Betel quid chewing, cigarette smoking and alcohol consumption related to oral cancer in Taiwan

Ko, Ying‐Chin; Huang, Yeou‐Lih; Lee, Chien-Hung; Chen, Mei-Ju; Lin, Li‐Min; Tsai, Chih-Cheng

doi:10.1111/j.1600-0714.1995.tb01132.x

Cited by 647 publications

(580 citation statements)

References 10 publications

Supporting

Mentioning

543

Contrasting

Unclassified

Order By: Relevance

“…3,27 In our study, although an especially strong risk (OR ϭ 41.2) of esophageal cancer was noticed among patients who concomitantly consumed the 3 substances, no sufficient data can be used for the exploration of 3-way interaction because there were no cancer cases in the category of non-drinking and nonsmoking chewers. Owing to areca nut chewing had a higher risk for contracting oral cancer 28 and certain oral precancers, such as oral leukoplakia and submucous fibrosis 9 than esophageal cancer. The competing causes of tumor occurrence from these diseases might explain the absence of this type of case in this population.…”

Section: Discussionmentioning

confidence: 99%

Independent and combined effects of alcohol intake, tobacco smoking and betel quid chewing on the risk of esophageal cancer in Taiwan

Lee

et al. 2004

Intl Journal of Cancer

Self Cite

208

175

View full text Add to dashboard Cite

A multicenter case-control study was conducted in northern and southern Taiwan to clarify the independent and combined effects of alcohol intake, tobacco smoking and betel quid chewing on the risk of esophageal cancer. A total of 513 patients with newly diagnosed and histopathologically confirmed squamous cell carcinoma of the esophagus and 818 gender, age and study hospitalmatched controls were included. We found a significant doseresponse relationship between the duration and intensity of consumption of the 3 substances and the development of this neoplasm in this site. Although the amount of alcohol consumed had a stronger effect on the risk of esophageal cancer than the number of years it was consumed, however, the number of years one smoked had a stronger effect on the risk than the amount of cigarettes consumed. The strongest risk factor of esophageal cancer was alcohol intake, with highest risk (OR ‫؍‬ 13.9) being for those who consumed more than 900 g/day-year. Combined exposure to any 2 of 3 substances brought the risks up to 8.8 -19.7 fold and, to all 3 substances, to 41.2-fold. A multiplicative interaction effect for alcohol drinkers who smoked on cancer risk was detected, whereas an additive interaction effect was found among drinkers who chewed. The combined effect of all 3 substances accounted for 83.7% of the attributable fraction of contracting esophageal cancer in this population. In conclusion, these results suggest that the intensity and the length of time alcohol and tobacco are used play different roles in the etiology of esophageal cancer. Alcohol separately interacts with tobacco and betel quid in a differently synergistic way in determining the development of this site of cancer.

show abstract

Section: Discussionmentioning

confidence: 99%

Independent and combined effects of alcohol intake, tobacco smoking and betel quid chewing on the risk of esophageal cancer in Taiwan

Lee

et al. 2004

Intl Journal of Cancer

Self Cite

208

175

View full text Add to dashboard Cite

show abstract

“…Tobacco smoking and alcohol abuse are involved in the pathogenesis of oral cavity cancer, and the two agents appear to act synergistically (Blot et al, 1988;Merletti et al, 1989;Ko et al, 1995). Although OL and OSF are both high-risk preneoplastic states, the independent and interactive associations between cigarette smoking, alcohol consumption and areca nut chewing have not been well established in these oral diseases.…”

mentioning

confidence: 99%

The precancer risk of betel quid chewing, tobacco use and alcohol consumption in oral leukoplakia and oral submucous fibrosis in southern Taiwan

