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Articles by Q Wei
Total Records ( 6 ) for Q Wei
  L. M Chen , G Li , L. R Reitzel , K. B Pytynia , M. E Zafereo , Q Wei and E. M. Sturgis
 

It is unknown whether population-level racial or ethnic disparities in mortality from squamous cell carcinoma of the head and neck (SCCHN) also occur in the setting of standardized multidisciplinary-team directed care. Therefore, we conducted a matched-pair study that controlled for several potentially confounding prognostic variables to assess whether a difference in survival exists for African American or Hispanic American compared with non-Hispanic white American SCCHN patients receiving similar care. Matched pairs were 81 African American case and 81 non-Hispanic white control patients and 100 Hispanic American cases and 100 matched non-Hispanic white controls selected from 1,833 patients of a prospective epidemiologic study of incident SCCHN within a single, large multidisciplinary cancer center. Matching variables included age (±10 years), sex, smoking status (never versus ever), site, tumor stage (T1-2 versus T3-4), nodal status (negative versus positive), and treatment. Cases and controls were not significantly different in proportions of comorbidity score, alcohol use, subsite distribution, overall stage, or tumor grade. Matched-pair and log-rank analyses showed no significant differences between cases and controls in recurrence-free, disease-specific, or overall survival. Site-specific analyses suggested that more aggressive oropharyngeal cancers occurred more frequently in minority than in non-Hispanic white patients. We conclude that minority and non-Hispanic white SCCHN patients receiving similar multidisciplinary-team directed care at a tertiary cancer center have similar survival results overall. These results encourage reducing health disparities in SCCHN through public-health efforts to improve access to multidisciplinary oncologic care (and to preventive measures) and through individual clinician efforts to make the best multidisciplinary cancer treatment choices available for their minority patients. The subgroup finding suggests a biologically based racial/ethnic disparity among oropharyngeal patients and that prevention and treatment strategies should be tailored to different populations of these patients.

  M Wang , W Zhang , L Yuan , G Fu , Q Wei and Z. Zhang
 

A recent genome-wide association study identified two common variants that confer susceptibility to bladder cancer. We hypothesized that these variants are associated with risk of bladder cancer in Chinese populations. We genotyped rs9642880 G>T on 8q24 and rs710521 A>G on 3q28 in a two-stage case–control study of bladder cancer to evaluate the association and further examined the expression of MYC. We found that the rs9642880 G>T, but not the rs710521 A>G polymorphism, was associated with an increased risk of bladder cancer. Compared with the rs9642880 GG genotype, the GT/TT genotypes were associated with an odds ratio of 1.65 (95% confidence interval = 1.25–2.17), and this risk was more pronounced in young men and for low-risk tumors. Additional experiments revealed that the rs9642880 GT/TT genotypes were associated with enhanced levels of both MYC mRNA and protein in bladder tissues. Our findings suggested that the rs9642880 G>T polymorphism on 8q24 was independently associated with the risk of bladder cancer in Chinese populations.

  D Lei , E. M Sturgis , Z Liu , M. E Zafereo , Q Wei and G. Li
 

p21 plays an important role in modulating cell cycle control, inducing apoptosis, and inhibiting cell growth, subsequently affecting cancer risk. We investigated the association between two putatively functional single-nucleotide polymorphisms (SNPs) of p21 (p21 C98A and p21 C70T) among 1282 patients diagnosed with incident squamous cell carcinoma of the head and neck (SCCHN) and risk of second primary malignancy (SPM) in an ongoing molecular epidemiology study. We used Log-rank test and Cox proportional hazard models to assess the association of these two SNPs with SPM-free survival and SPM risk. We found that patients with either p21 variant genotypes of the two polymorphisms had a significantly reduced SPM-free survival compared with patients with either p21 wild-type homozygous genotypes (Log-rank test, P = 0.0016). Compared with patients having the p21 98 CC and p21 70 CC genotypes, the patients having p21 98 CA/AA and p21 70 CT/TT variant genotypes had a significantly greater risk of developing SPM, respectively, [hazard ratio (HR) = 1.80, 95% CI = 1.14–2.82 for p21 C98A and HR = 1.82, 95% confidence interval (CI) = 1.16–2.85 for p21 C70T]. Moreover, after combining the variant genotypes of two SNPs, patients with variant genotypes had a significantly moderately increased risk for SPM compared with patients with no variant genotypes (HR = 2.00, 95% CI = 1.26–3.00), and the risk was particularly pronounced in several subgroups. Our results support an increased risk of SPM after index SCCHN with both p21 polymorphisms individually and in combination.

