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Qingyi Wei

Publications and source records attributed to Qingyi Wei.

118 records · Page 7Linked to original sources
PubMed2002

A variant of the DNA repair gene XRCC3 and risk of squamous cell carcinoma of the head and neck: a case-control analysis.

Individuals differ in their ability to repair DNA damage induced by carcinogens. Studies have shown that polymorphisms in DNA repair genes contribute to individual variation in DNA repair capacity and cancer risk. In a hospital-based case-control study, we tested the hypothesis that a C to T variant (Thr241Met) of DNA repair gene X-ray repair cross-complementing group 3 (XRCC3) is associated with risk of developing squamous cell carcinoma of the head and neck (SCCHN). We genotyped for this variant in 367 non-Hispanic white patients newly diagnosed with SCCHN and 354 frequency-matched cancer-free controls. Compared with the XRCC3 18067CC and 18607CT genotypes, the variant XRCC3 18067TT genotype was associated with a non-statistically significantly increased risk of SCCHN (adjusted odds ratio [ORadj], 1.36; 95% confidence interval [CI], 0.89-2.08), but this risk was significantly increased among female subjects (ORadj 2.23, 95% CI, 1.00-4.98) and current smokers (ORadj, 2.26; 95% CI, 1.02-4.99). These findings suggest that the variant XRCC3 18067TT genotype may not play a major role in the etiology of SCCHN but may contribute to a subset of SCCHN. Larger studies are needed to verify these findings.

Adult↗
PubMed2002

Expression of nucleotide excision repair genes and the risk for squamous cell carcinoma of the head and neck.

BACKGROUND: Phenotypic differences in the ability to repair genetic damage induced by tobacco carcinogens may reflect genetic differences in susceptibility to squamous cell carcinoma of the head and neck (SCCHN). The objective of this study was to assess the variation in baseline expression of five nucleotide excision repair genes between individuals with SCCHN and cancer free controls. METHODS: The authors conducted a hospital-based case-control study of 57 SCCHN patients and 105 cancer free controls. Using peripheral blood lymphocytes, a multiplex reverse transcriptase-polymerase chain reaction assay was used to quantitate in vitro the mRNA levels of five genes (ERCC1, XPB/ERCC3, XPG/ERCC5, CSB/ERCC6, and XPC) involved in the nucleotide excision repair pathway. RESULTS: The levels of ERCC1, XPB/ERCC3, XPG/ERCC5, and CSB/ERCC6 transcripts were lower in cases than in controls (P =0.0001, 0.096, 0.001, and 0.0001, respectively). In multivariate logistic regression analysis (adjusting for age, gender, race, smoking status, and alcohol use), low expression of ERCC1, XPB/ERCC3, XPG/ERCC5, and CSB/ERCC6 was associated with a statistically significant increased risk for SCCHN (adjusted odds ratios [95% confidence intervals] 6.42 [2.63-15.69], 2.86 [1.39-5.90], 3.69 [1.73-7.90], and 2.46 [1.19-5.09], respectively). CONCLUSIONS: Reduced expression of ERCC1, XPB/ERCC3, XPG/ERCC5, and CSB/ERCC6 is associated with a more than two-fold increased risk of SCCHN.

Adult↗
PubMed2002

DNA repair gene ERCC1 and ERCC2/XPD polymorphisms and risk of squamous cell carcinoma of the head and neck.

OBJECTIVE: To determine the effect of the ERCC1 C8092A polymorphism and the ERCC2/XPD G23591A polymorphism on the risk of squamous cell carcinoma of the head and neck (SCCHN). DESIGN: A hospital-based case-control study. SUBJECTS: A total of 330 newly diagnosed case subjects with SCCHN and 330 cancer-free control subjects matched on age (+/- 5 years), sex, smoking status, and alcohol use. All subjects were non-Hispanic whites. METHODS: After informed consent was obtained, blood was drawn for genotyping. The ERCC1 C8092A polymorphism was typed by single-strand conformational polymorphism analysis. The ERCC2/XPD G23591A polymorphism was typed by polymerase chain reaction-based restriction fragment length polymorphism analysis with the enzyme StyI. The chi(2) analysis was used to assess differences in genotype and allele frequencies. Multivariate logistic regression analysis was performed to estimate the risk of SCCHN for individuals having these genotypes after adjustment for age, sex, tobacco smoking, and alcohol use. RESULTS: The DNA was available and genotyping was ultimately successful for 313 case subjects and 313 control subjects. The ERCC1 8092CC genotype and the ERCC2/XPD 23591A allele were associated with nonsignificantly increased risks of SCCHN: odds ratios, 1.15 (95% confidence interval [CI], 0.84-1.59) and 1.28 (95% CI, 0.93-1.76), respectively, whereas having both risk genotypes was associated with an even higher risk of SCCHN: odds ratio, 1.78 (95% CI, 0.99-3.17). When considering both polymorphisms, we found a significant allele dose effect (P =.04). CONCLUSIONS: These 2 polymorphisms may contribute to the risk of SCCHN, but larger studies are needed to confirm their role in SCCHN. Combining common DNA repair gene polymorphisms into models of genetic risk of SCCHN may improve risk estimates.