et al. 2003

Br J Cancer

239

180

View full text Add to dashboard Cite

In areas where the practise of betel quid chewing is widespread and the chewers also often smoke and drink alcohol, the relation between oral precancerous lesion and condition to the three habits is probably complex. To explore such association and their attributable effect on oral leukoplakia (OL) and oral submucous fibrosis (OSF), a gender -age-matched case -control study was conducted at Kaohsiung, southern Taiwan. This study included 219 patients with newly diagnosed and histologically confirmed OL or OSF, and 876 randomly selected community controls. All information was collected by a structured questionnaire through in-person interviews. A preponderance of younger patients had OSF, while a predominance of older patients had OL. Betel quid chewing was strongly associated with both these oral diseases, the attributable fraction of OL being 73.2% and of OSF 85.4%. While the heterogeneity in risk for areca nut chewing across the two diseases was not apparent, betel quid chewing patients with OSF experienced a higher risk at each exposure level of chewing duration, quantity and cumulative measure than those who had OL. Alcohol intake did not appear to be a risk factor. However, cigarette smoking had a significant contribution to the risk of OL, and modified the effect of chewing based on an additive interaction model. For the two oral premalignant diseases combined, 86.5% was attributable to chewing and smoking. Our results suggested that, although betel quid chewing was a major cause for both OL and OSF, its effect might be difference between the two diseases. Cigarette smoking has a modifying effect in the development of oral leukoplakia.

show abstract

“…Epidemiological studies have clearly indicated that areca quid (AQ) chewing, cigarette smoking and alcohol are the major risk factors for oral squamous cell carcinoma (OSCC) (IARC, 1985;Ko et al, 1995). In Taiwan, approximately 80% of all oral cancer patients are associated with the AQ chewing habit (Ko et al, 1995).…”

mentioning

confidence: 99%

p53 polymorphisms associated with mutations in and loss of heterozygosity of the p53 gene in male oral squamous cell carcinomas in Taiwan

Huang

et al. 2004

Br J Cancer

View full text Add to dashboard Cite

The present study was designed to examine whether different p53 haplotypes of exon 4 -intron 3 -intron 6 affect the frequency of mutations and loss of heterozygosity (LOH) of the p53 gene in male oral squamous cell carcinomas (OSCCs) in Taiwan. We found that individuals without two Pro-W-G alleles had significantly higher frequency of p53 mutations than those with two Pro-W-G alleles (odds ratio (OR) ¼ 1.98; 95% confidence interval (CI), 1.10 -3.56). Out of the 172 p53 gene exon 4 informative male OSCCs, 72 (41.9%) showed LOH. Among these 72 OSCCs with LOH, the frequency of Pro allele loss was 73.6% (53/72). It is notable that alcohol drinking increased the frequency of Arg allele loss (OR ¼ 10.56; 95% CI, 1.23 -234.94) in OSCCs from patients who both smoked cigarettes and chewed areca quid (AQ). The frequency of LOH of p53 was not different between p53-mutated OSCCs and p53-normal OSCCs. Thus, the present study revealed that (a) the Arg allele is associated with p53 mutations, (b) the Pro allele is preferentially lost in OSCCs associated with cigarette smoking and AQ chewing, while the frequency of Arg allele loss is increased with alcohol drinking, and (c) haploinsufficiency of p53 is in itself likely to contribute to tumour progression in Taiwanese OSCCs.

show abstract

Betel quid chewing, cigarette smoking and alcohol consumption related to oral cancer in Taiwan

Cited by 647 publications

References 10 publications

Independent and combined effects of alcohol intake, tobacco smoking and betel quid chewing on the risk of esophageal cancer in Taiwan

Independent and combined effects of alcohol intake, tobacco smoking and betel quid chewing on the risk of esophageal cancer in Taiwan

The precancer risk of betel quid chewing, tobacco use and alcohol consumption in oral leukoplakia and oral submucous fibrosis in southern Taiwan

p53 polymorphisms associated with mutations in and loss of heterozygosity of the p53 gene in male oral squamous cell carcinomas in Taiwan

Contact Info

Product

Resources

About