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2.
Leukemia ; 33(8): 1910-1922, 2019 08.
Artigo em Inglês | MEDLINE | ID: mdl-30858550

RESUMO

Minimal residual disease (MRD) is a powerful prognostic factor in acute lymphoblastic leukemia (ALL) and is used for patient stratification and treatment decisions, but its precise role in Philadelphia chromosome positive ALL is less clear. This uncertainty results largely from methodological differences relating to the use of real-time quantitative PCR (qRT-PCR) to measure BCR-ABL1 transcript levels for MRD analysis. We here describe the first results by the EURO-MRD consortium on standardization of qRT-PCR for the e1a2 BCR-ABL1 transcript in Ph + ALL, designed to overcome the lack of standardisation of laboratory procedures and data interpretation. Standardised use of EAC primer/probe sets and of centrally prepared plasmid standards had the greatest impact on reducing interlaboratory variability. In QC1 the proportion of analyses with BCR-ABL1/ABL1 ratios within half a log difference were 40/67 (60%) and 52/67 (78%) at 10-3 and 36/67 (53%) and 53/67 (79%) at 10-4BCR-ABL1/ABL1. Standardized RNA extraction, cDNA synthesis and cycler platforms did not improve results further, whereas stringent application of technical criteria for assay quality and uniform criteria for data interpretation and reporting were essential. We provide detailed laboratory recommendations for the standardized MRD analysis in routine diagnostic settings and in multicenter clinical trials for Ph + ALL.


Assuntos
Proteínas de Fusão bcr-abl/genética , Cromossomo Filadélfia , Guias de Prática Clínica como Assunto , Leucemia-Linfoma Linfoblástico de Células Precursoras/genética , Reação em Cadeia da Polimerase em Tempo Real/métodos , Consenso , Humanos , Neoplasia Residual , RNA Mensageiro/análise
3.
Leukemia ; 20(6): 1061-6, 2006 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-16642048

RESUMO

The emergence of ABL point mutations is the most frequent cause for imatinib resistance in chronic myelogenous leukemia (CML) patients and can occur during any phase of the disease; however, their clinical impact remains controversial. In this study, we retrospectively analyzed the predictive impact of 94 BCR-ABL kinase domain mutations (18 T315I, 26 P-loop, 50 in other sites) found in 89 imatinib-resistant CML patients. At imatinib onset, 64% of patients (57/89) were in chronic phase (CP), 24% (21/89) in accelerated phase (AP) and 12% (11/89) in blastic phase (BP). T315I and P-loop mutations were preferentially discovered in accelerated phase of BP CML, and other types of mutations in CP (P=0.003). With a median follow-up of 39.2 months (6.3-67.2), since imatinib initiation, overall survival (OS) was significantly worse for P-loop (28.3 months) and for T315I (12.6 months), and not reached for other mutations (P=0.0004). For CP only, multivariate analysis demonstrated a worse OS for P-loop mutations (P=0.014), and a worse progression-free survival (PFS) for T315I mutations (P=0.014). Therefore, P-loop and T315I mutations selectively impair the outcome of imatinib-resistant CML patients, in contrast to other mutations, which may benefit from dose escalation of imatinib, able to improve or stabilize disease response.


Assuntos
Resistencia a Medicamentos Antineoplásicos/genética , Proteínas de Fusão bcr-abl/genética , Leucemia Mielogênica Crônica BCR-ABL Positiva/genética , Piperazinas/uso terapêutico , Mutação Puntual , Pirimidinas/uso terapêutico , Adolescente , Adulto , Idoso , Benzamidas , Análise Mutacional de DNA , Relação Dose-Resposta a Droga , Feminino , França , Humanos , Mesilato de Imatinib , Leucemia Mielogênica Crônica BCR-ABL Positiva/diagnóstico , Leucemia Mielogênica Crônica BCR-ABL Positiva/tratamento farmacológico , Masculino , Pessoa de Meia-Idade , Valor Preditivo dos Testes , Estudos Retrospectivos , Taxa de Sobrevida , Resultado do Tratamento
4.
Blood Cancer J ; 7(4): e555, 2017 04 21.
Artigo em Inglês | MEDLINE | ID: mdl-28430172

