Your browser doesn't support javascript.
loading
Mostrar: 20 | 50 | 100
Resultados 1 - 20 de 87
Filtrar
Más filtros

Banco de datos
Tipo del documento
Intervalo de año de publicación
1.
Haematologica ; 2024 Apr 11.
Artículo en Inglés | MEDLINE | ID: mdl-38618686

RESUMEN

Not available.

2.
Eur J Haematol ; 2024 Jul 05.
Artículo en Inglés | MEDLINE | ID: mdl-38967591

RESUMEN

Shwachman-Diamond syndrome (SDS) is an inherited bone marrow failure disorder that often presents at infancy. Progress has been made in revealing causal mutated genes (SBDS and others), ribosome defects, and hematopoietic aberrations in SDS. However, the mechanism underlying the hematopoietic failure remained unknown, and treatment options are limited. Herein, we investigated the onset of SDS embryonic hematopoietic impairments. We generated SDS and control human-derived induced pluripotent stem cells (iPSCs). SDS iPSCs recapitulated the SDS hematological phenotype. Detailed stepwise evaluation of definitive hematopoiesis revealed defects that started at the early emerging hematopoietic progenitor (EHP) stage after mesoderm and hemogenic endothelium were normally induced. Hematopoietic potential of EHPs was markedly reduced, and the introduction of SBDS in SDS iPSCs improved colony formation. Transcriptome analysis revealed reduced expression of ribosome and oxidative phosphorylation-related genes in undifferentiated and differentiated iPSCs. However, certain pathways (e.g., DNA replication) and genes (e.g., CHCHD2) were exclusively or more severely dysregulated in EHPs compared with earlier and later stages. To our knowledge, this study offers for the first time an insight into the embryonic onset of human hematopoietic defects in an inherited bone marrow failure syndrome and reveals cellular and molecular aberrations at critical stages of hematopoietic development toward EHPs.

3.
Pediatr Blood Cancer ; 71(8): e31070, 2024 Aug.
Artículo en Inglés | MEDLINE | ID: mdl-38757488

RESUMEN

Severe aplastic anemia (SAA) is a rare potentially fatal hematologic disorder. Although overall outcomes with treatment are excellent, there are variations in management approach, including differences in treatment between adult and pediatric patients. Certain aspects of treatment are under active investigation in clinical trials. Because of the rarity of the disease, some pediatric hematologists may have relatively limited experience with the complex management of SAA. The following recommendations reflect an up-to-date evidence-based approach to the treatment of children with newly diagnosed SAA.


Asunto(s)
Anemia Aplásica , Humanos , Anemia Aplásica/terapia , Anemia Aplásica/diagnóstico , Niño , Medicina Basada en la Evidencia , Guías de Práctica Clínica como Asunto/normas
4.
Pediatr Blood Cancer ; 71(8): e31075, 2024 Aug.
Artículo en Inglés | MEDLINE | ID: mdl-38764170

RESUMEN

Severe aplastic anemia (SAA) is a rare potentially fatal hematologic disorder. Although overall outcomes with treatment are excellent, there are variations in management approach, including differences in treatment between adult and pediatric patients. Certain aspects of treatment are under active investigation in clinical trials. Because of the rarity of the disease, some pediatric hematologists may have relatively limited experience with the complex management of SAA. The following recommendations reflect an up-to-date evidence-based approach to the treatment of children with relapsed or refractory SAA.


Asunto(s)
Anemia Aplásica , Humanos , Anemia Aplásica/terapia , Niño , Recurrencia , Medicina Basada en la Evidencia , Trasplante de Células Madre Hematopoyéticas
5.
Eur J Haematol ; 108(4): 278-287, 2022 Apr.
Artículo en Inglés | MEDLINE | ID: mdl-34897809

