Qingyi Wei

Overview:

Qingyi Wei, MD, PhD, Professor in the Department of Medicine, is Associate Director for Cancer Control and Population Sciences, Co-leader of CCPS and Co-leader of Epidemiology and Population Genomics (Focus Area 1). He is a professor of Medicine and an internationally recognized epidemiologist focused on the molecular and genetic epidemiology of head and neck cancers, lung cancer, and melanoma. His research focuses on biomarkers and genetic determinants for the DNA repair deficient phenotype and variations in cell death. He is Editor-in-Chief of the open access journal "Cancer Medicine" and Associate Editor-in-Chief of the International Journal of Molecular Epidemiology and Genetics.

Area of Expertise: Epidemiology

Positions:

Professor in Population Health Sciences

Population Health Sciences
School of Medicine

Research Professor of Global Health

Duke Global Health Institute
Institutes and Provost's Academic Units

Professor in Medicine

Medicine, Medical Oncology
School of Medicine

Member of the Duke Cancer Institute

Duke Cancer Institute
School of Medicine

Education:

B.M. 1983

Nanjing Medical University (China)

Ph.D. 1993

Johns Hopkins Unversity, Bloomberg School of Public Health

Grants:

Postdoctoral Training in Genomic Medicine Research

Administered By
Duke Center for Applied Genomics and Precision Medicine
Awarded By
National Institutes of Health
Role
Mentor
Start Date
End Date

Helicobacter pylori blood biomarker for gastric cancer risk in East Asia

Administered By
Duke Cancer Institute
Awarded By
National Institutes of Health
Role
Co Investigator
Start Date
End Date

The UGT2A and 3A metabolizing enzymes and tobacco-related cancer risk

Administered By
Duke Cancer Institute
Awarded By
Washington State University
Role
Principal Investigator
Start Date
End Date

Genotypes and Phenotypes of Apoptosis and Risk of Head and Neck Cancer

Administered By
Duke Cancer Institute
Awarded By
National Institutes of Health
Role
Principal Investigator
Start Date
End Date

Molecular Epidemiology of DNA Repair in Head and Neck Cancer

Administered By
Duke Cancer Institute
Awarded By
National Institutes of Health
Role
Principal Investigator
Start Date
End Date

Publications:

Genetic variants in glutamine metabolic pathway genes predict cutaneous melanoma-specific survival.

Glutamine dependence is a unique metabolic defect seen in cutaneous melanoma (CM), directly influencing the treatment and prognosis. Here, we investigated the associations between 6025 common single-nucleotide polymorphisms (SNPs) in 77 glutamine metabolic pathway genes with CM-specific survival (CMSS) using genotyping datasets from two published genome-wide association studies (GWASs). In the single-locus analysis, 76 SNPs were found to be significantly associated with CMSS (P < .050, false-positive report probability < 0.2 and Bayesian false discovery probability < 0.8) in the discovery dataset, of which seven SNPs were replicated in the validation dataset and three SNPs (HAL rs17676826T > C, LGSN rs12663017T > A, and NOXRED1 rs8012548A > G) independently predicted CMSS, with an effect-allele attributed adjusted hazards ratio of 1.52 (95% confidence interval = 1.19-1.93) and P < .001, 0.68 (0.54-0.87) and P = .002 and 0.62 (0.46-0.83) and P = .002, respectively. The model including the number of unfavorable genotypes (NUGs) of these three SNPs and covariates improved the five-year CMSS prediction (P = .012) than the one with other covariates only. Further expression quantitative trait loci (eQTL) analysis found that the LGSN rs12663017 A allele was significantly associated with increased messenger RNA (mRNA) expression levels (P = 8.89 × 10 -11 ) in lymphoblastoid cell lines of the 1000 Genomes Project database. In the analysis of the genotype tissue expression (GTEx) project datasets, HAL rs17676826 C and NOXRED1 rs8012548 G alleles were significantly associated with their mRNA expression levels in sun-exposed skin of the lower leg (P = 6.62 × 10-6 and 1.37 × 10-7 , respectively) and in sun-not-exposed suprapubic skin (P < .001 and 1.43 × 10-8 , respectively). Taken together, these genetic variants of glutamine-metabolic pathway genes may be promising predictors of survival in patients with CM.
Authors
Chen, K; Liu, H; Liu, Z; Bloomer, W; Amos, CI; Lee, JE; Li, X; Nan, H; Wei, Q
MLA Citation
Chen, Ka, et al. “Genetic variants in glutamine metabolic pathway genes predict cutaneous melanoma-specific survival.Mol Carcinog, vol. 58, no. 11, Nov. 2019, pp. 2091–103. Pubmed, doi:10.1002/mc.23100.
URI
https://scholars.duke.edu/individual/pub1406342
PMID
31435991
Source
pubmed
Published In
Molecular Carcinogenesis
Volume
58
Published Date
Start Page
2091
End Page
2103
DOI
10.1002/mc.23100

Genetic variants in CYP2B6 and HSD17B12 associated with risk of squamous cell carcinoma of the head and neck.

