Abstract
OBJECTIVES: To examine the profiles of K-ras mutations and p16 and preproenkephalin (ppENK) promoter hypermethylation and their associations with cigarette smoking in pancreatic cancer patients. METHODS: In plasma DNA of 83 patients with untreated primary pancreatic ductal adenocarcinoma, DNA hypermethylation was determined by methylation-specific polymerase chain reaction and K-ras codon 12 mutations by enriched-nested polymerase chain reaction followed by direct sequencing. Information on smoking exposure was collected by in-person interview. Pearson χ test and Fisher exact test were used in statistical analysis. RESULTS: K-ras mutations, ppENK, and p16 promoter hypermethylation were detected in 32.5%, 29.3%, and 24.6% of the patients, respectively. Sixty-three percent (52/83) of patients exhibited at least one of the alterations. Smoking was associated with the presence of K-ras mutations (P = 0.003). A codon 12 G-to-A mutation was predominantly observed in regular smokers and in heavy smokers (pack-year of smoking ≥36). Smoking was not associated with p16 or ppENK hypermethylation. CONCLUSIONS: These preliminary observations suggest that plasma DNA might be a useful surrogate in detecting genetic and epigenetic alterations of pancreatic cancer. The findings on the association between K-ras mutation and smoking were in consistency with previous studies. Further studies on environmental modulators of epigenetic changes in pancreatic cancer are warranted.
Original language | English (US) |
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Pages (from-to) | 55-62 |
Number of pages | 8 |
Journal | Pancreas |
Volume | 34 |
Issue number | 1 |
DOIs | |
State | Published - Jan 2007 |
Keywords
- Cigarette smoking
- DNA methylation
- K-ras mutation
- Pancreatic cancer
- Plasma DNA
- Preproenkephalin
- p16
ASJC Scopus subject areas
- Internal Medicine
- Endocrinology, Diabetes and Metabolism
- Hepatology
- Endocrinology