RESUMO

The histone methyltransferase EZH2 has an essential role in the development of follicular lymphoma (FL). Recurrent gain-of-function mutations in EZH2 have been described in 25% of FL patients and induce aberrant methylation of histone H3 lysine 27 (H3K27). We evaluated the role of EZH2 genomic gains in FL biology. Using RNA sequencing, Sanger sequencing and SNP-arrays, the mutation status, copy-number and gene-expression profiles of EZH2 were assessed in a cohort of 159 FL patients from the PRIMA trial. Immunohistochemical (IHC) EZH2 expression (n=55) and H3K27 methylation (n=63) profiles were also evaluated. In total, 37% of patients (59/159) harbored an alteration in the EZH2 gene (mutation n=46, gain n=23). Both types of alterations were associated with highly similar transcriptional changes, with increased proliferation programs. An H3K27me3/me2 IHC score fully distinguished mutated from wild-type samples, showing its applicability as surrogate for EZH2 mutation analysis. However, this score did not predict the presence of gains at the EZH2 locus. The presence of an EZH2 genetic alteration was an independent factor associated with a longer progression-free survival (hazard ratio 0.58, 95% confidence interval 0.36-0.93, P=0.025). We propose that the copy-number status of EZH2 should also be considered when evaluating patient stratification and selecting patients for EZH2 inhibitor-targeted therapies.


Assuntos
Proteína Potenciadora do Homólogo 2 de Zeste/genética , Histona-Lisina N-Metiltransferase/genética , Linfoma Folicular/genética , Adulto , Idoso , Linhagem Celular Tumoral , Intervalo Livre de Doença , Feminino , Regulação Neoplásica da Expressão Gênica/genética , Histona Metiltransferases , Humanos , Linfoma Folicular/tratamento farmacológico , Linfoma Folicular/patologia , Masculino , Metilação/efeitos dos fármacos , Pessoa de Meia-Idade , Mutação/genética , Polimorfismo de Nucleotídeo Único/genética , Análise de Sequência de RNA
5.
Oncogene ; 16(22): 2949-54, 1998 Jun 04.
Artigo em Inglês | MEDLINE | ID: mdl-9671416

RESUMO

We report here the molecular study of a t(11;19)(q13;p13) translocation observed in a case of B-cell chronic lymphocytic leukemia. This translocation leads to the juxtaposition of the CCND1 gene on chromosome 11 to a new transcriptional unit on chromosome 19. The cDNA of this new evolutionarily conserved gene (named FLRG for Follistatin-Related Gene) codes for a secreted glycoprotein of the follistatin-module-protein family. FLRG is expressed in a wide range of human and murine adult tissues and its expression seems to be tightly regulated during murine embryogenesis. Its transcripts could not be detected in hematopoietic cells from all lineages and in particular in cells from lymphoid B and T lineage except in the t(11;19)-carrying leukemia described here. A great variability of expression is observed among the other tumoral cell lines analysed. Besides the t(11;19)-carrying leukemia described in this work, structural rearrangements of the FLRG locus have been found in a non-Hodgkin lymphoma, suggesting that it may play a role in leukemogenesis.


Assuntos
Cromossomos Humanos Par 11 , Cromossomos Humanos Par 19 , Ciclina D1/genética , Glicoproteínas , Glicoproteínas/genética , Glicoproteínas/farmacologia , Leucemia Linfocítica Crônica de Células B/genética , Translocação Genética , Sequência de Aminoácidos , Animais , Sequência de Bases , Células COS , DNA Complementar , Folistatina , Proteínas Relacionadas à Folistatina , Glicoproteínas/metabolismo , Humanos , Linfoma de Células B/genética , Dados de Sequência Molecular , Homologia de Sequência de Aminoácidos
6.
Oncogene ; 19(38): 4446-50, 2000 Sep 07.
Artigo em Inglês | MEDLINE | ID: mdl-10980622

RESUMO

In haematopoietic malignancies the MLL gene, located on chromosome 11q23, is frequently disrupted by chromosome rearrangement, generally resulting in fusion to various partner genes. We have previously reported a t(11;15)(q23;q14) in a case of acute myeloblastic leukaemia. Here, we report the cloning of a novel MLL partner, AF15q14, at chromosome 15q14. In this translocation, the breakpoint occurred in exon 8 of MLL and exon 10 of AF15q14. The normal AF15q14 transcripts of approximately 8.5 kb in size, are expressed in different tumoral cell lines, in a variety of normal tissues, and in all the foetal tissues tested. Sequencing of AF15q14 cDNA revealed a putative open reading frame of 1833 amino acids that had no homology with any other known protein. The C-terminal end of the putative AF15q14 contained a bipartite nuclear localization site. The translocation t(11;15) preserved the open reading frame between MLL and the 3' end of AF15q14. The contribution of AF15q14 to the fusion protein was only 85 amino acids. Immunofluorescence staining experiments with expression vectors encoding these 85 amino acids confirmed the functionality of the predicted nuclear localization site.