Polycyclic aromatic hydrocarbons (PAH) and tobacco-specific nitrosamines (TSNA) metabolism-related genes play an important role in the development of cancers. We assessed the associations of genetic variants in genes involved in the metabolism of PAHs and TSNA with risk of squamous cell carcinoma of the head and neck (SCCHN) in European populations using two published genome-wide association study datasets. In the single-locus analysis, we identified two SNPs (rs145533669 and rs35246205) in CYP2B6 to be associated with risk of SCCHN (P = 1.57 × 10-4 and .004, respectively), two SNPs (EPHX1 rs117522494 and CYP2B6 rs145533669) to be associated with risk of oropharyngeal cancer (P = .001 and .004, respectively), and one SNP (rs4359199 in HSD17B12) to be associated with risk of oral cancer (P = .006). A significant interaction effect was found between rs4359199 and drinking status on risks of SCCHN and oropharyngeal cancer (P < .05). eQTL and sQTL analyzes revealed that two SNPs (CYP2B6 rs35246205 and HSD17B12 rs4359199) were correlated with alternative splicing or mRNA expression levels of the corresponding genes in liver cells (P < .05 for both). In silico functional annotation suggested that these two SNPs may regulate mRNA expression by affecting the binding of transcription factors. Results from phenome-wide association studies presented significant associations between these genes and risks of other cancers, smoking behavior and alcohol dependence (P < .05). Thus, our study provided some insight into the underlying genetic mechanism of head and neck cancer, which warrants future functional validation.
Authors
Liu, H; Li, G; Sturgis, EM; Shete, S; Dahlstrom, KR; Du, M; Amos, CI; Christiani, DC; Lazarus, P; Wei, Q
MLA Citation
Liu, Hongliang, et al. “Genetic variants in CYP2B6 and HSD17B12 associated with risk of squamous cell carcinoma of the head and neck.Int J Cancer, vol. 151, no. 4, Aug. 2022, pp. 553–64. Pubmed, doi:10.1002/ijc.34023.
URI
https://scholars.duke.edu/individual/pub1518323
PMID
35404482
Source
pubmed
Published In
Int J Cancer
Volume
151
Published Date
Start Page
553
End Page
564
DOI
10.1002/ijc.34023

Potentially functional genetic variants of the Notch signaling pathway genes predict survival of Chinese patients with Esophageal Squamous Cell Carcinoma.

BACKGROUND: The Notch signaling pathway is involved in progression of esophageal squamous cell carcinoma (ESCC), but the roles of single nucleotide polymorphisms (SNPs) of the Notch signaling pathway genes in the process remain unknown. METHODS: The present study included 1,009 patients with histopathologically diagnosed ESCC at Fudan University Shanghai Cancer Center (FUSCC). The two-stage multivariate Cox proportional hazards regression analysis was used to estimate associations between 13,248 SNPs in 103 Notch signaling pathway genes and overall survival of the patients. RESULTS: We found that overall survival of the patients was significantly associated with genotypes of HDAC9 rs1729318 (AT+TT vs AA: HR = 1.44, 95% CI = 1.16-1.80, Pcombined = 0.001) and HDAC9 rs1339555498 (GT +TT vs GG: HR = 1.38, 95% CI = 1.10-1.74, Pcombined = 0.005). Further receiver operator characteristic (ROC) curve analysis indicated that the model with both available clinical factors and these two SNPs improved the area under the ROC curve, compared with the model with clinical factors only (1-year: 0.66 vs. 0.64, P = 0.034). Additional expression quantitative trait loci (eQTL) analysis showed that the rs1729318 T variant genotypes were associated with increased mRNA expression levels of HDAC9 in normal esophageal muscular tissue (P = 0.003). CONCLUSIONS: The results suggest that these two potential functional SNPs on HDAC9 may serve as biomarkers for predicting survival of ESCC patients. However, further studies are needed to confirm these findings.
Authors
Wu, Y; Liu, M; Zhang, R; Sun, M; Wei, Q; Zhao, K; Wang, M
MLA Citation
URI
https://scholars.duke.edu/individual/pub1526274
PMID
35821600
Source
pubmed
Published In
J Gene Med
Published Date
Start Page
e3438
DOI
10.1002/jgm.3438

Genetic variants in DDO and PEX5L in peroxisome-related pathways predict non-small cell lung cancer survival.