RESUMEN

Classification of inherited bone marrow failure syndromes (IBMFSs) according to clinical and genetic diagnoses enables proper adjustment of treatment. Unfortunately, 30% of patients enrolled in the Canadian Inherited Marrow Failure Registry (CIMFR) with features suggesting hereditability could not be classified with a specific syndromic diagnosis. We analyzed the outcome of hematopoietic stem cell transplantation (HSCT) in unclassified IBMFSs (uIBMFSs) and the factors associated with outcome. Twenty-two patients with uIBMFSs and 70 patients with classified IBMFSs underwent HSCT. Five-year overall survival of uIBMFS patients after HSCT was inferior to that of patients with classified IBMFSs (56% vs 76.5%). The outcome of patients with uIBMFS who received cord blood was significantly lower than that of patients who received other stem cell sources (14.8% vs 90.9%). Engraftment failure was higher among patients with uIBMFS who received cord blood than those who received bone marrow. None of the following factors were significantly associated with poor survival: transfusion load, transplant indication, the intensity of conditioning regimen, human leukocyte antigen-identical sibling/alternative donor. We suggest that identifying the genetic diagnosis is essential to modulate the transplant procedure including conditioning agents and stem cell sources for better outcome and the standard cord blood transplantation (CBT) should be avoided in uIBMFS.


Asunto(s)
Enfermedad Injerto contra Huésped , Trasplante de Células Madre Hematopoyéticas , Trasplante de Médula Ósea , Canadá/epidemiología , Síndromes Congénitos de Insuficiencia de la Médula Ósea , Enfermedad Injerto contra Huésped/diagnóstico , Enfermedad Injerto contra Huésped/etiología , Antígenos HLA , Trasplante de Células Madre Hematopoyéticas/efectos adversos , Trasplante de Células Madre Hematopoyéticas/métodos , Humanos , Estudios Retrospectivos , Acondicionamiento Pretrasplante/métodos
6.
Am J Hematol ; 96(11): 1491-1504, 2021 11 01.
Artículo en Inglés | MEDLINE | ID: mdl-34342889

RESUMEN

The North American Pediatric Aplastic Anemia Consortium (NAPAAC) is a group of pediatric hematologist-oncologists, hematopathologists, and bone marrow transplant physicians from 46 institutions in North America with interest and expertise in aplastic anemia, inherited bone marrow failure syndromes, and myelodysplastic syndromes. The NAPAAC Bone Marrow Failure Diagnosis and Care Guidelines Working Group was established with the charge of harmonizing the approach to the diagnostic workup of aplastic anemia in an effort to standardize best practices in the field. This document outlines the rationale for initial evaluations in pediatric patients presenting with signs and symptoms concerning for severe aplastic anemia.


Asunto(s)
Anemia Aplásica/diagnóstico , Anemia Aplásica/patología , Médula Ósea/patología , Niño , Diagnóstico Diferencial , Hemoglobina Fetal/análisis , Antígenos HLA/análisis , Humanos , América del Norte , Índice de Severidad de la Enfermedad
7.
Br J Haematol ; 189(5): 976-981, 2020 06.
Artículo en Inglés | MEDLINE | ID: mdl-32128787

RESUMEN

Progressive cytopenia is a serious complication among paediatric patients with inherited bone marrow failure syndromes (IBMFS). Androgens have been used to improve blood counts in different bone marrow failure conditions. Little is known about efficacy and toxicity with new androgens (i.e., danazol) in different types of IBMFS. We identified 29 patients from the Canadian Inherited Marrow Failure Registry, who received oxymetholone or danazol. Sixteen (55%) had haematological response including patients with unclassified IBMFS (45%). Danazol showed a better toxicity profile and similar efficacy compared to oxymetholone. Androgens are an effective and safe option to ameliorate bone marrow failure in IBMFS.


Asunto(s)
Andrógenos/uso terapéutico , Trastornos de Fallo de la Médula Ósea/tratamiento farmacológico , Adolescente , Adulto , Andrógenos/efectos adversos , Trastornos de Fallo de la Médula Ósea/sangre , Trastornos de Fallo de la Médula Ósea/genética , Trastornos de Fallo de la Médula Ósea/terapia , Canadá/epidemiología , Linaje de la Célula , Niño , Preescolar , Terapia Combinada , Danazol/efectos adversos , Danazol/uso terapéutico , Progresión de la Enfermedad , Sustitución de Medicamentos , Femenino , Trasplante de Células Madre Hematopoyéticas , Humanos , Lactante , Masculino , Persona de Mediana Edad , Oximetolona/efectos adversos , Oximetolona/uso terapéutico , Pancitopenia/tratamiento farmacológico , Pancitopenia/etiología , Sistema de Registros , Trombocitopenia/tratamiento farmacológico , Trombocitopenia/etiología , Resultado del Tratamiento , Virilismo/inducido químicamente
8.
Pediatr Blood Cancer ; 67(10): e28652, 2020 10.
Artículo en Inglés | MEDLINE | ID: mdl-32779892

