Nature genetics · 2009
Germline genomic variants associated with childhood acute lymphoblastic leukemia.
СтатьяПоддержка NIH: внешняя программаПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод пока не подготовлен
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Treviño Lisa R, Yang Wenjian, French Deborah, Hunger Stephen P, Carroll William L, Devidas Meenakshi, Willman Cheryl, Neale Geoffrey, Downing James, Raimondi Susana C, Pui Ching-Hon, Evans William E, Relling Mary V
Аннотация
Using the Affymetrix 500K Mapping array and publicly available genotypes, we identified 18 SNPs whose allele frequency differed significantly(P < 1 x 10(-5)) between pediatric acute lymphoblastic leukemia (ALL) cases (n = 317) and non-ALL controls (n = 17,958). Two SNPs in ARID5B not only differed between ALL and non-ALL groups (rs10821936, P = 1.4 x 10(-15), odds ratio (OR) = 1.91; rs10994982, P = 5.7 x 10(-9), OR = 1.62) but also distinguished B-hyperdiploid ALL from other subtypes (rs10821936, P = 1.62 x 10(-5), OR = 2.17; rs10994982, P = 0.003, OR 1.72). These ARID5B SNPs also distinguished B-hyperdiploid ALL from other subtypes in an independent validation cohort (n = 124 children with ALL; P = 0.003 and P = 0.0008, OR 2.45 and 2.86, respectively) and were associated with methotrexate accumulation and gene expression pattern in leukemic lymphoblasts. We conclude that germline variants affect susceptibility to, and characteristics of, specific ALL subtypes.
Предметные рубрики MeSH
AllelesAntimetabolites, AntineoplasticCase-Control StudiesChildChild, PreschoolChromosomes, Human, Pair 10Chromosomes, Human, Pair 7Cohort StudiesDNA-Binding ProteinsDopa DecarboxylaseGene DosageGene Expression Regulation, NeoplasticGene FrequencyGenetic Predisposition to DiseaseGenetic VariationGenome-Wide Association StudyGerm CellsGerm-Line MutationHaplotypesHumansIkaros Transcription FactorLinkage DisequilibriumMethotrexateOdds RatioOncogene Proteins, FusionPolyglutamic AcidPolymorphism, Single NucleotidePrecursor Cell Lymphoblastic Leukemia-LymphomaProbabilityReproducibility of ResultsRisk FactorsTrans-ActivatorsTranscription FactorsWhite People