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Association between p53 immunostaining and cigarette smoking in squamous cell carcinoma of the esophagus.

AbstractBACKGROUND:
It is generally accepted that cigarette smoking is closely associated with esophageal squamous cell carcinoma. This study investigated the molecular targets of cigarette smoke in carcinogenesis of the esophagus.
METHODS:
Seventy-four patients with esophageal squamous cell carcinoma (SCC) were grouped according to daily cigarette consumption: heavy smoking group (group H) (n = 26), moderate smoking group (group M) (n = 39) and non-smoking group (group N) (n = 9). We compared p53 and retinoblastoma (RB) expression among the three groups by immunohistochemistry. In addition, fresh tumor tissues from 30 smokers with esophageal SCC were tested for p53 mutations in exons 5-8 by direct sequencing.
RESULTS:
Staining for the p53 product was positive in 65.4% of group H, 38.5% of group M and 44.4% of group N. The frequency of positive staining in the group H was significantly higher than in group M (p = 0.033) and in group M + group N (p = 0.034). The difference with respect to the frequency of overexpression of RB was not significant. The patterns of p53 base-pair mutations in direct sequencing study were of five types, most commonly G:C to T:A transversion (35.3%).
CONCLUSIONS:
Our study suggests that one of the molecular targets of cigarette smoke is the p53 gene. The pattern of p53 point mutations involved a wide range of base-pair changes.
AuthorsS Mizobuchi, M Furihata, H Sonobe, Y Ohtsuki, T Ishikawa, H Murakami, A Kurabayashi, S Ogoshi, S Sasaguri
JournalJapanese journal of clinical oncology (Jpn J Clin Oncol) Vol. 30 Issue 10 Pg. 423-8 (Oct 2000) ISSN: 0368-2811 [Print] England
PMID11185887 (Publication Type: Journal Article)
Chemical References
  • Tumor Suppressor Protein p53
Topics
  • Aged
  • Carcinoma, Squamous Cell (genetics, metabolism)
  • Esophageal Neoplasms (genetics, metabolism)
  • Female
  • Genes, p53
  • Humans
  • Immunohistochemistry
  • Male
  • Middle Aged
  • Mutation
  • Retrospective Studies
  • Smoking (adverse effects, genetics)
  • Tumor Suppressor Protein p53 (metabolism)

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