title: Association of p53 codon Arg72Pro and p73 G4C14-to-A4T14 at exon 2 genetic polymorphisms with the risk of Japanese breast cancer.
abstract: BACKGROUND
  The association between breast cancer risk and genetic polymorphisms of p53 at codon 72 (Arg72Pro) has been investigated by several studies, but the results are not consistent. The aim of this case-control study conducted in Nagoya, Japan, was to reconfirm the results of prior studies of polymorphisms of p53 Arg72Pro, and to test if polymorphisms of p73 G4C14-to-A4T14 at exon 2 (G4A) were also associated with breast cancer risk.
  
  
  METHODS
  The cases were 200 breast cancer patients who visited Aichi Cancer Center Hospital. The controls were 282 local citizens who underwent a health check-up. All cases and controls were recruited from Chubu Japan. Genotyping was carried out by polymerase chain reaction with confronting two-pair primers.
  
  
  RESULTS
  The p53 genotype distribution was 40.4% for Arg72 homozygous, 48.9% for heterozygous, and 10.7% for Pro72 homozygous in controls, and 32.0%, 50.0%, and 18.0% in cases, respectively. A comparison between cases and controls indicated a significantly increased risk for Pro72 homozygosity in cases (odds ratio=2.14; 95% confidence interval=1.21-3.79). The genotypic frequencies for p73 G4A were 54.3% for G/G, 39.7% for G/A, and 6.0% for A/A in controls; and 59.0%, 32.0%, and 9.0% in cases, respectively. There were no significant differences in p73 G4A frequency between cases and controls.
  
  
  CONCLUSIONS
  This study implies an association of breast cancer risk with the p53 polymorphism Arg72Pro, but not with p73 G4A.
authors.affiliation: Department of Health Promotion and Preventive Medicine, Nagoya City University Graduate School of Medical Sciences, 1 Kawasumi, Mizuho-ku, Nagoya 467-8601, Japan. huangxinen06@yahoo.com.cn
authors.forename: Xin-En
authors.initials: XE
authors.lastname: Huang
authors.forename: Nobuyuki
authors.initials: N
authors.lastname: Hamajima
authors.forename: Nobuyuki
authors.initials: N
authors.lastname: Katsuda
authors.forename: Keitaro
authors.initials: K
authors.lastname: Matsuo
authors.forename: Kaoru
authors.initials: K
authors.lastname: Hirose
authors.forename: Mitsuhiro
authors.initials: M
authors.lastname: Mizutani
authors.forename: Hiroji
authors.initials: H
authors.lastname: Iwata
authors.forename: Shigeto
authors.initials: S
authors.lastname: Miura
authors.forename: Jin
authors.initials: J
authors.lastname: Xiang
authors.forename: Shinkan
authors.initials: S
authors.lastname: Tokudome
authors.forename: Kazuo
authors.initials: K
authors.lastname: Tajima
mesh_terms: D000225:Adenine / Q000378:metabolism; D000328:Adult; D000368:Aged; D001120:Arginine / Q000235:genetics; D001943:Breast Neoplasms / Q000235:genetics*; D044584:Carcinoma, Ductal / Q000235:genetics*; D016022:Case-Control Studies; D003062:Codon; D003596:Cytosine / Q000378:metabolism; D017931:DNA Primers; D004268:DNA-Binding Proteins / Q000235:genetics*; D005091:Exons; D005260:Female; D016147:Genes, Tumor Suppressor; D005838:Genotype; D006147:Guanine / Q000378:metabolism; D006720:Homozygote; D006801:Humans; D016015:Logistic Models; D008875:Middle Aged; D009687:Nuclear Proteins / Q000235:genetics*; D016017:Odds Ratio; D016133:Polymerase Chain Reaction; D011110:Polymorphism, Genetic; D012150:Polymorphism, Restriction Fragment Length; D011392:Proline / Q000235:genetics; D013941:Thymine / Q000378:metabolism; D000072160:Tumor Protein p73; D016159:Tumor Suppressor Protein p53 / Q000235:genetics*; D025521:Tumor Suppressor Proteins
chemical_list: D003062:Codon; D017931:DNA Primers; D004268:DNA-Binding Proteins; D009687:Nuclear Proteins; C000606460:TP73 protein, human; D000072160:Tumor Protein p73; D016159:Tumor Suppressor Protein p53; D025521:Tumor Suppressor Proteins; D006147:Guanine; D003596:Cytosine; D001120:Arginine; D011392:Proline; D000225:Adenine; D013941:Thymine