title: E-cadherin polymorphisms and haplotypes influence risk for prostate cancer.
abstract: BACKGROUND
  The E-cadherin (CDH1) gene has been implicated in prostate cancer (PCA) risk, however, the exact mechanism is unknown. Several polymorphisms, such as the C/A variant -160 base pairs from the transcription start site, in the CDH1 gene promoter region have been associated with cancer risk, mainly in European descent populations.
  
  
  METHODS
  We screened the entire coding region and 3.0 kilobases of the CDH1 promoter for polymorphisms in 48 African Americans using dHPLC. Twenty-one (21) polymorphisms were observed. Four polymorphisms, including -160C/A, were genotyped in a genetic association study using incident PCA cases (N = 427) and unaffected controls (N = 337) of similar age from three different ethnic groups consisting of African Americans, Jamaicans, and European Americans.
  
  
  RESULTS
  We observed a significantly higher frequency of the -160A allele among European American PCA patients (27.5%) compared to the control group (19.7%) (P = 0.04). More importantly, among men of European ancestry under the age of 65 who possess the -160 A allele there was over three times increased risk for prostate cancer (P = 0.05). Also, the AACT haplotype bearing the -160A allele was significantly associated with PCA in European Americans (P = 0.04).
  
  
  CONCLUSIONS
  Our data indicate that CDH1 likely is a low-penetrant PCA susceptibility gene, however, population differences in linkage disequilibrium within the CDH1 gene region may influence the effect of susceptibility alleles such as -160A.
authors.affiliation: Human Cancer Genetics, Comprehensive Cancer Center, The Ohio State University, Columbus 43210, USA.
authors.forename: Carolina
authors.initials: C
authors.lastname: Bonilla
authors.forename: Tshela
authors.initials: T
authors.lastname: Mason
authors.forename: Layron
authors.initials: L
authors.lastname: Long
authors.forename: Chiledum
authors.initials: C
authors.lastname: Ahaghotu
authors.forename: Weidong
authors.initials: W
authors.lastname: Chen
authors.forename: Aiqiu
authors.initials: A
authors.lastname: Zhao
authors.forename: Aoua
authors.initials: A
authors.lastname: Coulibaly
authors.forename: Frankly
authors.initials: F
authors.lastname: Bennett
authors.forename: William
authors.initials: W
authors.lastname: Aiken
authors.forename: Trevor
authors.initials: T
authors.lastname: Tullock
authors.forename: Kathleen
authors.initials: K
authors.lastname: Coard
authors.forename: Vincent
authors.initials: V
authors.lastname: Freeman
authors.forename: Rick A
authors.initials: RA
authors.lastname: Kittles
mesh_terms: D001741:Black or African American / Q000235:genetics; D000368:Aged; D015820:Cadherins / Q000235:genetics*; D005091:Exons; D020022:Genetic Predisposition to Disease; D006801:Humans; D007438:Introns; D008297:Male; D008875:Middle Aged; D011110:Polymorphism, Genetic; D011401:Promoter Regions, Genetic; D017430:Prostate-Specific Antigen / Q000097:blood; D011471:Prostatic Neoplasms / Q000097:blood / Q000453:epidemiology* / Q000235:genetics*; D012307:Risk Factors; D017384:Sequence Deletion; D014481:United States
chemical_list: D015820:Cadherins; D017430:Prostate-Specific Antigen