title: [P53 codon 72 polymorphism in cervical cancers and its correlation with HPV16,18E6].
abstract: OBJECTIVE
  To examine p53 codon 72 polymorphism in cervical cancers and its correlation with HPV16/18 E6.
  
  
  METHODS
  Cervical specimens were taken from 81 patients with cervical squamous cancer, 18 patients with cervical adenocarcinoma, 88 patients with CIN II - III and 60 patients without cancers. PCR was used to examine the p53 genotypes and the expression of HPV16 and 18 E6.
  
  
  RESULTS
  The frequencies of p53 Arg homozygosity in cervical squamous cancer, cervical adenocarcinoma and CIN (II - III) were 58.020%, 55.55% and 59.09% respectively, greater than those of p53 Arg/Pro heterozygosity (30.86%, 27.78%, 21.59%) and those of p53 Pro homozygosity (11.12%, 16.67%, 19.32%). The normal cervical samples also showed less frequency of p53 Arg homozygosity (23.33%) than cervical squamous cancer. There were no significant differences in the frequencies of p53 Arg homozygosity, p53 Arg/Pro heterozygosity and p53 Pro homozygosity (23.33%, 40.00% and 36.67% respectively). The frequency of HPV16,18 E6-positive in cervical cancer and CIN was much higher than that in control group (81.84%, 50.00% and 53.41%) for the normal cervical samples. The expression of HPV16 and 18 E6 in cervical squamous cancers was more frequent than in CIN. The frequency of p53 Arg homozygosity in HRHPV E6-positive cervical squamous cancers (64.06%) was greater than in HRHPV E6-negative cervical squamous cancers (35.29%) and in HRHPV E6-positive normal samples (33.33%). The p53 codon 72 polymorphism showed no differences in samples with different FIGO staging and grades.
  
  
  CONCLUSIONS
  p53 Arg homozygosity could serve as a risk indicator for the tumorigenesis of cervix. In combination with HRHPV E6, it might be able to predict the progression of cervical lesions. p53 codon 72 polymorphism is not associated with FIGO staging and grades of cervical cancers.
authors.affiliation: Department of Obstetrics and Gynecology, West China Second University Hospital, Sichuan University, Chengdu 610041, China.
authors.forename: Min-min
authors.initials: MM
authors.lastname: Hou
authors.forename: Ming-rong
authors.initials: MR
authors.lastname: Xi
authors.forename: Ze-yi
authors.initials: ZY
authors.lastname: Cao
authors.forename: Kai-xuan
authors.initials: KX
authors.lastname: Yang
authors.forename: Zhi-lin
authors.initials: ZL
authors.lastname: Sun
mesh_terms: D000230:Adenocarcinoma / Q000235:genetics / Q000821:virology; D002294:Carcinoma, Squamous Cell / Q000235:genetics / Q000821:virology; D003062:Codon; D004268:DNA-Binding Proteins / Q000235:genetics*; D005260:Female; D016158:Genes, p53 / Q000235:genetics*; D052162:Human papillomavirus 16 / Q000235:genetics; D052161:Human papillomavirus 18 / Q000235:genetics; D006801:Humans; D009856:Oncogene Proteins, Viral / Q000235:genetics*; D030361:Papillomavirus Infections / Q000821:virology; D011110:Polymorphism, Genetic; D012097:Repressor Proteins / Q000235:genetics*; D002583:Uterine Cervical Neoplasms / Q000235:genetics* / Q000821:virology; D002578:Uterine Cervical Dysplasia / Q000235:genetics / Q000821:virology
chemical_list: D003062:Codon; D004268:DNA-Binding Proteins; C068651:E6 protein, Human papillomavirus type 16; C052603:E6 protein, Human papillomavirus type 18; D009856:Oncogene Proteins, Viral; D012097:Repressor Proteins