RESUMEN

BACKGROUND: Myelodysplastic syndromes (MDS) represent a group of clonal hematopoietic stem cell disorders that commonly progress to acute myeloid leukemia (AML). The diagnostics, prognostics, and treatment of adult MDS are established but do not directly translate to children and adolescents. Pediatric MDS is a rare disease, characterized by unique cytogenetics and histology compared with adult MDS, and often arises secondary to germline predisposition or cytotoxic exposures. Our objective was to highlight aspects of diagnosis/management that would benefit from further systematic review toward the development of clinical practice guidelines for pediatric MDS. PROCEDURE: The North American Pediatric Aplastic Anemia Consortium (NAPAAC) is composed of collaborative institutions with a strong interest in pediatric bone marrow failure syndromes and hematologic malignancies. The NAPAAC MDS working group developed a national survey distributed to 35 NAPAAC institutions to assess data on (1) clinical presentation of pediatric MDS, (2) diagnostic evaluation, (3) criteria for diagnosis, (4) supportive care and treatment decisions, and (5) role of hematopoietic stem cell transplantation (HSCT). RESULTS: Twenty-eight of 35 institutions returned the survey. Most centers agreed on a common diagnostic workup, though there was considerable variation regarding the criteria for diagnosis. Although there was consensus on supportive care, treatment strategies, including the role of cytoreduction and HSCT, varied across centers surveyed. CONCLUSIONS: There is lack of national consensus on diagnosis and treatment of pediatric MDS. This survey identified key aspects of MDS management that will warrant systematic review toward the goal of developing national clinical practice guidelines for pediatric MDS.


Asunto(s)
Toma de Decisiones , Trasplante de Células Madre Hematopoyéticas/métodos , Síndromes Mielodisplásicos/diagnóstico , Síndromes Mielodisplásicos/terapia , Pautas de la Práctica en Medicina/estadística & datos numéricos , Anemia Aplásica/diagnóstico , Anemia Aplásica/terapia , Niño , Humanos , Pronóstico , Estudios Retrospectivos , Encuestas y Cuestionarios , Tasa de Supervivencia
9.
J Pediatr Hematol Oncol ; 42(3): 170-174, 2020 04.
Artículo en Inglés | MEDLINE | ID: mdl-32134844

RESUMEN

The distinction between myelodysplastic syndrome (MDS) and acute myeloid leukemia (AML) often relies on an arbitrary marrow blast cutoff of 30% in pediatrics and 20% in adults. There is little data about the treatment of children with extramedullary myeloid malignancy that has features of both, MDS and AML. Herein, we report for the first time 2 patients MDS/AML (1 with Shwachman-Diamond syndrome and 1 with idiopathic MDS and monosomy 7) who presented with extramedullary complications, received treatment with azacitidine, achieved complete remission and subsequently underwent hematopoietic stem cell transplantation.


Asunto(s)
Antimetabolitos Antineoplásicos/uso terapéutico , Azacitidina/uso terapéutico , Leucemia Mieloide Aguda/tratamiento farmacológico , Síndromes Mielodisplásicos/tratamiento farmacológico , Adolescente , Preescolar , Deleción Cromosómica , Cromosomas Humanos Par 7 , Humanos , Leucemia Mieloide Aguda/genética , Masculino , Síndromes Mielodisplásicos/genética , Síndrome de Shwachman-Diamond/complicaciones
10.
J Med Genet ; 56(5): 340-346, 2019 05.
Artículo en Inglés | MEDLINE | ID: mdl-30327448

RESUMEN

BACKGROUND: Dandy-Walker malformation features agenesis/hypoplasia of the cerebellar vermis, cystic dilatation of the fourth ventricle and enlargement of posterior fossa. Although Dandy-Walker malformation is relatively common and several genes were linked to the syndrome, the genetic cause in the majority of cases is unknown. OBJECTIVE: To identify the mutated gene responsible for Dandy-Walker malformation, kidney disease and bone marrow failure in four patients from two unrelated families. METHODS: Medical assessment, sonographic, MRI and pathological studies were used to define phenotype. Chromosomal microarray analysis and whole-exome sequence were performed to unravel the genotype. RESULTS: We report four subjects from two unrelated families with homozygous mutations in the Exocyst Complex Component 3-Like-2 gene (EXOC3L2).EXOC3L2 functions in trafficking of post-Golgi vesicles to the plasma membrane. In the first family a missense mutation in a highly conserved amino acid, p.Leu41Gln, was found in three fetuses; all had severe forms of Dandy-Walker malformation that was detectable by prenatal ultrasonography and confirmed by autopsy. In the second family, the affected child carried a nonsense mutation, p.Arg72*, and no detected protein. He had peritrigonal and cerebellar white matter abnormalities with enlargement of the ventricular trigones, developmental delay, pituitary hypoplasia, severe renal dysplasia and bone marrow failure. CONCLUSION: We propose that biallelic EXOC3L2 mutations lead to a novel syndrome that affects hindbrain development, kidney and possibly the bone marrow.


