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1.
Blood ; 119(4): 1029-31, 2012 Jan 26.
Artículo en Inglés | MEDLINE | ID: mdl-22144180

RESUMEN

Women treated at young ages with supradiaphragmatic radiotherapy for Hodgkin lymphoma (HL) have a highly increased risk of breast cancer. For personalized advice and follow-up regimens for patients, information is needed on how the radiotherapy-related risk is affected by other breast cancer risk factors. Genome-wide association studies have identified 14 independently replicated common single nucleotide polymorphisms that influence breast cancer risk. To examine whether these variants contribute to risk of radiation-associated breast cancer in HL, we analyzed 2 independent case-control series, from the United Kingdom and The Netherlands, totaling 693 HL patients, 232 with breast cancer and 461 without. rs1219648, which annotates the FGFR2 gene, was associated with risk in both series (combined per-allele odds ratio = 1.59, 95% confidence interval: 1.26-2.02; P = .000111). These data provide evidence that genetic variation in FGFR2 influences radiation-induced breast cancer risk.


Asunto(s)
Neoplasias de la Mama/genética , Enfermedad de Hodgkin/radioterapia , Glándulas Mamarias Humanas/efectos de la radiación , Polimorfismo de Nucleótido Simple , Receptor Tipo 2 de Factor de Crecimiento de Fibroblastos/genética , Adulto , Factores de Edad , Neoplasias de la Mama/complicaciones , Neoplasias de la Mama/etiología , Estudios de Casos y Controles , Femenino , Predisposición Genética a la Enfermedad , Enfermedad de Hodgkin/complicaciones , Enfermedad de Hodgkin/genética , Humanos , Persona de Mediana Edad , Países Bajos/epidemiología , Medicina de Precisión , Riesgo , Reino Unido/epidemiología
2.
PLoS Genet ; 7(6): e1002105, 2011 Jun.
Artículo en Inglés | MEDLINE | ID: mdl-21655089

RESUMEN

Genome-wide association studies (GWAS) have identified 14 tagging single nucleotide polymorphisms (tagSNPs) that are associated with the risk of colorectal cancer (CRC), and several of these tagSNPs are near bone morphogenetic protein (BMP) pathway loci. The penalty of multiple testing implicit in GWAS increases the attraction of complementary approaches for disease gene discovery, including candidate gene- or pathway-based analyses. The strongest candidate loci for additional predisposition SNPs are arguably those already known both to have functional relevance and to be involved in disease risk. To investigate this proposition, we searched for novel CRC susceptibility variants close to the BMP pathway genes GREM1 (15q13.3), BMP4 (14q22.2), and BMP2 (20p12.3) using sample sets totalling 24,910 CRC cases and 26,275 controls. We identified new, independent CRC predisposition SNPs close to BMP4 (rs1957636, P = 3.93×10(-10)) and BMP2 (rs4813802, P = 4.65×10(-11)). Near GREM1, we found using fine-mapping that the previously-identified association between tagSNP rs4779584 and CRC actually resulted from two independent signals represented by rs16969681 (P = 5.33×10(-8)) and rs11632715 (P = 2.30×10(-10)). As low-penetrance predisposition variants become harder to identify-owing to small effect sizes and/or low risk allele frequencies-approaches based on informed candidate gene selection may become increasingly attractive. Our data emphasise that genetic fine-mapping studies can deconvolute associations that have arisen owing to independent correlation of a tagSNP with more than one functional SNP, thus explaining some of the apparently missing heritability of common diseases.


Asunto(s)
Proteína Morfogenética Ósea 2/genética , Proteína Morfogenética Ósea 4/genética , Neoplasias Colorrectales/genética , Predisposición Genética a la Enfermedad , Péptidos y Proteínas de Señalización Intercelular/genética , Anciano , Proteína Morfogenética Ósea 2/metabolismo , Proteína Morfogenética Ósea 4/metabolismo , Estudios de Casos y Controles , Neoplasias Colorrectales/metabolismo , Frecuencia de los Genes , Variación Genética , Estudio de Asociación del Genoma Completo , Humanos , Masculino , Persona de Mediana Edad , Polimorfismo de Nucleótido Simple , Carácter Cuantitativo Heredable , Transducción de Señal
3.
Blood ; 118(19): 5211-7, 2011 Nov 10.
Artículo en Inglés | MEDLINE | ID: mdl-21921049