Assuntos
Cromossomos Humanos Par 15 , Proteínas de Ligação a DNA/genética , Leucemia Mielomonocítica Aguda/genética , Proto-Oncogenes , Fatores de Transcrição , Sequência de Aminoácidos , Fusão Gênica Artificial , Sequência de Bases , Cromossomos Humanos Par 11 , Clonagem Molecular , Histona-Lisina N-Metiltransferase , Humanos , Masculino , Pessoa de Meia-Idade , Dados de Sequência Molecular , Proteína de Leucina Linfoide-Mieloide , Análise de Sequência de DNA , Homologia de Sequência de Aminoácidos , Transcrição Gênica , Translocação Genética
7.
Oncogene ; 20(39): 5409-19, 2001 Sep 06.
Artigo em Inglês | MEDLINE | ID: mdl-11571638

RESUMO

The FLRG gene encodes a secreted glycoprotein that binds to activin and is highly homologous to follistatin, an activin ligand. We cloned the promoter region of the human FLRG gene, and defined the minimal region necessary for transcription activation in a reporter-system assay. We showed that the fragment between positions -130 and +6, which consists of multiple consensus Sp1-binding sites, is required for the constitutive expression of the FLRG gene. We demonstrate here that FLRG mRNA expression is rapidly induced by TGFbeta or by transfection with Smad protein expression vectors in human HepG2 cells. We investigated the transcription-regulation mechanism of FLRG expression in HepG2 cells following treatment with TGFbeta. By deletion and point-mutation analysis of the FLRG promoter, we identified a Smad-binding element involved in the TGFbeta-inducible expression of the FLRG gene. Moreover, transactivation of the FLRG promoter by TGFbeta was compromised by dominant-negative mutants of Smad3 and Smad4 proteins. In addition, gel electrophoresis mobility-shift assays demonstrated the specific interaction of Smad3 and Smad4 proteins with the Smad-binding element consensus motif found in the FLRG promoter. Taken together, our data imply that Smad proteins participate in the regulation of expression of FLRG, a new target of TGFbeta transcription activation.


Assuntos
Proteínas de Ligação a DNA/fisiologia , Glicoproteínas/genética , Transativadores/fisiologia , Fator de Crescimento Transformador beta/farmacologia , Ativinas , Sequência de Bases , Clonagem Molecular , Sequência Consenso , Proteínas Relacionadas à Folistatina , Genes Reporter , Glicoproteínas/metabolismo , Humanos , Inibinas/metabolismo , Dados de Sequência Molecular , Regiões Promotoras Genéticas , RNA Mensageiro/biossíntese , Elementos de Resposta , Proteína Smad3 , Proteína Smad4 , Ativação Transcricional , Células Tumorais Cultivadas , Regulação para Cima
8.
Bone Marrow Transplant ; 35(6): 601-8, 2005 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-15756285

RESUMO

In order to study efficacy, toxicity and the long-term results of donor lymphocyte infusions (DLI), we retrospectively analyzed DLI given for relapse after conventional allogeneic hematopoietic stem cell transplantation (HSCT) in 30 patients with a median delay of 107.5 months after transplant and 58 months after DLI. After DLI, 15 patients established full donor chimerism, three patients developed grade III and one grade IV acute GVHD. A total of 15 patients achieved a disease response. Among the 14 patients with chronic myeloid leukemia (CML), 11 are alive at the last follow-up: five are in complete molecular response (CMR) and two in complete cytogenetic response (CCR) with no other intervention after DLI, three in CMR after imatinib mesylate given after DLI and one in complete hematological response after imatinib mesylate and reduced-intensity conditioning allogeneic SCT performed after DLI. At the time of the last follow-up, 19 (63%) patients died and 11 (37%) remain alive. The 3-year probability of survival for the entire population, CML patients and non-CML patients, was 60, 93, 62% after transplantation, and 48, 80 and 48% after DLI, respectively. A multivariate analysis demonstrated a significantly worse survival rate after transplantation for female recipients, advanced disease and acute leukemia before transplantation.


