[Analysis of p53 mutational spectra of esophageal squamous cell carcinomas from Linzhou, comparison with esophageal and other cancers from other areas].
OBJECTIVE
To study the etiological clues involved (in esophageal cancer in Linzhou, Henan, a high-incidence area for esophageal cancer) by analyzing p53 mutational spectrum from esophageal precancerous and cancerous lesions.


METHODS
Using bolt bioinformatic and Monte Carlo methods to analyze p53 mutation spectra from "The IARC Database of Somatic p53 Mutations in Human Tumors and Cell Lines", "p53 Database at Institute Curic" and to establish a local database based on these data using the FileMark Pro 3.0 software to allow fast and off-line analysis on a PC from the authors' laboratory.


RESULTS
We found that esophageal squamous cell carcinomas from Linzhou had a lower prevalence of base substitutions associated with strand bias than those from other areas (32.8% vs 39.8%). However, a higher prevalence of G:C-->A:T transitions at CpG site (29.6% vs16.4%) was found. Esophageal squamous cell carcinomas from Linzhou displayed a distinctive profile of mutation hotspots, including codons 273 (covers 11.3% of all missense mutations), 175 (9.7%), 158 (9.7%), 159 (6.5%) and 282 (6.5%), all of which were at the CpG site. Statistical analysis showed that the p53 mutation profiles between esophageal squamous cell carcinomas from Linzhou and those from other areas were different (P = 0.02). The p53 mutation profiles of esophageal squamous cell carcinomas from Linzhou and from other areas were also different from cancer of the head and neck.


CONCLUSIONS
Data showed that the p53 mutational spectrum of esophageal squamous cell carcinomas from Linzhou baring the characteristics of those caused both by endogenous and exogenous mutagenic agents, suggesting the potential involvement of chronic inflammation, unique dietary habits and carcinogen exposure in the pathogenesis of esophageal squamous cell carcinoma in Linzhou.
Wang
Li-dong
LD
Cancer Institute, College of Medicine, Zhejiang University, Hangzhou 310009, China.
Liu
Bin
B
Zheng
Shu
S
D002274:Carcinogens, Environmental / Q000633:toxicity; D002294:Carcinoma, Squamous Cell / Q000453:epidemiology / Q000209:etiology / Q000235:genetics*; D002681:China / Q000453:epidemiology; D004252:DNA Mutational Analysis; D004938:Esophageal Neoplasms / Q000453:epidemiology / Q000209:etiology / Q000235:genetics*; D005247:Feeding Behavior; D005260:Female; D016158:Genes, p53 / Q000235:genetics*; D006801:Humans; D008297:Male; D017354:Point Mutation; D011230:Precancerous Conditions / Q000235:genetics* / Q000378:metabolism; D016159:Tumor Suppressor Protein p53 / Q000378:metabolism
D002274:Carcinogens, Environmental; D016159:Tumor Suppressor Protein p53