RESUMEN

The pathogenesis of classical Hodgkin lymphoma (cHL) involves environmental and genetic factors. To explore the role of the human leukocyte antigen (HLA) genes, we performed a case-control genotyping study in 338 Dutch cHL patients and more than 5000 controls using a PCR-based sequence-specific oligonucleotide probe hybridization approach. HLA-A68 and HLA-DR11 (5) were significantly increased in the cHL patient population compared with the controls. Three class II associations were observed in the EBV(-) cHL population with an increase of HLA-DR15 (2) and a decrease of HLA-DR4 and HLA-DR7. Allele frequencies of HLA-A1, HLA-B37, and HLA-DR10 were significantly increased in the EBV(+) cHL population; these alleles are in strong linkage disequilibrium and form a common haplotype in whites. The allele frequency of HLA-A2 was significantly decreased in the EBV(+) cHL population. Sequence-specific oligonucleotide probe analysis revealed significant differences between EBV(+) and EBV(-) cHL patients for 19 probes that discriminate between HLA-A*01 and HLA-A*02. In conclusion, the HLA-A1 and HLA-A2 antigens and not specific single nucleotide variants shared by multiple alleles are responsible for the association with EBV(+) cHL. Furthermore, several new protective and predisposing HLA class I and II associations for the EBV(+), the EBV(-), and the entire cHL population were identified.


Asunto(s)
Genes MHC Clase II , Genes MHC Clase I , Enfermedad de Hodgkin/genética , Enfermedad de Hodgkin/inmunología , Adolescente , Adulto , Anciano , Anciano de 80 o más Años , Estudios de Casos y Controles , Infecciones por Virus de Epstein-Barr/genética , Infecciones por Virus de Epstein-Barr/inmunología , Femenino , Frecuencia de los Genes , Estudios de Asociación Genética , Predisposición Genética a la Enfermedad , Herpesvirus Humano 4/aislamiento & purificación , Herpesvirus Humano 4/patogenicidad , Enfermedad de Hodgkin/clasificación , Enfermedad de Hodgkin/virología , Humanos , Desequilibrio de Ligamiento , Masculino , Persona de Mediana Edad , Países Bajos , Adulto Joven
4.
PLoS Genet ; 6(9): e1001126, 2010 Sep 16.
Artículo en Inglés | MEDLINE | ID: mdl-20862326

RESUMEN

Common genetic variation at human 8q23.3 is significantly associated with colorectal cancer (CRC) risk. To elucidate the basis of this association we compared the frequency of common variants at 8q23.3 in 1,964 CRC cases and 2,081 healthy controls. Reporter gene studies showed that the single nucleotide polymorphism rs16888589 acts as an allele-specific transcriptional repressor. Chromosome conformation capture (3C) analysis demonstrated that the genomic region harboring rs16888589 interacts with the promoter of gene for eukaryotic translation initiation factor 3, subunit H (EIF3H). We show that increased expression of EIF3H gene increases CRC growth and invasiveness thereby providing a biological mechanism for the 8q23.3 association. These data provide evidence for a functional basis for the non-coding risk variant rs16888589 at 8q23.3 and provides novel insight into the etiological basis of CRC.


Asunto(s)
Alelos , Cromosomas Humanos Par 8/genética , Neoplasias Colorrectales/genética , Factor 3 de Iniciación Eucariótica/genética , Predisposición Genética a la Enfermedad , Variación Genética , Secuencias Reguladoras de Ácidos Nucleicos/genética , Línea Celular Tumoral , Proliferación Celular , Neoplasias Colorrectales/patología , Ensayo de Cambio de Movilidad Electroforética , Femenino , Regulación Neoplásica de la Expresión Génica , Genes Reporteros/genética , Sitios Genéticos/genética , Humanos , Desequilibrio de Ligamiento/genética , Masculino , Persona de Mediana Edad , Polimorfismo de Nucleótido Simple/genética , Unión Proteica , Factores de Riesgo
5.
Blood ; 116(26): 5957-60, 2010 Dec 23.
Artículo en Inglés | MEDLINE | ID: mdl-20855867

