title: HPV infection and p53 inactivation in pterygium.
abstract: OBJECTIVE
  Our recent report indicated that tumor suppressor gene (p53) mutations and protein aberrant expression were detected in pterygium. Inactivation of p53 by Human papillomavirus (HPV) 16/18 E6 plays a crucial role in cervical tumorigenesis. In this study, we further speculate that p53 inactivation may be linked with HPV infection in pterygium pathogenesis. To investigate the involvement of HPV 16/18 E6 in p53 inactivation in pterygium, the association between HPV 16 or HPV 18 infection, the HPV E6 oncoprotein, and p53 protein expression was analyzed in this study.
  
  
  METHODS
  HPV 16/18 infection was detected by nested-polymerase chain reaction (nested-PCR), the p53 mutation was detected by direct sequencing, and the p53 and the HPV 16/18 E6 proteins were studied using immunohistochemistry on 129 pterygial specimens and 20 normal conjunctivas.
  
  
  RESULTS
  The HPV 16/18 was detected in 24% of the pterygium tissues (31 of 129) but not in the normal conjunctiva, and the HPV16/18 E6 oncoprotein was detected in 48.3% of HPV 16/18 DNA-positive pterygium tissues (15 of 31). In addition, p53 protein negative expression in pterygium was correlated with HPV16/18 E6 oncoprotein expression but not with a p53 mutation.
  
  
  CONCLUSIONS
  HPV 16/18 E6 contributes to HPV-mediated pterygium pathogenesis as it is partly involved in p53 inactivation and is expressed in HPV DNA-positive pterygium.
authors.affiliation: Institute of Medicine, Chung Shan Medical University, Taichung, Taiwan.
authors.forename: Yi-Yu
authors.initials: YY
authors.lastname: Tsai
authors.forename: Chi-Chung
authors.initials: CC
authors.lastname: Chang
authors.forename: Chun-Chi
authors.initials: CC
authors.lastname: Chiang
authors.forename: Kun-Tu
authors.initials: KT
authors.lastname: Yeh
authors.forename: Pei-Liang
authors.initials: PL
authors.lastname: Chen
authors.forename: Chi-Huang
authors.initials: CH
authors.lastname: Chang
authors.forename: Ming-Chih
authors.initials: MC
authors.lastname: Chou
authors.forename: Huei
authors.initials: H
authors.lastname: Lee
authors.forename: Ya-Wen
authors.initials: YW
authors.lastname: Cheng
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D004252:DNA Mutational Analysis; D004268:DNA-Binding Proteins / Q000235:genetics; D005260:Female; D020868:Gene Silencing; D016158:Genes, p53; D052162:Human papillomavirus 16 / Q000235:genetics / Q000378:metabolism / Q000472:pathogenicity; D052161:Human papillomavirus 18 / Q000235:genetics / Q000378:metabolism / Q000472:pathogenicity; D006801:Humans; D007150:Immunohistochemistry; D008297:Male; D008875:Middle Aged; D009856:Oncogene Proteins, Viral / Q000235:genetics; D030361:Papillomavirus Infections / Q000378:metabolism* / Q000821:virology; D016133:Polymerase Chain Reaction; D011625:Pterygium / Q000235:genetics / Q000378:metabolism* / Q000821:virology*; D012097:Repressor Proteins / Q000235:genetics; D017422:Sequence Analysis, DNA; D016159:Tumor Suppressor Protein p53 / Q000235:genetics / Q000378:metabolism*
chemical_list: 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; D016159:Tumor Suppressor Protein p53