  S Zhang , J Lu , X Zhao , W Wu , H Wang , Q Wu , X Chen , W Fan , H Chen , F Wang , Z Hu , L Jin , Q Wei , H Shen , W Huang and D. Lu
 

Checkpoint kinase (CHEK) 2, a tumor suppressor gene, plays an essential role in the DNA damage checkpoint response cascade. We first investigated two polymorphisms in the proximal promoter of the CHEK2 gene and evaluated their associations with the risk of lung cancer in a case–control study using 500 incident lung cancer cases and 517 cancer-free controls. We found that CHEK2 rs2236141 –48 G > A was significantly associated with lung cancer risk (P = 0.0018). Similar results were obtained in a follow-up replication study in 575 lung cancer patients and 589 controls (P = 0.042). Quantitative polymerase chain reaction showed that individuals with the G allele had lower levels of CHEK2 transcripts in peripheral blood mononuclear cells and normal lung tissues. The –48 G->A variant eliminated a methylation site and thereby relieve the transcriptional repression of CHEK2. Therefore, this polymorphism affected downstream transcription through genetic and epigenetic modifications. Luciferase reporter assays demonstrated that the major G allele significantly attenuated reporter gene expression when methylated. Electrophoretic Mobility shift assays and surface plasmon resonance revealed that the methylated G allele increased transcription factor accessibility. We used in vivo chromatin immunoprecipitation to confirm that the relevant transcription factor was Sp1. Using lung tissue heterozygous for the G/A single-nucleotide polymorphism, we found that Sp1 acted as a repressor and had a stronger binding affinity for the G allele. These results support our hypothesis that the CHEK2 rs2236141 variant modifies lung cancer susceptibility in the Chinese population by affecting CHEK2 expression.

  B Liu , D Chen , L Yang , Y Li , X Ling , L Liu , W Ji , Y Wei , J Wang , Q Wei , L Wang and J. Lu
 

Mitogen-activated protein kinase kinase 4 (MKK4) is a critical mediator of stress-activated protein kinase signals that regulate apoptosis, inflammations and tumorigenesis. Several polymorphisms have been identified in the MKK4 gene. We hypothesized that genetic variants in the MKK4 promoter may alter its expression and thus cancer risk. In a case–control study of 1056 lung cancer cases and 1056 sex and age frequency-matched cancer-free controls, we genotyped two common polymorphisms in the MKK4 promoter region (–1304T>G and –1044A>T) with the Taqman assay, and we found that compared with the most common –1304TT genotype, carriers of –1304G variant genotypes had a decreased risk of lung cancer [odds ratio (OR) = 0.74; 95% confidence interval (CI) = 0.61–0.90 for TG, and OR = 0.62; 95% CI = 0.41–0.94 for GG] in an allele dose–response manner (adjusted Ptrend = 0.0005). Further stratification analysis showed that the protective role of the –1304G variant allele was more evident in low or normal body mass index (BMI) but restrained in the overweighters and that the –1304G variant genotypes interacted with BMI in reducing cancer risk (adjusted Pinteraction = 0.003). Moreover, the luciferase assay showed that the G allele in the promoter significantly increased the transcription activity of the MKK4 gene in vitro and that the MKK4 protein expression levels of the G variant carriers was significantly higher in tumor tissues than those of the –1304TT genotype. However, no significant association was observed between the –1044A>T polymorphism and risk of lung cancer. Our data suggest that the functional –1304G variant in the MKK4 promoter contributes to a decreased risk of lung cancer by increasing the promoter activity and that the G variant may be a marker for susceptibility to lung cancer.

  Y Liu , S Shete , L. E Wang , R El Zein , C. J Etzel , F. W Liang , G Armstrong , S Tsavachidis , M. R Gilbert , K. D Aldape , J Xing , X Wu , Q Wei and M. L. Bondy
 

Background: DNA strand breaks pose the greatest threat to genomic stability. Genetically determined mutagen sensitivity predisposes individuals to a variety of cancers, including glioma. However, polymorphisms in DNA strand break repair genes that may determine mutagen sensitivity are not well studied in cancer risk, especially in gliomas.

Methods: We correlated genotype data for tag single-nucleotide polymorphisms (tSNPs) of DNA strand break repair genes with a gamma-radiation-induced mutagen sensitivity phenotype [expressed as mean breaks per cell (B/C)] in samples from 426 glioma patients. We also conducted analysis to assess joint and haplotype effects of single-nucleotide polymorphisms (SNPs) on mutagen sensitivity. We further validate our results in an independent external control group totaling 662 subjects.

Results: Of the 392 tSNPs examined, we found that mutagen sensitivity was modified by one tSNP in the EME2 gene and six tSNPs in the RAD51L1 gene (P < 0.01). Among the six RAD51L1 SNPs tested in the validation set, one (RAD51L1 rs2180611) was significantly associated with mutagen sensitivity (P = 0.025). Moreover, we found a significant dose–response relationship between the mutagen sensitivity and the number of adverse tSNP genotypes. Furthermore, haplotype analysis revealed that RAD51L1 haplotypes F-A (zero adverse allele) and F-E (six adverse alleles) exhibited the lowest (0.42) and highest (0.93) mean B/C values, respectively. A similar dose–response relationship also existed between the mutagen sensitivity and the number of adverse haplotypes.

Conclusion: These results suggest that polymorphisms in and haplotypes of the RAD51L1 gene, which is involved in the double-strand break repair pathway, modulate gamma-radiation-induced mutagen sensitivity.

 
 
 
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