RESUMEN

Monoclonal B-cell lymphocytosis (MBL) is detectable in > 3% of the general population. Recent data are compatible, at least in a proportion of cases, with MBL being a progenitor lesion for chronic lymphocytic leukemia (CLL) and a surrogate for inherited predisposition. Common single nucleotide polymorphisms (SNPs) at 2q13 (rs17483466), 2q37.1 (rs13397985), 2q37.3 (rs757978), 6p25.3 (rs872071), 8q24.21 (rs2456449), 11q24.1 (rs735665), 15q21.3 (rs7169431), 15q23 (rs7176508), 16q24.1 (rs305061), and 19q13.32 (rs11083846) have been shown to confer a modest but significant increase in CLL risk. To examine the impact of these 10 SNPs on MBL, we analyzed 3 case-control series totaling 419 cases and 1753 controls. An association between genotype and MBL risk was seen for 9 SNPs, 6 of which were statistically significant: rs17483466 (odds ratio [OR] =1.27; P = .02), rs13397985 (OR = 1.40; P = 1.72 × 10(-3)), rs757978 (OR = 1.38; P = .02), rs872071 (OR = 1.27; P = 7.75 × 10(-3)), rs2456449 (OR = 1.31; P = 3.14 × 10(-3)), and rs735665 (OR = 1.63; P = 6.86 × 10(-6)). Collectively, these data provide support for genetic variation influencing CLL risk through predisposition to MBL.


Asunto(s)
Linfocitos B/patología , Aberraciones Cromosómicas , Cromosomas Humanos/genética , Predisposición Genética a la Enfermedad , Linfocitosis/genética , Polimorfismo de Nucleótido Simple/genética , Anciano , Estudios de Casos y Controles , Femenino , Genotipo , Humanos , Linfocitosis/patología , Masculino
6.
Hum Mutat ; 32(1): E1928-38, 2011 Jan.
Artículo en Inglés | MEDLINE | ID: mdl-20949628

RESUMEN

Transforming growth factor-ß (TGF-ß) signalling plays a key role in colorectal cancer (CRC). Bone morphogenetic protein-4 (BMP4) is a member of the TGF-ß family of signal transduction molecules. To examine if germline mutation in BMP4 causes CRC we analysed 504 genetically enriched CRC cases (by virtue of early-onset disease, family history of CRC) for mutations in the coding sequence of BMP4. We identified three pathogenic mutations, p.R286X (g.8330C>T), p.W325C (g.8449G>T) and p.C373S (g.8592G>C), amongst the CRC cases which were not observed in 524 healthy controls. p.R286X localizes to the N-terminal of the TGF-ß1 prodomain truncating the protein prior to the active domain. p.W325C and p.C373S mutations are predicted from protein homology modelling with BMP2 to impact deleteriously on BMP4 function. Segregation of p.C373S with adenoma and hyperplastic polyp in first-degree relatives of the case suggests germline mutations may confer a juvenile polyposis-type phenotype. These findings suggest mutation of BMP4is a cause of CRC and the value of protein-based modelling in the elucidation of rare disease-causing variants.


Asunto(s)
Proteína Morfogenética Ósea 4/genética , Proteína Morfogenética Ósea 4/metabolismo , Neoplasias Colorrectales/genética , Mutación de Línea Germinal/genética , Adulto , Anciano , Secuencia de Aminoácidos , Femenino , Humanos , Masculino , Persona de Mediana Edad , Datos de Secuencia Molecular , Mutación , Estructura Terciaria de Proteína , Alineación de Secuencia , Factor de Crecimiento Transformador beta/genética
7.
Br J Haematol ; 154(2): 229-33, 2011 Jul.
Artículo en Inglés | MEDLINE | ID: mdl-21554262

RESUMEN

A genome-wide association study of chronic lymphocytic leukaemia (CLL) suggested that common variants at 15q25.2 (rs783540) and 18q21.1 (rs1036935) influence CLL. To validate these associations and explore their relationship with CLL risk we genotyped case-control datasets from Poland, UK and Italy totalling 1428 cases and 1920 controls. Combined data from these and previously genotyped series (2503 cases and 5789 controls) provided evidence for an association between 15q25.2 and 18q21.1 loci and CLL risk (P(combined) = 1·10 × 10(-7) and 1·30 × 10(-5) respectively). These data provide further evidence for the involvement of common genetic variants in CLL risk and insight into the biological basis of disease development.