Assuntos
Transplante de Células-Tronco Hematopoéticas/métodos , Transfusão de Linfócitos , Adolescente , Adulto , Feminino , Seguimentos , Doença Enxerto-Hospedeiro , Neoplasias Hematológicas/complicações , Neoplasias Hematológicas/mortalidade , Neoplasias Hematológicas/terapia , Transplante de Células-Tronco Hematopoéticas/efeitos adversos , Transplante de Células-Tronco Hematopoéticas/mortalidade , Humanos , Masculino , Pessoa de Meia-Idade , Recidiva , Estudos Retrospectivos , Fatores de Risco , Análise de Sobrevida , Quimeras de Transplante , Condicionamento Pré-Transplante/métodos , Transplante Homólogo , Resultado do Tratamento
9.
Leukemia ; 11(8): 1214-9, 1997 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-9264372

RESUMO

B cell chronic lymphocytic leukemias (B-CLL) like other blood cell malignancies are characterized by chromosomal anomalies directly involved in tumor pathogenesis. We report here the molecular characterization of a t(7;14)(q21;q32) chromosomal translocation observed during the course of a B-CLL. We show that this translocation led to the juxtaposition of the immunoglobulin heavy chain locus on chromosome 14 to an endogenous retroviral sequence belonging to the THE family (transposable-like human element) on chromosome 7q21. RT-PCR analysis demonstrated that this sequence is transcribed in most of the tumoral and normal tissue analyzed and in the B-CLL described here. These data raise the question of the role of transposable elements in the pathogeny of some leukemias or at least, in the occurrence of chromosomal rearrangements. Structural rearrangements of the 7q21-22 region are frequently encountered in myeloid disorders, and the work presented here could help in their characterization.


Assuntos
Aberrações Cromossômicas/genética , Cromossomos Humanos Par 14 , Cromossomos Humanos Par 7 , Leucemia Linfocítica Crônica de Células B/genética , Sequências Repetitivas de Ácido Nucleico , Retroviridae/genética , Translocação Genética , Sequência de Bases , Southern Blotting , Transtornos Cromossômicos , Clonagem Molecular , Citogenética , DNA de Neoplasias/genética , Feminino , Expressão Gênica , Humanos , Pessoa de Meia-Idade , Dados de Sequência Molecular , RNA Mensageiro/genética , RNA Neoplásico/genética , Mapeamento por Restrição
10.
Leukemia ; 11(10): 1696-9, 1997 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-9324291

RESUMO

Recurrent anomalies of the short arm of chromosome 9, including interstitial deletions and translocations, have often been described. Recently two cyclin-dependent kinase inhibitors, known as P16 (INK4A/MTS1) and P15 (INK4B/MTS2), which map to 9p21, have been found deleted in a wide range of tumors and particularly in leukemic cells. We report here Southern blot analyses of cyclin-dependent kinase inhibitors (P16, P15, P21, and P27) status in primary tumoral cells of 121 patients with acute lymphoblastic leukemias, 85 patients with acute myeloid leukemias and 42 patients with B-chronic lymphocytic leukemias. P16 inactivation was found in 25 of 38 T-ALLs and in 28 of 83 B-lineage ALLs. In eight cases (three T-ALLs and five B-lineage ALLs), one or both alleles of P16 locus were rearranged. In these cases, breakpoints occurred within the two major breakpoints cluster regions previously described in T-ALLs. Homozygous P16 deletions were observed in two of 85 AMLs but in none of the 42 B-CLL cases tested. Our results suggest that P16 inactivation are the most frequent event observed in ALL (44%), are quite rare in AML (<2%) and seem to be absent in CLL. Search for P27 and P21 deletion was negative in B/T-lineage ALLs and monoallelic deletions of P27 were found in four AML cases (5%).


