Abstract
Chromoendoscopy with Lugol iodine staining provides important information on the development of squamous cell carcinoma (SCC). In particular, distinct iodine-unstained lesions (DIULs) larger than 10 mm show a high prevalence in high-grade intraepithelial neoplasia. It has also been reported that inactive ALDH2*1/*2 and less-active ADH1B*1/*1, and smoking, are risk factors for esophageal SCC. We previously examined telomere shortening in the esophageal epithelium of alcoholics, and suggested a high prevalence of chromosomal instability in such individuals. In the present study, we attempted to analyze telomere lengths in 52 DIULs with reference to both their size and multiplicity, ALDH2 and ADH1B genotypes, and smoking history. Patients with DIULs <10 mm (n = 42) had significantly longer telomeres than those with DIULs ≥10 mm (n = 10, p = 0.008). No significant differences in telomere length were recognized between the ALDH2 and ADH1B genotypes (ALDH2 active/inactive = 35/17, ADH1B active/inactive = 32/20; p = 0.563, 0.784, respectively) or among four groups of patients divided according to smoking history (never-, ex-, light, and heavy smokers = 3, 6, 21, and 22 patients, respectively; p = 0.956). Patients without multiple DIULs (n = 17) had significantly longer telomeres than patients with multiple DIULs (n = 35, p = 0.040). It is suggested that alcoholism reduces telomere length in the esophagus, irrespective of genotype or smoking habit. Telomere shortening may not generate cancer directly, but may create conditions under which SCC can develop more easily, depending on subsequent exposure to carcinogens.
Highlights
Squamous cell carcinoma (SCC) is still the predominant histologic type of esophageal cancer in areas where there is a high risk of developing it
Using Southern blotting and quantitative fluorescence in situ hybridization (Q-FISH), we have demonstrated that telomere shortening occurs in almost all human organs and tissues, including esophageal epithelium, with aging [8,9,10], and have confirmed that the annual telomere reduction rate is 60 bp in normal esophageal epithelium [8]
We demonstrated telomere shortening in the esophageal epithelium of alcoholics relative to non-alcoholics, and indicated that alcohol intake shortens telomeres in the esophageal epithelium [18]
Summary
Squamous cell carcinoma (SCC) is still the predominant histologic type of esophageal cancer in areas where there is a high risk of developing it. Telomeres in uninvolved lingual [11] and esophageal [17] epithelium (background) from cases of SCC in situ (CIS) have been shown to be significantly shorter than those in age-matched controls. These results have confirmed that our method for telomere measurement is accurate and reproducible. It has been reported that the risk factors for esophageal SCC in Japanese drinkers include the inactive ALDH2*1/*2 and less-active ADH1B*1/*1 genotypes, smoking, and frequent drinking of strong alcoholic beverages straight [27]. We attempted to clarify whether the inactive ALDH2*1/*2 and/or less-active ADH1B*1/ *1 genotype, and smoking, are risk factors associated with telomere shortening in alcoholics
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