Asunto(s)
Cromosomas Humanos Par 15/genética , Leucemia Linfocítica Crónica de Células B/genética , Anciano , Estudios de Casos y Controles , Cromosomas Humanos Par 18/genética , Femenino , Predisposición Genética a la Enfermedad , Estudio de Asociación del Genoma Completo , Genotipo , Humanos , Masculino , Persona de Mediana Edad , Polimorfismo de Nucleótido Simple
8.
PLoS One ; 7(7): e39986, 2012.
Artículo en Inglés | MEDLINE | ID: mdl-22808081

RESUMEN

The pathogenesis of classical Hodgkin lymphoma (cHL) involves environmental and genetic factors. To explore the role of the human leukocyte antigen (HLA) genes, we performed a case-control genotyping study in 338 Dutch cHL patients using a PCR-based sequence-specific oligonucleotide probe (SSOP) hybridization approach. The allele frequencies were compared to HLA typings of more than 6,000 controls. The age of the cHL patients varied between 13 and 81 years with a median of 35 years. Nodular sclerosis subtype was the most common subtype (87%) and EBV was detected in 25% of the cHL patients. HLA-B5 was significantly increased and HLA-DR7 significantly decreased in the total cHL patient population as compared to controls. Two class II associations were observed to be specific for the EBV- cHL population with an increase of HLA-DR2 and HLA-DR5. Allele frequencies of HLA-A1, HLA-B37 and HLA-DR10 were significantly increased in the EBV+ cHL population; these alleles are in strong linkage disequilibrium and form a common haplotype in Caucasians. The allele frequency of HLA-A2 was significantly decreased in the EBV+ cHL population. Analysis of haplotypes with a frequency of >1% revealed a significant increase of HLA-A2-B7-DR2 in EBV- cHL as compared to controls. SSOP association analysis revealed significant differences between EBV+ and EBV- cHL patients for 19 probes that discriminate between HLA-A*01 and HLA-A*02. In conclusion, the HLA-A1 and HLA-A2 antigens and not specific single nucleotide variants shared by multiple alleles are responsible for the association with EBV+ cHL. Furthermore several new protective and predisposing HLA class I and II associations for the EBV+, the EBV- and the entire cHL population were identified.


Asunto(s)
Antígenos HLA/genética , Herpesvirus Humano 4/fisiología , Enfermedad de Hodgkin/genética , Mononucleosis Infecciosa/genética , Adolescente , Adulto , Anciano , Anciano de 80 o más Años , Alelos , Estudios de Casos y Controles , Femenino , Frecuencia de los Genes , Antígenos HLA/inmunología , Haplotipos , Prueba de Histocompatibilidad , Enfermedad de Hodgkin/complicaciones , Enfermedad de Hodgkin/inmunología , Enfermedad de Hodgkin/virología , Humanos , Mononucleosis Infecciosa/complicaciones , Mononucleosis Infecciosa/inmunología , Mononucleosis Infecciosa/virología , Desequilibrio de Ligamiento , Masculino , Persona de Mediana Edad , Población Blanca
9.
Nat Genet ; 44(7): 770-6, 2012 May 27.
Artículo en Inglés | MEDLINE | ID: mdl-22634755

RESUMEN

We performed a meta-analysis of five genome-wide association studies to identify common variants influencing colorectal cancer (CRC) risk comprising 8,682 cases and 9,649 controls. Replication analysis was performed in case-control sets totaling 21,096 cases and 19,555 controls. We identified three new CRC risk loci at 6p21 (rs1321311, near CDKN1A; P = 1.14 × 10(-10)), 11q13.4 (rs3824999, intronic to POLD3; P = 3.65 × 10(-10)) and Xp22.2 (rs5934683, near SHROOM2; P = 7.30 × 10(-10)) This brings the number of independent loci associated with CRC risk to 20 and provides further insight into the genetic architecture of inherited susceptibility to CRC.


Asunto(s)
Neoplasias Colorrectales/genética , Inhibidor p21 de las Quinasas Dependientes de la Ciclina/genética , ADN Polimerasa III/genética , Proteínas de la Membrana/genética , Estudios de Casos y Controles , Sitios Genéticos , Predisposición Genética a la Enfermedad , Variación Genética , Estudio de Asociación del Genoma Completo/métodos , Humanos
10.
Nat Genet ; 43(9): 825-7, 2011 Jul 31.
Artículo en Inglés | MEDLINE | ID: mdl-21804547

RESUMEN

To identify susceptibility loci for meningioma, we conducted a genome-wide association study of 859 affected individuals (cases) and 704 controls with validation in two independent sample sets totaling 774 cases and 1,764 controls. We identified a new susceptibility locus for meningioma at 10p12.31 (MLLT10, rs11012732, odds ratio = 1.46, P(combined) = 1.88 × 10(-14)). This finding advances our understanding of the genetic basis of meningioma development.


