Oral Cancer Risk (oral + cancer_risk)

Distribution by Scientific Domains


Selected Abstracts


Genetic and environmental interactions on oral cancer in Southern Thailand

ENVIRONMENTAL AND MOLECULAR MUTAGENESIS, Issue 2 2001
Suparp Kietthubthew
Abstract Many countries are interested in understanding the relationship between genetic susceptibility and their prevalent environmental cancers for disease prevention. In Thailand we conducted a population-based case-control study of 53 matched pairs to assess the risk of oral cancer in relation to genetic polymorphism of the glutathione-S-transferase genes (GSTM1 and GSTT1) in cigarette smokers, alcohol drinkers, and betel quid chewers. Interaction of the genes with other potential risk factors such as local bean consumption were also elucidated. Homozygous deletion of GSTM1 has a frequency of 56.6% (n = 30 over 53) among the patients and 30.2% (16/53) among the controls. This gene is associated with a 2.6-fold higher risk for development of oral cancer (95% CI 1.04,6.5). Among the null GSTM1 individuals, those who smoke, consume alcohol, and/or chew betel quid have a significantly increased risk for oral cancer with an odd ratio (OR) = 4.0 (95% CI = 1.2,13.7), OR = 7.2 (95% CI = 1.5,33.8), and OR = 4.4 (95% CI = 1.1,17.8), respectively. Interactions between any two of the lifestyle habits for oral cancer risk, however, are not found. The frequency of the GSTT1 null genotype is 34.0% (18/53) among the patients and 47.2% (25/53) among our controls. There is no association between the GSTT1 null allele and oral cancer risk. In conclusion, our study provides data to indicate that individuals who have homozygous deletion of the GSTM1 gene have increased risk for oral cancer. The risk increases further when these individuals are exposed to environmental toxicants such as chemicals in cigarette smoke, alcohol, and betel quid. These baseline data can be applied to a larger population-based study, both to verify the observation and to conduct mechanistic investigations. Environ. Mol. Mutagen. 37:111,116, 2001 2001 Wiley-Liss, Inc. [source]


Glutathione S-transferase P1 and alpha gene variants; role in susceptibility and tumor size development of oral cancer

HEAD & NECK: JOURNAL FOR THE SCIENCES & SPECIALTIES OF THE HEAD AND NECK, Issue 8 2010
Mu-Kuan Chen MD
Abstract Background. The aim of this study was to estimate the relationship of glutathione S-transferases (GST)P1, GSTA1, GSTM1, and GSTT1 gene polymorphisms to oral cancer risk. Methods. Polymerase chain reaction,restriction fragment length polymorphism (PCR-RFLP) was used to measure these 4 gene polymorphisms in 274 controls and 164 oral cancer patients. Results. Individuals with at least 1 varied G allele of GSTP1 had a 1.53-fold risk (95% confidence interval [CI] = 1.01,2.31) of developing oral cancer compared with patients with wild-type A/A homozygotes. Oral cancer patients with at least 1 varied T allele of GSTA1 gene had a 0.42-fold risk (95% CI = 0.18,0.95) of having a tumor size >2 cm compared with patients with C/C homozygotes. Conclusions. The varied G allele of GSTP1 may be considered as a factor contributing to increased susceptibility, whereas the T allele of GSTA1 could be a protective factor for tumor size progression in Taiwanese with oral cancer. 2009 Wiley Periodicals, Inc. Head Neck, 2010 [source]


Combinational polymorphisms of four DNA repair genes XRCC1, XRCC2, XRCC3, and XRCC4 and their association with oral cancer in Taiwan

JOURNAL OF ORAL PATHOLOGY & MEDICINE, Issue 5 2008
Ching-Yu Yen
Background:, Many single nucleotide polymorphisms (SNPs) have been found to be associated with oral cancer but the biological interactions through SNPs are seldom addressed. In this study, we focused on the joint effect for SNP combinations of four DNA repair genes, X-ray repair cross-complementing groups (XRCCs) 1,4, involved in major cancer-related pathways. Methods:, Single nucleotide polymorphism genotyping was determined using by polymerase chain reaction-restriction fragment length polymorphism in this study (case = 103, control = 98). Different numbers of combinational SNPs with genotypes called the pseudo-haplotypes from these chromosome-wide genes were used to evaluate their joint effect on oral cancer risk. Results:, Except for XRCC2 rs2040639-AG, none of these SNPs was found to individually contribute to oral cancer risk. However, for two combined SNPs, the proportion of subjects with oral cancer was significantly higher in the pseudo-haplotype with AG-CC genotypes in rs2040639-rs861539 (XRCC2,XRCC3) compared with those with non-AG-CC genotypes. Similarly, the pseudo-haplotype of rs2040639,rs861539,rs2075685 (XRCC2,XRCC3,XRCC4) and rs2040639,rs861539,rs2075685,rs1799782 (XRCCs 1,4) with specific genotype pattern (AG-CC-TG and CT-AG-CC-TG) among three and four combinational SNPs were significantly associated with oral cancer. After controlling for age, gender, smoking, drinking, and betel nut chewing, the estimated odds ratio of oral cancer were 2.45, 5.03, and 10.10 for two, three and four specific SNP combinations, respectively, comparing these specific pseudo-haplotypes to their corresponding non-pseudo-haplotypes. Conclusion:, We have identified the potential combined XRCCs 1,4 SNPs with genotypes that were associated with oral cancer risk and may have an impact on identification of a high-risk population. [source]


On the natural course of oral lichen lesions in a Swedish population-based sample

JOURNAL OF ORAL PATHOLOGY & MEDICINE, Issue 5 2006
A. Roosaar
Objectives:, The aim was to assess the natural course of oral lichen lesions (OLL) among unselected, non-consulting individuals. Subjects and methods:, A cohort of 327 subjects with OLL, confirmed in 1973,1974 during a population-based survey in two Swedish municipalities, was followed through January 2002 via record linkages with nationwide and essentially complete registers. A sample of 80 drawn from the 194 surviving subjects who still resided in the area in 1993,1995 was invited for interview and oral re-examination. Results:, At the end of follow-up, one case of oral cancer was detected, while 0.4 were expected. The overall mortality among subjects with OLL was not significantly different from that in the 15 817 OLL-free subjects who participated in the initial population based survey in 1973,1974. The lesion had disappeared in 14 (39%) of 36 re-examined subjects with white OLLs in 1973,1974, and four (11%) had transformed into red types. In the corresponding group of 19 with red forms initially, five (26%) had become lesion free and four (21%) had switched to white types. Although the cohort size does not permit firm conclusions regarding oral cancer risk, the natural course over up to 30 years appears to be benign in the great majority. [source]