Adult↗
PubMed2002

Polymorphism of DNA ligase I and risk of lung cancer--a case-control analysis.

DNA ligases catalyze the joining of single and double-strand DNA breaks, which is an essential step in DNA replication, recombination and repair. Recently, a common single nucleotide polymorphism (A-->C) in exon 6 of DNA ligase I (LIG1) was identified, but its functional relevance remains to be determined. Because LIG1 participates in DNA repair and reduced DNA repair capacity is associated with risk of lung cancer, we evaluated in a non-population-based case-control study of 530 lung cancer cases and 570 cancer-free controls the role of this polymorphism in susceptibility to lung cancer. All of the subjects were non-Hispanic whites and the controls were frequency-matched to cases on age, sex and smoking status. Using the polymerase chain reaction-restriction fragment length polymorphism method, we found that this LIGI A-->C substitution was very common in healthy controls and that the A and C allele frequencies were close to 0.5. However, there was no significant difference in the frequency distributions of LIGI genotypes between lung cancer cases and controls (25.7, 49.8 and 24.5% in cases and 26.1, 49.7 and 24.2% in controls for the AA, AC and CC genotypes, respectively). Therefore, there was no evidence to support an association between this polymorphism and the risk of lung cancer (adjusted odds ratio (OR)=1.06, 95% confidence interval (CI)=0.76-1.49 for AC versus CC and OR=0.93, 95% CI=0.64-1.36 for AA versus CC) neither in all cases nor in different histopathologic types. The results of this large case-control study suggest that this LIG1 polymorphism may not play an important role in susceptibility to lung cancer.

Adult↗
PubMed2002

Polymorphisms of the DNA repair gene XPD and risk of lung cancer in a Chinese population.

Previous studies suggested that suboptimal DNA repair capacity is associated with cancer risk and that the Asp312Asn and Lys751Gln polymorphisms in the xeroderma pigmentosum complementary group D (XPD) gene may influence DNA repair capacity. We therefore tested the hypothesis that these two XPD polymorphisms are associated with susceptibility to lung cancer in a hospital-based, case-control study in a Chinese population. Genotypes were determined by polymerase chain reaction-based restriction fragment length polymorphism methods in 383 healthy controls and 351 patients with lung cancer. We found that those who carried at least one 312Asn variant allele had an increased risk of squamous cell carcinoma (SCC) of the lung compared with those with the 312Asp/Asp genotype (adjusted odds ratio (OR), 1.80; 95% confidence interval (CI), 1.10-2.96). Compared with those having the 751Lys/Lys genotype, subjects carrying at least one variant 751 Gln allele were at a borderline increased risk of SCC of the lung (adjusted OR, 1.52; 95% CI, 0.94-2.46). Furthermore, stratified analysis suggested a multiplicative interaction between tobacco smoking and the Asp312Asn polymorphism on risk of SCC of the lung. The adjusted ORs of SCC of the lung for the variant XPD 312Asn genotype alone, for smoking > or = 29 pack-years alone, and for both the factors combined were 1.04 (95% CI, 0.37-2.94), 4.74 (95% CI, 2.88-9.49), and 14.32 (95% CI, 5.80-35.2), respectively. Similar results were evident for the Lys751Gln polymorphism that was in the linkage disequilibrium with the variant 312Asn allele. These data suggest that the two polymorphisms in the XPD gene may influence risk of smoking-related SCC of the lung.

Aged↗
PubMed2002

XPD/ERCC2 EXON 8 Polymorphisms: rarity and lack of significance in risk of squamous cell carcinoma of the head and neck.

BACKGROUND: Inherited polymorphisms of DNA repair genes may contribute to genetic susceptibility to squamous cell carcinoma of the head and neck (SCCHN). The objective was to assess whether two polymorphisms in the nucleotide excision repair gene XPD (ERCC2) are markers of SCCHN risk. METHODS: We performed a hospital-based case-control study of 180 SCCHN patients and 400 cancer-free controls frequency matched on age, sex, smoking, and alcohol use. All subjects were non-Hispanic whites. XPD alleles 23047 and 23051 were assessed by digestion with the restriction enzymes XhoII and SphI after PCR amplification. RESULTS: The XPD 23047 G and XPD 23051 T alleles were extremely rare among both the cases and controls (allele frequencies<1.0%), and not statistically different between groups (P>0.6). CONCLUSIONS: The 23047 and 23051 variants of the DNA repair gene XPD are extremely rare and do not contribute significantly to the risk of SCCHN in the non-Hispanic white population.