Asunto(s)
Cromosomas Humanos Par 10/genética , Predisposición Genética a la Enfermedad , Neoplasias Meníngeas/genética , Meningioma/genética , Factores de Transcripción/genética , Sitios Genéticos , Estudio de Asociación del Genoma Completo , Humanos , Masculino , Neoplasias Meníngeas/epidemiología , Meningioma/epidemiología , Polimorfismo Genético , Polimorfismo de Nucleótido Simple , Riesgo
11.
Nat Genet ; 44(1): 58-61, 2011 Nov 27.
Artículo en Inglés | MEDLINE | ID: mdl-22120009

RESUMEN

To identify risk variants for multiple myeloma, we conducted a genome-wide association study of 1,675 individuals with multiple myeloma and 5,903 control subjects. We identified risk loci for multiple myeloma at 3p22.1 (rs1052501 in ULK4; odds ratio (OR) = 1.32; P = 7.47 × 10(-9)) and 7p15.3 (rs4487645, OR = 1.38; P = 3.33 × 10(-15)). In addition, we observed a promising association at 2p23.3 (rs6746082, OR = 1.29; P = 1.22 × 10(-7)). Our study identifies new genomic regions associated with multiple myeloma risk that may lead to new etiological insights.


Asunto(s)
Cromosomas Humanos Par 3 , Cromosomas Humanos Par 7 , Variación Genética , Mieloma Múltiple/genética , Estudios de Casos y Controles , Predisposición Genética a la Enfermedad , Estudio de Asociación del Genoma Completo , Humanos , Polimorfismo de Nucleótido Simple , Proteínas Serina-Treonina Quinasas/genética , Factores de Riesgo
12.
Fam Cancer ; 9(3): 413-21, 2010 Sep.
Artículo en Inglés | MEDLINE | ID: mdl-20455025

RESUMEN

There is increasing recognition of familial propensity to glioma as a distinct clinical entity beyond a few rare syndromes; however its genetic basis is poorly understood. The role of p16(INK4A)/p14(ARF) and p53 mutations in sporadic glioma provides a strong rationale for investigating germline mutations in these genes as a cause of familial glioma. To survey the familial glioma phenotype and examine the contribution of germline mutation in p16(INK4A)/p14(ARF) and p53 to the disease we have analyzed a series of 101 index familial cases collected through the GLIOGENE Consortium (http://braintumor.epigenetic.org/). There was little evidence for within family correlations for tumour histology, suggesting generic susceptibility to glial tumors. We did not detect any functional mutations in p16(INK4A) or p14(ARF). One index case with glioblastoma multiforme (GBM) diagnosed at age 54 and had a family history comprised of a paternal aunt with GBM at age 55, carried the p53 R158H mutation, which is predicted to be functional and has previously been implicated as a cause of Li-Fraumeni syndrome. Our findings provide no evidence that p16(INK4A)/p14(ARF) and p53 mutations contribute significantly to familial glioma.


Asunto(s)
Neoplasias Encefálicas/genética , Genes p16 , Genes p53 , Predisposición Genética a la Enfermedad , Glioma/genética , Adolescente , Adulto , Anciano , Niño , Preescolar , Análisis Mutacional de ADN , Femenino , Mutación de Línea Germinal , Humanos , Masculino , Persona de Mediana Edad , Linaje , Reacción en Cadena de la Polimerasa , Adulto Joven
13.
Nat Genet ; 42(11): 973-7, 2010 Nov.
Artículo en Inglés | MEDLINE | ID: mdl-20972440

RESUMEN

Genome-wide association studies (GWAS) have identified ten loci harboring common variants that influence risk of developing colorectal cancer (CRC). To enhance the power to identify additional CRC risk loci, we conducted a meta-analysis of three GWAS from the UK which included a total of 3,334 affected individuals (cases) and 4,628 controls followed by multiple validation analyses including a total of 18,095 cases and 20,197 controls. We identified associations at four new CRC risk loci: 1q41 (rs6691170, odds ratio (OR) = 1.06, P = 9.55 × 10⁻¹° and rs6687758, OR = 1.09, P = 2.27 × 10⁻9, 3q26.2 (rs10936599, OR = 0.93, P = 3.39 × 10⁻8), 12q13.13 (rs11169552, OR = 0.92, P = 1.89 × 10⁻¹° and rs7136702, OR = 1.06, P = 4.02 × 10⁻8) and 20q13.33 (rs4925386, OR = 0.93, P = 1.89 × 10⁻¹°). In addition to identifying new CRC risk loci, this analysis provides evidence that additional CRC-associated variants of similar effect size remain to be discovered.