Peroxisomes play a role in lipid metabolism and regulation of reactive oxygen species, but its role in development and progression of non-small cell lung cancer (NSCLC) is not well understood. Here, we investigated the associations between 9708 single-nucleotide polymorphisms (SNPs) in 113 genes in the peroxisome-related pathways and survival of NSCLC patients from the Prostate, Lung, Colorectal, and Ovarian Cancer Screening Trial (PLCO) and the Harvard Lung Cancer Susceptibility (HLCS) study. In 1185 NSCLC patients from the PLCO trial, we found that 213 SNPs were significantly associated with NSCLC overall survival (OS) (p ≤ 0.05, Bayesian false discovery probability [BFDP] ≤ 0.80), of which eight SNPs were validated in the HLCS data set. In a multivariate Cox proportional hazards regression model, two independent SNPs (rs9384742 DDO and rs9825224 PEX5L) were significantly associated with NSCLC survival (hazards ratios [HR] of 1.17 with 95% CI [confidence interval] of 1.06-1.28 and 0.86 with 95% CI of 0.77-0.96, respectively). Patients with one or two protective genotypes had a significantly higher OS (HR: 0.787 [95% CI: 0.620-0.998] and 0.691 [95% CI: 0.543-0.879], respectively). Further expression quantitative trait loci analysis using whole blood and lung tissue showed that the minor allele of rs9384742 DDO was significantly associated with decreased messenger RNA (mRNA) expression levels and that DDO expression was also decreased in NSCLC tumor tissue. Additionally, high PEX5L expression levels were significantly associated with lower survival of NSCLC. Our data suggest that variants in these peroxisome-related genes may influence gene regulation and are potential predictors of NSCLC OS, once validated by additional studies.
Authors
Chen, AS; Liu, H; Wu, Y; Luo, S; Patz, EF; Glass, C; Su, L; Du, M; Christiani, DC; Wei, Q
MLA Citation
Chen, Allan S., et al. “Genetic variants in DDO and PEX5L in peroxisome-related pathways predict non-small cell lung cancer survival.Mol Carcinog, vol. 61, no. 7, July 2022, pp. 619–28. Pubmed, doi:10.1002/mc.23400.
URI
https://scholars.duke.edu/individual/pub1520237
PMID
35502931
Source
pubmed
Published In
Molecular Carcinogenesis
Volume
61
Published Date
Start Page
619
End Page
628
DOI
10.1002/mc.23400

Deciphering associations between three RNA splicing-related genetic variants and lung cancer risk.

Limited efforts have been made in assessing the effect of genome-wide profiling of RNA splicing-related variation on lung cancer risk. In the present study, we first identified RNA splicing-related genetic variants linked to lung cancer in a genome-wide profiling analysis and then conducted a two-stage (discovery and replication) association study in populations of European ancestry. Discovery and validation were conducted sequentially with a total of 29,266 cases and 56,450 controls from both the Transdisciplinary Research in Cancer of the Lung and the International Lung Cancer Consortium as well as the OncoArray database. For those variants identified as significant in the two datasets, we further performed stratified analyses by smoking status and histological type and investigated their effects on gene expression and potential regulatory mechanisms. We identified three genetic variants significantly associated with lung cancer risk: rs329118 in JADE2 (P = 8.80E-09), rs2285521 in GGA2 (P = 4.43E-08), and rs198459 in MYRF (P = 1.60E-06). The combined effects of all three SNPs were more evident in lung squamous cell carcinomas (P = 1.81E-08, P = 6.21E-08, and P = 7.93E-04, respectively) than in lung adenocarcinomas and in ever smokers (P = 9.80E-05, P = 2.70E-04, and P = 2.90E-05, respectively) than in never smokers. Gene expression quantitative trait analysis suggested a role for the SNPs in regulating transcriptional expression of the corresponding target genes. In conclusion, we report that three RNA splicing-related genetic variants contribute to lung cancer susceptibility in European populations. However, additional validation is needed, and specific splicing mechanisms of the target genes underlying the observed associations also warrants further exploration.
Authors
Yang, W; Liu, H; Zhang, R; Freedman, JA; Han, Y; Hung, RJ; Brhane, Y; McLaughlin, J; Brennan, P; Bickeboeller, H; Rosenberger, A; Houlston, RS; Caporaso, NE; Landi, MT; Brueske, I; Risch, A; Christiani, DC; Amos, CI; Chen, X; Patierno, SR; Wei, Q
MLA Citation
Yang, Wenjun, et al. “Deciphering associations between three RNA splicing-related genetic variants and lung cancer risk.Npj Precis Oncol, vol. 6, no. 1, June 2022, p. 48. Pubmed, doi:10.1038/s41698-022-00281-9.
URI
https://scholars.duke.edu/individual/pub1526275
PMID
35773316
Source
pubmed
Published In
Npj Precis Oncol
Volume
6
Published Date
Start Page
48
DOI
10.1038/s41698-022-00281-9