Adult↗
PubMed2002

Modulation of repair of ultraviolet damage in the host-cell reactivation assay by polymorphic XPC and XPD/ERCC2 genotypes.

DNA repair capacity (DRC) plays an important role in genetic susceptibility to cancer. Polymorphisms of a number of DNA repair genes involved in several distinct pathways have been identified. However, their effects on repair function have not been well characterized. We demonstrated previously that DRC for removal of benzo[a]pyrene diol epoxide-induced DNA damage measured by a host-cell reactivation assay was modulated by two XPD/ERCC2 polymorphisms in lung cancer. In this report, we investigated the association between the repair phenotype of ultraviolet (UV)-induced damage and genotypes of three DNA repair genes, XPC and XPD [involved in nucleotide excision repair (NER)] and XRCC1 [involved in base excision repair (BER)]. We measured DRC for removal of UV photoproducts by the host-cell reactivation assay in cryopreserved lymphocytes from 102 healthy non-Hispanic white subjects. We also typed these subjects for five polymorphisms in these three DNA repair genes (at intron 9 of XPC; exons 6, 10 and 23 of XPD and exon 10 of XRCC1). Compared with wild-type homozygotes, subjects homozygous for polymorphisms of the two NER genes consistently had suboptimal DRC. The DRC was consistently lower in subjects homozygous for XPC, XPD or both than in subjects with other genotypes, although the difference was not statistically significant for XPD variants. In contrast, the polymorphic allele of the BER gene, XRCC1, had no consistent effect on DRC. We concluded that these NER polymorphisms may modulate DRC and may be useful biomarkers for identifying individuals at risk of developing cancer.

DNA Damage↗
PubMed2002

Genetic susceptibility--molecular epidemiology of head and neck cancer.

In parts of the developing world (South Central Asia in particular), squamous cell carcinoma of the head and neck (SCCHN) is one of the most common malignancies encountered. Although tobacco and alcohol are clearly defined as etiologic factors in these malignancies, clinical observations have suggested that inherited genetic factors put some individuals at increased risk for SCCHN. Emerging data (both phenotypic and genotypic) support this concept of genetic susceptibility to SCCHN and point to differences in DNA repair ability, carcinogen metabolism, and cell cycle control as the systems important to the risk of tobacco-induced malignancies. The ability to identify such high-risk individuals will have major influences on the practice of cancer prevention in the future.

Carcinoma, Squamous Cell↗
PubMed2002

Haplotypes of two variants in p16 (CDKN2/MTS-1/INK4a) exon 3 and risk of squamous cell carcinoma of the head and neck: a case-control study.

The frequent loss or promoter methylation of the tumor suppressor gene p16 in head and neck cancer suggests an etiologic role of p16 in this disease. Two adjacent polymorphisms of p16 exon 3, C540G and C580T, were identified recently. C540G is associated with low expression of p53, and both polymorphisms are associated with tumor aggressiveness, suggesting a possible functional relevance. We hypothesized that these two polymorphisms, particularly their haplotypes, are associated with the risk of developing squamous cell carcinoma of the head and neck (SCCHN). To test this hypothesis, we conducted a hospital-based case-control study of 208 patients with SCCHN and 224 cancer-free control subjects to evaluate the association between p16 genotypes/haplotypes and the risk of SCCHN, using a PCR-single strand conformation polymorphism-based genotyping assay. However, our results suggested that no significant differences exist in the distribution of p16 C540G and C580T genotypes between cases and controls. For the C540G polymorphism, the CC, CG, and GG genotype frequencies were 76.9%, 22.1%, and 1.0%, respectively, in the cases, compared with 76.8%, 21.9%, and 1.3%, respectively, for the controls. For the C580T polymorphism, the CC, CT, and TT genotype frequencies were 83.6%, 15.9%, and 0.5%, respectively, in the cases, compared with 82.6%, 16.5%, and 0.9%, respectively, for the controls. The frequencies of three predominant 540C/580C, 540G/580C, and 540C/580T haplotype alleles were distributed similarly in the cases (79.6%, 12.0%, and 8.4%) and in the controls (78.6%, 12.3%, and 9.1%). None of these differences were statistically significant. We conclude that these polymorphic p16 genotypes or haplotypes may not play a major role in the etiology of SCCHN, if any. However, our limited sample size and power call for larger studies for additional verification of our findings.

Aged↗