title: Polymorphisms in CYP1A1 and ethnic-specific susceptibility to acute lymphoblastic leukemia in children.
abstract: BACKGROUND
  Acute lymphoblastic leukemia (ALL) is the most common childhood malignancy. The U.S. Surveillance Epidemiology and End Results (SEER) registry reports that Hispanic children have the highest incidence of ALL, however, it is unclear if this is due to genetic factors, unique environmental exposures, or both. Previous reports have shown an association between CYP1A1 variants and ALL.
  
  
  METHODS
  To explore the contribution of CYP1A1 polymorphisms to ALL susceptibility in different ethnic groups, we conducted a case-control analysis in Caucasian, Hispanic, and African-American children.
  
  
  RESULTS
  Increased risk of developing ALL was found in the whole sample group for homozygosity of variant alleles at CYP1A1*2C (OR 2.51, 95% CI 1.18-5.33, P = 0.016) and CYP1A1*2B (OR 3.24, 95% CI 1.43-7.34, P = 0.005). Stratified analyses showed increased risks in the Hispanic group (CYP1A1*2A, OR 2.70, 95% CI 1.27-5.74, P = 0.010; CYP1A1*2C, OR 2.47, 95% CI 1.13-5.38, P = 0.023; and CYP1A1*2B, OR 3.28, 95% CI 1.40-7.69, P = 0.006) but not for the other ethnic groups. Hispanic control subjects were significantly more likely to be carriers of variant alleles as compared to Caucasians (P < 0.0001) and African Americans (P = 0.005).
  
  
  CONCLUSIONS
  Our study suggests that polymorphisms in CYP1A1 may contribute to the increased risk of ALL in Hispanic children due to both their impact on leukemia susceptibility and the increased prevalence of the at-risk alleles in the Hispanic population.
  
  
  CONCLUSIONS
  Our study provides a novel and specific link between CYP1A1 polymorphisms and ethnic influence on ALL risk that may help explain varying susceptibilities across groups to environmental toxins.
authors.affiliation: Department of Pediatrics and Hamon Center for Therapeutic Oncology Research, University of Texas Southwestern Medical Center, Dallas, Texas, USA.
authors.forename: Ryan M
authors.initials: RM
authors.lastname: Swinney
authors.forename: Joke
authors.initials: J
authors.lastname: Beuten
authors.forename: Anderson B
authors.initials: AB
authors.lastname: Collier
authors.forename: Tina T-L
authors.initials: TT
authors.lastname: Chen
authors.forename: Naomi J
authors.initials: NJ
authors.lastname: Winick
authors.forename: Brad H
authors.initials: BH
authors.lastname: Pollock
authors.forename: Gail E
authors.initials: GE
authors.lastname: Tomlinson
mesh_terms: D001741:Black or African American / Q000208:ethnology / Q000235:genetics; D016022:Case-Control Studies; D002648:Child; D019363:Cytochrome P-450 CYP1A1 / Q000235:genetics*; D020022:Genetic Predisposition to Disease; D005838:Genotype; D006630:Hispanic or Latino / Q000208:ethnology / Q000235:genetics; D006801:Humans; D020641:Polymorphism, Single Nucleotide; D054198:Precursor Cell Lymphoblastic Leukemia-Lymphoma / Q000208:ethnology* / Q000235:genetics*; D044465:White People / Q000208:ethnology / Q000235:genetics
chemical_list: D019363:Cytochrome P-450 CYP1A1