Assuntos
Proteínas de Transporte/genética , Proteínas de Ciclo Celular , Leucemia/enzimologia , Leucemia/genética , Proteínas Supressoras de Tumor , Adulto , Alelos , Southern Blotting , Criança , Inibidor de Quinase Dependente de Ciclina p15 , Inibidor p16 de Quinase Dependente de Ciclina , Deleção de Genes , Regulação Leucêmica da Expressão Gênica , Homozigoto , Humanos , Leucemia Mieloide Aguda/enzimologia , Leucemia Mieloide Aguda/genética , Leucemia de Células T/embriologia , Leucemia de Células T/genética , Leucemia-Linfoma Linfoblástico de Células Precursoras/enzimologia , Leucemia-Linfoma Linfoblástico de Células Precursoras/genética
11.
Leukemia ; 11(3): 370-5, 1997 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-9067576

RESUMO

It is well known that loss of tumor suppressor genes and more generally of antiproliferative genes plays a key role in the development of most tumors. We report here the cloning of the mouse BTG3 gene and show that its human counterpart maps on chromosome 21. This evolutionarily conserved gene codes for a 30 kDa protein and is expressed in most adult murine and human tissues analyzed. However, we demonstrate that its expression is cell cycle dependent and peaks at the end of the G1 phase. This gene is homologous to the human BTG1, BTG2 and TOB genes which were demonstrated to act as inhibitors of cell proliferation. Its description allowed us to define better this seven gene family (the BTG gene family) at the structural level and to speculate about its physiological role in normal and tumoral cells. This family is mainly characterized by the presence of two conserved domains (BTG boxes A and B) of as yet undetermined function which are separated by a non-conserved 20-25 amino acid sequence.


Assuntos
DNA Complementar/genética , DNA Complementar/isolamento & purificação , Genes Supressores de Tumor , Sequência de Aminoácidos , Animais , Sequência de Bases , Northern Blotting , Ciclo Celular/fisiologia , Cromossomos Humanos Par 21 , Clonagem Molecular , Humanos , Camundongos , Dados de Sequência Molecular , Filogenia
12.
Leukemia ; 29(2): 369-76, 2015 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-25036192

RESUMO

Serial quantification of BCR-ABL1 mRNA is an important therapeutic indicator in chronic myeloid leukaemia, but there is a substantial variation in results reported by different laboratories. To improve comparability, an internationally accepted plasmid certified reference material (CRM) was developed according to ISO Guide 34:2009. Fragments of BCR-ABL1 (e14a2 mRNA fusion), BCR and GUSB transcripts were amplified and cloned into pUC18 to yield plasmid pIRMM0099. Six different linearised plasmid solutions were produced with the following copy number concentrations, assigned by digital PCR, and expanded uncertainties: 1.08±0.13 × 10(6), 1.08±0.11 × 10(5), 1.03±0.10 × 10(4), 1.02±0.09 × 10(3), 1.04±0.10 × 10(2) and 10.0±1.5 copies/µl. The certification of the material for the number of specific DNA fragments per plasmid, copy number concentration of the plasmid solutions and the assessment of inter-unit heterogeneity and stability were performed according to ISO Guide 35:2006. Two suitability studies performed by 63 BCR-ABL1 testing laboratories demonstrated that this set of 6 plasmid CRMs can help to standardise a number of measured transcripts of e14a2 BCR-ABL1 and three control genes (ABL1, BCR and GUSB). The set of six plasmid CRMs is distributed worldwide by the Institute for Reference Materials and Measurements (Belgium) and its authorised distributors (https://ec.europa.eu/jrc/en/reference-materials/catalogue/; CRM code ERM-AD623a-f).


Assuntos
Proteínas de Fusão bcr-abl/genética , Proteínas de Fusão bcr-abl/metabolismo , Plasmídeos/genética , Reação em Cadeia da Polimerase em Tempo Real/normas , Calibragem , Clonagem Molecular , DNA , Proteínas de Escherichia coli/genética , Dosagem de Genes , Humanos , Proteínas de Membrana Transportadoras/genética , Proteínas Proto-Oncogênicas c-bcr/genética , RNA Mensageiro/metabolismo , Padrões de Referência
13.
Int J Hematol ; 61(4): 165-78, 1995 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-8547605

