Joke BeutenJonathan A L GelfondDuangjai PiwkhamBrad H. PollockNaomi J. WinickAnderson B. CollierGail E. TomlinsonUniversity of Texas Health Science Center at San AntonioMahidol UniversityUT Southwestern Medical SchoolLehigh Valley Hospital and Health Network2018-05-032018-05-032011-09-09Carcinogenesis. Vol.32, No.9 (2011), 1349-135314602180014333342-s2.0-80052409831https://repository.li.mahidol.ac.th/handle/20.500.14594/11474To 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 5 1.79, P 5 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. © The Author 2011. Published by Oxford University Press. All rights reserved.Mahidol UniversityBiochemistry, Genetics and Molecular BiologyArticleSCOPUS10.1093/carcin/bgr091