Asunto(s)
Alelos , Síndrome de Dandy-Walker/diagnóstico , Síndrome de Dandy-Walker/genética , Mutación , Fenotipo , Proteínas de Transporte Vesicular/genética , Biopsia , Encéfalo/patología , Variaciones en el Número de Copia de ADN , Homocigoto , Humanos , Riñón/metabolismo , Imagen por Resonancia Magnética , Evaluación de Síntomas , Síndrome , Ultrasonografía , Proteínas de Transporte Vesicular/metabolismo , Secuenciación del Exoma
11.
Angiogenesis ; 22(1): 95-102, 2019 02.
Artículo en Inglés | MEDLINE | ID: mdl-30168024

RESUMEN

Vascular complications such as bleeding due to gastrointestinal telangiectatic anomalies, pulmonary arteriovenous malformations, hepatopulmonary syndrome, and retinal vessel abnormalities are being reported in patients with telomere biology disorders (TBDs) more frequently than previously described. The international clinical care consortium of telomere-associated ailments and family support group Dyskeratosis Congenita Outreach, Inc. held a workshop on vascular abnormalities in the TBDs at the National Cancer Institute in October 2017. Clinicians and basic scientists reviewed current data on vascular complications, hypotheses for the underlying biology and developed new collaborations to address the etiology and clinical management of vascular complications in TBDs.


Asunto(s)
Fístula Arteriovenosa , Arteria Pulmonar/anomalías , Venas Pulmonares/anomalías , Telangiectasia , Telómero , Animales , Fístula Arteriovenosa/genética , Fístula Arteriovenosa/metabolismo , Fístula Arteriovenosa/patología , Educación , Humanos , Arteria Pulmonar/metabolismo , Arteria Pulmonar/patología , Venas Pulmonares/metabolismo , Venas Pulmonares/patología , Telangiectasia/genética , Telangiectasia/metabolismo , Telangiectasia/patología , Telómero/genética , Telómero/metabolismo , Telómero/patología
14.
Pediatr Blood Cancer ; 64(2): 302-305, 2017 02.
Artículo en Inglés | MEDLINE | ID: mdl-27577695

RESUMEN

To study the prevalence of pediatric cancer patients who have underlying inherited bone marrow failure syndrome (IBMFS), we retrospectively reviewed the medical records of newly diagnosed pediatric cancer patients at The Hospital for Sick Children from June 2009 to May 2010, focusing on clinical, laboratory, and treatment-related findings which may indicate underlying IBMFS. We found five (1.8%) patients out of 276 who had two or more findings suggestive of IBMFS. We conclude that a small fraction of patients with cancer have clinical features that indicate investigations to rule out underlying IBMFSs. A prospective study is needed to determine their prevalence.


Asunto(s)
Enfermedades de la Médula Ósea/diagnóstico , Neoplasias/complicaciones , Adolescente , Enfermedades de la Médula Ósea/etiología , Niño , Preescolar , Femenino , Estudios de Seguimiento , Humanos , Masculino , Neoplasias/patología , Pronóstico , Estudios Retrospectivos
15.
Haematologica ; 101(12): 1508-1515, 2016 12.
Artículo en Inglés | MEDLINE | ID: mdl-27540140

