 mutation may not play a role in the tumorigenesis of common solid cancers |
|
127. |
overexpressed in acute myeloid leukemia while translocations associated with this gene are absent |
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128. |
BRCA1-BARD1 catalyzes the polyubiquitination of nucleolar phosphoprotein nucleophosmin/B23 |
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129. |
NPM1 mutations represent a common genetic abnormality in adult acute myeloid leukemia and appears to identify patients with improved response toward treatment. |
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130. |
results suggest that B23 plays an important role in the intracellular localization of the core protein and replication of Japanese encephalitis virus |
|
131. |
The sensitive RQ-PCR assays for NPM1 mutations can now monitor and quantify MRD in AML patients with normal karyotype and NPM1 gene mutations. |
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132. |
NPM/ALK-carrying T cell lymphoma (ALK+TCL) cells secrete IL-10 and TGF-beta and express FoxP3, indicating their T regulatory (Treg) cell phenotype. |
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133. |
NPM1 gene mutations cause a frame shift in the C-terminus of exon 12, disrupting the NPM nucleolar-localization signal or generating a leucine-rich nuclear export motif, resulting in abnormal cytoplasmic accumulation of NPM. |
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134. |
PAI-1 downregulates B23 in LnCAP prostatic cancer. |
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135. |
These findings suggest that an NPM/MLF1 fusion is the primary molecular abnormality in t(3;5) MDS and AML with multilineage dysplasia, and that cases with NPM/MLF1 may be clinically distinct from other MDS-associated disease |
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136. |
NPM/ALK-mediated induction of Bcl-XL |
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137. |
NPM inhibits hypoxia-induced p53 phosphorylation at Ser-15 and interacts with p53 in hypoxic cells; hypoxia-driven cancer progression may require increased expression of NPM to suppress p53 activation and maintain cell survival |
|
138. |
Cytoplasmic NPM is a characteristic feature of a large subgroup of patients with AML who have a normal karyotype, NPM gene mutations, and responsiveness to induction chemotherapy. |
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139. |
overexpression of NPM suppressed PKR activity, enhanced protein synthesis, and inhibited apoptosis. Fanconi anemia lymphoblasts expressed low levels of NPM, which correlated with high ground-state activation of PKR and hypersensitivity to apoptotic cues |
|
140. |
c-Myc-mediated expression of NPM decreases during retinoic acid-induced differentiation of HL-60 cells. |
|
141. |
Nucleophosmin (NPM) may be a Ran-Crm1 substrate that controls centrosome duplication. |
|
142. |
Loss of SHP1 enhances JAK3/STAT3 signaling and decreases proteosome degradation of JAK3 and NPM-ALK in ALK+ anaplastic large-cell lymphoma. |
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143. |
nucleophosmin is an NF-kappaB co-activator for the induction of the human SOD2 gene |
|
144. |
a novel association of B23 and Gadd45a and implicate B23 as an important regulator in Gadd45a nuclear import. |
|
145. |
NPM1 mutations may be also involved in the pathogenesis of myelodysplastic syndromes. |
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146. |
constitutive expression of C/EBPbeta in ALK-positive anaplastic large cell lymphoma and its relationship to NPM-ALK |
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147. |
AUF1 was phosphorylated by ALK in vitro and was hyperphosphorylated in NPM-ALK-expressing cells. |
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148. |
study could not find any NPM gene mutations in pediatric acute myeloid leukemia with normal karyotype |
|
149. |
Protein B23 is an abundant, multifunctional nucleolar phosphoprotein that behaves like a molecular chaperone, an activity that may be related to its role in ribosome biogenesis |