Asunto(s)
Cromosomas Humanos Par 12/genética , Cromosomas Humanos Par 13/genética , Cromosomas Humanos Par 1/genética , Cromosomas Humanos Par 3/genética , Neoplasias Colorrectales/genética , Predisposición Genética a la Enfermedad , Estudio de Asociación del Genoma Completo , Mapeo Cromosómico/métodos , Femenino , Estudio de Asociación del Genoma Completo/métodos , Genotipo , Humanos , Masculino , Metaanálisis como Asunto , Oportunidad Relativa , Análisis de Secuencia por Matrices de Oligonucleótidos , Polimorfismo de Nucleótido Simple , Medición de Riesgo
14.
Nat Genet ; 42(12): 1126-1130, 2010 Dec.
Artículo en Inglés | MEDLINE | ID: mdl-21037568

RESUMEN

To identify susceptibility loci for classical Hodgkin's lymphoma (cHL), we conducted a genome-wide association study of 589 individuals with cHL (cases) and 5,199 controls with validation in four independent samples totaling 2,057 cases and 3,416 controls. We identified three new susceptibility loci at 2p16.1 (rs1432295, REL, odds ratio (OR) = 1.22, combined P = 1.91 × 10(-8)), 8q24.21 (rs2019960, PVT1, OR = 1.33, combined P = 1.26 × 10(-13)) and 10p14 (rs501764, GATA3, OR = 1.25, combined P = 7.05 × 10(-8)). Furthermore, we confirmed the role of the major histocompatibility complex in disease etiology by revealing a strong human leukocyte antigen (HLA) association (rs6903608, OR = 1.70, combined P = 2.84 × 10(-50)). These data provide new insight into the pathogenesis of cHL.


Asunto(s)
Cromosomas Humanos/genética , Factor de Transcripción GATA3/genética , Sitios Genéticos/genética , Predisposición Genética a la Enfermedad , Estudio de Asociación del Genoma Completo , Enfermedad de Hodgkin/genética , Proteínas Proto-Oncogénicas c-rel/genética , Adulto , Cromosomas Humanos Par 10/genética , Cromosomas Humanos Par 2/genética , Cromosomas Humanos Par 8/genética , Femenino , Genoma Humano/genética , Humanos , Masculino , Polimorfismo de Nucleótido Simple/genética , Recombinación Genética
15.
Nat Genet ; 41(9): 1006-10, 2009 Sep.
Artículo en Inglés | MEDLINE | ID: mdl-19684604

RESUMEN

To identify risk variants for childhood acute lymphoblastic leukemia (ALL), we conducted a genome-wide association study of two case-control series, analyzing the genotypes with respect to 291,423 tagging SNPs in a total of 907 ALL cases and 2,398 controls. We identified risk loci for ALL at 7p12.2 (IKZF1, rs4132601, odds ratio (OR) = 1.69, P = 1.20 x 10(-19)), 10q21.2 (ARID5B, rs7089424, OR = 1.65, P = 6.69 x 10(-19)) and 14q11.2 (CEBPE, rs2239633, OR = 1.34, P = 2.88 x 10(-7)). The 10q21.2 (ARID5B) risk association appears to be selective for the subset of B-cell precursor ALL with hyperdiploidy. These data show that common low-penetrance susceptibility alleles contribute to the risk of developing childhood ALL and provide new insight into disease causation of this specific hematological cancer. Notably, all three risk variants map to genes involved in transcriptional regulation and differentiation of B-cell progenitors.


Asunto(s)
Cromosomas Humanos Par 10 , Cromosomas Humanos Par 14 , Cromosomas Humanos Par 7 , Predisposición Genética a la Enfermedad , Leucemia-Linfoma Linfoblástico de Células Precursoras/etiología , Alelos , Emparejamiento Base , Secuencia de Bases , Proteínas Potenciadoras de Unión a CCAAT/genética , Estudios de Casos y Controles , Niño , Preescolar , Intervalos de Confianza , Proteínas de Unión al ADN/genética , Frecuencia de los Genes , Variación Genética , Estudio de Asociación del Genoma Completo , Genotipo , Haplotipos , Humanos , Factor de Transcripción Ikaros/genética , Intrones , Desequilibrio de Ligamiento , Metaanálisis como Asunto , Datos de Secuencia Molecular , Oportunidad Relativa , Mapeo Físico de Cromosoma , Polimorfismo de Nucleótido Simple , Leucemia-Linfoma Linfoblástico de Células Precursoras/genética , Probabilidad , Recombinación Genética , Factores de Riesgo , Factores de Transcripción/genética
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