RESUMEN

Advanced myelodysplastic syndrome harbors a high risk of progression to acute myeloid leukemia and poor prognosis. In children, there is no established treatment to prevent or delay progression to leukemia prior to hematopoietic stem cell transplantation. Azacitidine is a hypomethylating agent, which was shown to slow progression to leukemia in adults with myelodysplastic syndrome. There is little data on the efficacy of azacitidine in children. We reviewed 22 pediatric patients with advanced myelodysplastic syndrome from a single center, diagnosed between January 2000 and December 2015. Of those, eight patients received off-label azacitidine before hematopoietic stem cell transplantation. A total of 31 cycles were administered and modification or delay occurred in four of them due to cytopenias, infection, nausea/vomiting, and transient renal impairment. Bone marrow blast percentages in azacitidine-treated patients decreased significantly from a median of 15% (range 9-31%) at the start of treatment to 5.5% (0-12%, P=0.02) before hematopoietic stem cell transplantation. Following azacitidine treatment, four patients (50%) achieved marrow remission, and none progressed. In contrast, three untreated patients (21.4%) had progressive disease characterized by >50% increase in blast counts or progression to leukemia. Azacitidine-treated patients had significantly increased 4-year event-free survival (P=0.04); predicted 4-year overall survival was 100% versus 69.3% in untreated patients (P=0.1). In summary, azacitidine treatment prior to hematopoietic stem cell transplantation was well tolerated in pediatric patients with advanced myelodysplastic syndrome, led to partial or complete bone marrow response in seven of eight patients (87.5%), and correlated with superior event-free survival in this cohort.


Asunto(s)
Antimetabolitos Antineoplásicos/uso terapéutico , Azacitidina/uso terapéutico , Síndromes Mielodisplásicos/tratamiento farmacológico , Adolescente , Antimetabolitos Antineoplásicos/administración & dosificación , Antimetabolitos Antineoplásicos/efectos adversos , Azacitidina/administración & dosificación , Azacitidina/efectos adversos , Recuento de Células Sanguíneas , Médula Ósea/patología , Niño , Preescolar , Femenino , Trasplante de Células Madre Hematopoyéticas , Humanos , Lactante , Masculino , Síndromes Mielodisplásicos/diagnóstico , Síndromes Mielodisplásicos/mortalidad , Síndromes Mielodisplásicos/terapia , Cuidados Preoperatorios , Índice de Severidad de la Enfermedad , Análisis de Supervivencia , Resultado del Tratamiento
16.
J Med Genet ; 52(11): 738-48, 2015 Nov.
Artículo en Inglés | MEDLINE | ID: mdl-26342108

RESUMEN

BACKGROUND: Deadenylation regulates RNA function and fate. Poly(A)-specific ribonuclease (PARN) is a deadenylase that processes mRNAs and non-coding RNA. Little is known about the biological significance of germline mutations in PARN. METHODS: We identified mutations in PARN in patients with haematological and neurological manifestations. Genomic, biochemical and knockdown experiments in human marrow cells and in zebrafish have been performed to clarify the role of PARN in the human disease. RESULTS: We identified large monoallelic deletions in PARN in four patients with developmental delay or mental illness. One patient in particular had a severe neurological phenotype, central hypomyelination and bone marrow failure. This patient had an additional missense mutation on the non-deleted allele and severely reduced PARN protein and deadenylation activity. Cells from this patient had impaired oligoadenylation of specific H/ACA box small nucleolar RNAs. Importantly, PARN-deficient patient cells manifested short telomeres and an aberrant ribosome profile similar to those described in some variants of dyskeratosis congenita. Knocking down PARN in human marrow cells and zebrafish impaired haematopoiesis, providing further evidence for a causal link with the human disease. CONCLUSIONS: Large monoallelic mutations of PARN can cause developmental/mental illness. Biallelic PARN mutations cause severe bone marrow failure and central hypomyelination.


Asunto(s)
Enfermedades de la Médula Ósea/genética , Discapacidades del Desarrollo/genética , Exorribonucleasas/genética , Mutación Missense , Eliminación de Secuencia , Alelos , Animales , Enfermedades de la Médula Ósea/metabolismo , Niño , Análisis Mutacional de ADN , Discapacidades del Desarrollo/metabolismo , Femenino , Pruebas Genéticas , Humanos , Lactante , Masculino , Persona de Mediana Edad , Vaina de Mielina/genética , Vaina de Mielina/patología , Homeostasis del Telómero/genética , Adulto Joven , Pez Cebra
17.
J Med Genet ; 52(9): 575-84, 2015 Sep.
Artículo en Inglés | MEDLINE | ID: mdl-26136524

