Candidate gene association analysis of acute lymphoblastic leukemia identifies new susceptibility locus at 11p15 (LMO1)

To determine the contribution of susceptibility loci in explaining the genetic basis of acute lymphoblastic leukemia (ALL), we genotyped 29 high-potential candidate genes with 672 tagged single-nucleotide polymorphisms (SNPs) in a sample (163 cases and 251 healthy controls) of Caucasian children. Fi...

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Bibliographic Details
Published in:Carcinogenesis (New York) 2011-09, Vol.32 (9), p.1349-1353
Main Authors: BEUTEN, Joke, GELFOND, Jonathan A. L, PIWKHAM, Duangjai, POLLOCK, Brad H, WINICK, Naomi J, COLLIER, Anderson B, TOMLINSON, Gail E
Format: Article
Language:English
Subjects:
Acute lymphatic leukemia
Adolescent
Adult
Biological and medical sciences
Carcinogenesis, carcinogens and anticarcinogens
Child
Child, Preschool
Chromosome Mapping
Chromosomes, Human, Pair 11
DNA-Binding Proteins - genetics
Female
Gene Frequency
Genetic Predisposition to Disease
Haplotypes
Hematologic and hematopoietic diseases
Humans
Infant
Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis
LIM Domain Proteins
Linkage Disequilibrium
Male
Medical sciences
Polymorphism, Single Nucleotide
Precursor Cell Lymphoblastic Leukemia-Lymphoma - etiology
Precursor Cell Lymphoblastic Leukemia-Lymphoma - genetics
Quality Control
Transcription Factors - genetics
Tumors
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Summary:To determine the contribution of susceptibility loci in explaining the genetic basis of acute lymphoblastic leukemia (ALL), we genotyped 29 high-potential candidate genes with 672 tagged single-nucleotide polymorphisms (SNPs) in a sample (163 cases and 251 healthy controls) of Caucasian children. Fifty SNPs in 15 genes were significantly associated with ALL risk at the P < 0.05 level. After correction for multiple testing, rs442264 within the LIM domain only 1 (LMO1) gene at 11p15 remained significant [odds ratio (OR) = 1.90, P = 3 × 10(-5)]. In addition, a major haplotype within LMO1 comprising 14 SNPs with individual risk associations was found to significantly increase ALL risk (OR = 1.79, P = 0.0006). A stratified analysis on subtype indicated that risk associations of LMO1 variants are significant in children with precursor B-cell leukemia. These data show that genetic variants within LMO1 are associated with ALL and identify this gene as a strong candidate for precursor B-cell leukemogenesis.
ISSN:0143-3334
1460-2180
DOI:10.1093/carcin/bgr091