about
Upstream open reading frames: molecular switches in (patho)physiologyTribbles homolog 2 inactivates C/EBPalpha and causes acute myelogenous leukemiaAberrant nuclear factor-kappa B activity in acute myeloid leukemia: from molecular pathogenesis to therapeutic targetPrognostic implications of CEBPA mutations in pediatric acute myeloid leukemia: a report from the Japanese Pediatric Leukemia/Lymphoma Study GroupPharmacological targeting of the Wdr5-MLL interaction in C/EBPα N-terminal leukemia.EVI2B is a C/EBPα target gene required for granulocytic differentiation and functionality of hematopoietic progenitors.Characterizing disease states from topological properties of transcriptional regulatory networks.Identification of a myeloid committed progenitor as the cancer-initiating cell in acute promyelocytic leukemia.The biological effects of C/EBPalpha in K562 cells depend on the potency of the N-terminal regulatory region, not on specificity of the DNA binding domain.Clinical relevance of mutant NPM1 and CEBPA in patients with acute myeloid leukaemia - preliminary reportC/EBPα and MYB regulate FLT3 expression in AMLThe multifaceted functions of C/EBPα in normal and malignant haematopoiesis.Characterization of CEBPA mutations and promoter hypermethylation in pediatric acute myeloid leukemia.Gene mutations and molecularly targeted therapies in acute myeloid leukemia.Double CEBPA mutations, but not single CEBPA mutations, define a subgroup of acute myeloid leukemia with a distinctive gene expression profile that is uniquely associated with a favorable outcome.The gene signature in CCAAT-enhancer-binding protein α dysfunctional acute myeloid leukemia predicts responsiveness to histone deacetylase inhibitors.Synergistic induction of galectin-1 by CCAAT/enhancer binding protein alpha and hypoxia-inducible factor 1alpha and its role in differentiation of acute myeloid leukemic cells.Distinct patterns of mutations occurring in de novo AML versus AML arising in the setting of severe congenital neutropenia.Molecular genetic analysis of haematological malignancies: I. Acute leukaemias and myeloproliferative disorders.NAD(P)H:quinone oxidoreductase 1 (NQO1) competes with 20S proteasome for binding with C/EBPα leading to its stabilization and protection against radiation-induced myeloproliferative disease.C/EBPγ deregulation results in differentiation arrest in acute myeloid leukemia.Detection of CEBPA double mutants in acute myeloid leukemia using a custom gene expression arrayTranscriptional repression of c-Myb and GATA-2 is involved in the biologic effects of C/EBPalpha in p210BCR/ABL-expressing cells.Differential contributions of haematopoietic stem cells to foetal and adult haematopoiesis: insights from functional analysis of transcriptional regulators.EVI1 Interferes with Myeloid Maturation via Transcriptional Repression of Cebpa, via Binding to Two Far Downstream Regulatory Elements.Nanochannel Electroporation as a Platform for Living Cell Interrogation in Acute Myeloid Leukemia.CCAAT/enhancer-binding proteins and the pathogenesis of retrovirus infection.Predictive factors of relapse and survival in childhood acute myeloid leukemia: role of minimal residual disease.Origins of aberrant DNA methylation in acute myeloid leukemia.Molecular pathogenesis of atypical CML, CMML and MDS/MPN-unclassifiable.Transcription factor mutations in myelodysplastic/myeloproliferative neoplasmsBiomarkers in Hematological Malignancies: A Review of Molecular Testing in Hematopathology.CEBPA gene mutations in Egyptian acute myeloid leukemia patients: impact on prognosis.E6AP, an E3 ubiquitin ligase negatively regulates granulopoiesis by targeting transcription factor C/EBPα for ubiquitin-mediated proteasome degradation.A tumor suppressor role for C/EBPα in solid tumors: more than fat and blood.The presence of C/EBPα and its degradation are both required for TRIB2-mediated leukaemia.NPM1, FLT3 and CEBPA mutations in pediatric patients with AML from Argentina: incidence and prognostic value.Acute myeloid leukemia with the t(8;21) translocation: clinical consequences and biological implications.Overexpression of wild-type or mutants forms of CEBPA alter normal human hematopoiesis.Ectopic expression of C/EBPalpha and ID1 is sufficient to restore defective neutrophil development in low-risk myelodysplasia
P2860
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P2860
description
2005 nî lūn-bûn
@nan
2005 թուականի Մարտին հրատարակուած գիտական յօդուած
@hyw
2005 թվականի մարտին հրատարակված գիտական հոդված
@hy
2005年の論文
@ja
2005年論文
@yue
2005年論文
@zh-hant
2005年論文
@zh-hk
2005年論文
@zh-mo
2005年論文
@zh-tw
2005年论文
@wuu
name
CEBPA point mutations in hematological malignancies.
@ast
CEBPA point mutations in hematological malignancies.
@en
CEBPA point mutations in hematological malignancies.
@nl
type
label
CEBPA point mutations in hematological malignancies.
@ast
CEBPA point mutations in hematological malignancies.
@en
CEBPA point mutations in hematological malignancies.
@nl
prefLabel
CEBPA point mutations in hematological malignancies.
@ast
CEBPA point mutations in hematological malignancies.
@en
CEBPA point mutations in hematological malignancies.
@nl
P2093
P2860
P356
P1433
P1476
CEBPA point mutations in hematological malignancies.
@en
P2093
P2860
P2888
P304
P356
10.1038/SJ.LEU.2403614
P577
2005-03-01T00:00:00Z
P5875
P6179
1049861833