RESUMO

A novel mutation of 523 GAT-->TAT (175 Asp-->Tyr) in exon 4 of the band 4.2 gene was detected in a 37-year-old Japanese patient with total lack of band 4.2 protein, designated as allele 4.2 Komatsu. In this patient, moderate uncompensated hemolytic anemia (red cell count 3.38 x 10(6)/microliters, hemoglobin 10.8 g/dl, hematocrit 30.9%, reticulocytes 12.4%, indirect bilirubin 1.84 mg/dl) with ovalostomatocytosis and increased osmotic fragility had been noted since birth. Family studies revealed no overt hemolytic anemia in other family members, essentially normal red cell morphology, and a normal profile of red cell membrane proteins including band 4.2. Genetic studies proved that the proband was homozygous and all the family members studied were heterozygous with respect to the mutation of 523 GAT-->TAT of the band 4.2 gene. Although band 4.2 was completely absent in the proband, trace amounts of 72 kDa and 74 kDa peptides were detected in the red cells of all the family members, in which the mutation of 424 GCT-->ACT at exon 3 of the band 4.2 gene (Nippon type) was not present. Electron microscopic studies with the surface replica method and the quick-freeze deep-etching method showed the most marked disorganization of the cytoskeletal network in the patient's red cells in situ among the cases of band 4.2 deficiencies we have studied. This suggests that the amino acid of the band 4.2 protein, which was affected by the present mutation in exon 4, is much more crucial for the functioning of band 4.2 protein than that at codon 142 in exon 3. The cytoplasmic domain of band 3 in the proband's red cells was essentially normal in protein chemistry and in gene analysis with single-stranded conformation polymorphism (SSCP).


Assuntos
Anemia Hemolítica Congênita/genética , Proteínas Sanguíneas/deficiência , Proteínas Sanguíneas/genética , Citoesqueleto/ultraestrutura , Eritrócitos Anormais/ultraestrutura , Adulto , Alelos , Anemia Hemolítica Congênita/sangue , Sequência de Bases , Proteínas do Citoesqueleto , Feminino , Técnica de Congelamento e Réplica , Genes , Genótipo , Humanos , Masculino , Proteínas de Membrana , Dados de Sequência Molecular , Linhagem , Mutação Puntual , Polimorfismo Conformacional de Fita Simples
16.
Leukemia ; 26(6): 1247-54, 2012 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-22289988

RESUMO

Recently, DNA methyltransferase 3A (DNMT3A) mutations have been identified in acute myeloid leukemia (AML), the highest frequency being found within cytogenetically normal (CN) AML. In this study, diagnostic samples from 123 adults younger than 60 years with primary CN-AML homogeneously treated in the Acute Leukemia French Association-9801 and -9802 trials were screened for mutations in DNMT3A-conserved domains by direct sequencing. Patients were also assessed for the presence of FLT3 (fms-like tyrosine kinase receptor-3), NPM1 (nucleophosmin), CEBPA, WT1 (Wilms tumor 1), IDH1 (isocitrate dehydrogenase 1) and IDH2 mutations. Thirty-eight mutations were detected in 36 patients (29%): 36 nucleotide substitutions, mostly affecting amino-acid residue R882 and two frameshift deletions. DNMT3A mutations were significantly associated with the French-American-British subtypes M4/M5 and the presence of NPM1 mutations. In the whole cohort, DNMT3A mutated patients had a shorter event-free survival (5-year EFS: 13% vs 32%, P = 0.02) and overall survival (5-year OS: 23% vs 45%, P = 0.02) compared with DNMT3A wild-type patients. In multivariate analysis including age, white blood cell count, NPM1/FLT3-internal tandem duplication/CEBPA risk group and DNMT3A mutational status, the presence of a DNMT3A mutation remained an independent adverse prognostic factor for EFS and OS, suggesting that testing for DNMT3A mutations could help further improve risk stratification in CN-AML.


Assuntos
Biomarcadores Tumorais/genética , Análise Citogenética , DNA (Citosina-5-)-Metiltransferases/genética , Leucemia Mieloide Aguda/genética , Leucemia Mieloide Aguda/mortalidade , Mutação/genética , Adolescente , Adulto , DNA Metiltransferase 3A , DNA de Neoplasias/genética , Feminino , Seguimentos , Humanos , Leucemia Mieloide Aguda/classificação , Masculino , Pessoa de Meia-Idade , Nucleofosmina , Reação em Cadeia da Polimerase , Prognóstico , Estudos Prospectivos , Estudos Retrospectivos , Fatores de Risco , Taxa de Sobrevida , Adulto Jovem , Tirosina Quinase 3 Semelhante a fms/genética
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