RESUMEN

BACKGROUND: Phenotypic overlap among the inherited bone marrow failure syndromes (IBMFSs) frequently limits the ability to establish a diagnosis based solely on clinical features. >70 IBMFS genes have been identified, which often renders genetic testing prolonged and costly. Since correct diagnosis, treatment and cancer surveillance often depend on identifying the mutated gene, strategies that enable timely genotyping are essential. METHODS: To overcome these challenges, we developed a next-generation sequencing assay to analyse a panel of 72 known IBMFS genes. Cases fulfilling the clinical diagnostic criteria of an IBMFS but without identified causal genotypes were included. RESULTS: The assay was validated by detecting 52 variants previously found by Sanger sequencing. A total of 158 patients with unknown mutations were studied. Of 75 patients with known IBMFS categories (eg, Fanconi anaemia), 59% had causal mutations. Among 83 patients with unclassified IBMFSs, we found causal mutations and established the diagnosis in 18% of the patients. The assay detected mutant genes that had not previously been reported to be associated with the patient phenotypes. In other cases, the assay led to amendments of diagnoses. In 20% of genotype cases, the results indicated a cancer surveillance programme. CONCLUSIONS: The novel assay is efficient, accurate and has a major impact on patient care.


Asunto(s)
Hemoglobinuria Paroxística , Análisis de Secuencia de ADN/métodos , Anemia Aplásica , Enfermedades de la Médula Ósea , Trastornos de Fallo de la Médula Ósea , Hemoglobinuria Paroxística/diagnóstico , Hemoglobinuria Paroxística/genética , Hemoglobinuria Paroxística/terapia , Secuenciación de Nucleótidos de Alto Rendimiento/métodos , Humanos , Mutación , Atención al Paciente , Sensibilidad y Especificidad
18.
Haematologica ; 100(5): 633-42, 2015 May.
Artículo en Inglés | MEDLINE | ID: mdl-25682607

RESUMEN

Inherited bone marrow failure syndromes are a group of rare, heterogeneous genetic disorders with a risk of clonal and malignant myeloid transformation including clonal marrow cytogenetic abnormalities, myelodysplastic syndrome and acute myeloid leukemia. The clinical characteristics, risk classification, prognostic factors and outcome of clonal and malignant myeloid transformation associated with inherited bone marrow failure syndromes are largely unknown. The aims of this study were to determine the impact of category, cytopathology and cytogenetics, the three components of the "Category Cytology Cytogenetics" classification of pediatric myelodysplastic syndrome, on the outcome of clonal and malignant myeloid transformation associated with inherited bone marrow failure. We used data from the Canadian Inherited Marrow Failure Registry. Among 327 patients with inherited bone marrow failure syndrome enrolled in the registry, the estimated risk of clonal and malignant myeloid transformation by the age of 18 years was 37%. The risk of clonal and malignant myeloid transformation varied according to the type of inherited bone marrow failure syndrome but was highest in Fanconi anemia. The development of clonal and malignant myeloid transformation significantly affected overall survival. Mortality varied based on cytopathological group. The largest group of patients had refractory cytopenia. Clonal marrow cytogenetic abnormalities were identified in 87% of patients with clonal and malignant myeloid transformation, and different cytogenetic groups had different impacts on disease progression. We conclude that category, cytopathology and cytogenetics in cases of clonal and malignant myeloid transformation associated with inherited bone marrow failure syndromes have an important impact on outcome and that the classification of such cases should incorporate these factors.


Asunto(s)
Transformación Celular Neoplásica/genética , Aberraciones Cromosómicas , Evolución Clonal , Hemoglobinuria Paroxística/congénito , Hemoglobinuria Paroxística/diagnóstico , Leucemia Mieloide Aguda/diagnóstico , Leucemia Mieloide Aguda/etiología , Adolescente , Adulto , Anemia Aplásica , Médula Ósea/patología , Enfermedades de la Médula Ósea , Trastornos de Fallo de la Médula Ósea , Canadá/epidemiología , Niño , Preescolar , Análisis Citogenético , Progresión de la Enfermedad , Hemoglobinuria Paroxística/epidemiología , Humanos , Lactante , Recién Nacido , Estimación de Kaplan-Meier , Leucemia Mieloide Aguda/epidemiología , Evaluación del Resultado de la Atención al Paciente , Pronóstico , Sistema de Registros , Riesgo , Adulto Joven
SELECCIÓN DE REFERENCIAS
DETALLE DE LA BÚSQUEDA