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

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

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

Publications:

Genetic Variants of CLEC4E and BIRC3 in Damage-Associated Molecular Patterns-Related Pathway Genes Predict Non-Small Cell Lung Cancer Survival.

Accumulating evidence supports a role of various damage-associated molecular patterns (DAMPs) in progression of lung cancer, but roles of genetic variants of the DAMPs-related pathway genes in lung cancer survival remain unknown. We investigated associations of 18,588 single-nucleotide polymorphisms (SNPs) in 195 DAMPs-related pathway genes with non-small cell lung cancer (NSCLC) survival in a subset of genotyping data for 1,185 patients from the Prostate, Lung, Colorectal and Ovarian (PLCO) Cancer Screening Trial and validated the findings in another independent subset of genotyping data for 984 patients from Harvard Lung Cancer Susceptibility Study. We performed multivariate Cox proportional hazards regression analysis, followed by expression quantitative trait loci (eQTL) analysis, Kaplan-Meier survival analysis and bioinformatics functional prediction. We identified that two SNPs (i.e., CLEC4E rs10841847 G>A and BIRC3 rs11225211 G>A) were independently associated with NSCLC overall survival, with adjusted allelic hazards ratios of 0.89 (95% confidence interval=0.82-0.95 and P=0.001) and 0.82 (0.73-0.91 and P=0.0003), respectively; so were their combined predictive alleles from discovery and replication datasets (P trend=0.0002 for overall survival). We also found that the CLEC4E rs10841847 A allele was associated with elevated mRNA expression levels in normal lymphoblastoid cells and whole blood cells, while the BIRC3 rs11225211 A allele was associated with increased mRNA expression levels in normal lung tissues. Collectively, these findings indicated that genetic variants of CLEC4E and BIRC3 in the DAMPs-related pathway genes were associated with NSCLC survival, likely by regulating the mRNA expression of the corresponding genes.
Authors
Liu, L; Liu, H; Luo, S; Patz, EF; Glass, C; Su, L; Lin, L; Christiani, DC; Wei, Q
MLA Citation
Liu, Lihua, et al. “Genetic Variants of CLEC4E and BIRC3 in Damage-Associated Molecular Patterns-Related Pathway Genes Predict Non-Small Cell Lung Cancer Survival.Front Oncol, vol. 11, 2021, p. 717109. Pubmed, doi:10.3389/fonc.2021.717109.
URI
https://scholars.duke.edu/individual/pub1499279
PMID
34692492
Source
pubmed
Published In
Frontiers in Oncology
Volume
11
Published Date
Start Page
717109
DOI
10.3389/fonc.2021.717109

Comparative Effectiveness of 5 Local-Regional Control Strategies for IIIA (N2) Non-small Cell Lung Cancer Using SEER Data: Outcomes After Treatment of 20,468 Patients

Authors
Kang, X; Wang, Y; Wei, Q; D'Amico, T; Chen, K
MLA Citation
Kang, Xiaozheng, et al. “Comparative Effectiveness of 5 Local-Regional Control Strategies for IIIA (N2) Non-small Cell Lung Cancer Using SEER Data: Outcomes After Treatment of 20,468 Patients.” Chest, vol. 149, no. 4, Elsevier BV, 2016, pp. A275–A275. Crossref, doi:10.1016/j.chest.2016.02.287.
URI
https://scholars.duke.edu/individual/pub1498211
Source
crossref
Published In
Chest
Volume
149
Published Date
Start Page
A275
End Page
A275
DOI
10.1016/j.chest.2016.02.287

Abstract 3284: Genome-wide association study identifies new susceptibility loci of epithelial ovarian cancer in Han Chinese

Authors
Li, L; Chen, K; Zang, R; Hao, Q; Hu, Z; Lin, D; Ma, D; Jia, W; Shen, H; Wei, Q
MLA Citation
Li, Lian, et al. “Abstract 3284: Genome-wide association study identifies new susceptibility loci of epithelial ovarian cancer in Han Chinese.” Epidemiology, American Association for Cancer Research, 2014. Crossref, doi:10.1158/1538-7445.am2014-3284.
URI
https://scholars.duke.edu/individual/pub1498216
Source
crossref
Published In
Epidemiology
Published Date
DOI
10.1158/1538-7445.am2014-3284

A pleiotropic ATM variant (rs1800057 C>G) is associated with risk of multiple cancers.

ATM (ataxia-telangiectasia mutated) is an important cell-cycle checkpoint kinase required for cellular response to DNA damage. Activated by DNA double strand breaks, ATM regulates the activities of many downstream proteins involved in various carcinogenic events. Therefore, ATM or its genetic variants may have a pleiotropic effect in cancer development. We conducted a pleiotropic analysis to evaluate associations between genetic variants of ATM and risk of multiple cancers. With genotyping data extracted from previously published genome-wide association studies of various cancers, we performed multivariate logistic regression analysis, followed by a meta-analysis for each cancer site, to identify cancer risk-associated single-nucleotide polymorphisms (SNPs). In the ASSET two-sided analysis, we found that two ATM SNPs were significantly associated with risk of multiple cancers. One tagging SNP (rs1800057 C>G) was associated with risk of multiple cancers (two-sided P=5.27×10 -7). Because ATM rs1800057 is a missense variant, we also explored the intermediate phenotypes through which this variant may confer risk of multiple cancers and identified a possible immune-mediated effect of this variant. Our findings indicate that genetic variants of ATM may have a pleiotropic effect on cancer risk and thus provide an important insight into common mechanisms of carcinogenesis.
Authors
Qian, D; Liu, H; Zhao, L; Luo, S; Walsh, KM; Huang, J; Li, C-Y; Wei, Q
MLA Citation
Qian, Danwen, et al. “A pleiotropic ATM variant (rs1800057 C>G) is associated with risk of multiple cancers.Carcinogenesis, Oct. 2021. Pubmed, doi:10.1093/carcin/bgab092.
URI
https://scholars.duke.edu/individual/pub1499401
PMID
34643693
Source
pubmed
Published In
Carcinogenesis
Published Date
DOI
10.1093/carcin/bgab092

Association of genetic variants of FBXO32 and FOXO6 in the FOXO pathway with breast cancer risk.

Forkhead box class O (FOXO) transcription factors play a pivotal role in regulating a variety of biological processes, including organismal development, cell signaling, cell metabolism, and tumorigenesis. Therefore, we hypothesize that genetic variants in FOXO pathway genes are associated with breast cancer (BC) risk. To test this hypothesis, we conducted a large meta-analysis using 14 published genome-wide association study (GWAS) data sets in the Discovery, Biology, and Risk of Inherited Variants in Breast Cancer (DRIVE) study. We assessed associations between 5214 (365 genotyped in DRIVE and 4849 imputed) common single-nucleotide polymorphisms (SNPs) in 55 FOXO pathway genes and BC risk. After multiple comparison corrections by the Bayesian false-discovery probability method, we found five SNPs to be significantly associated with BC risk. In stepwise multivariate logistic regression analysis with adjustment for age, principal components, and previously published SNPs in the same data set, three independent SNPs (i.e., FBXO32 rs10093411 A>G, FOXO6 rs61229336 C>T, and FBXO32 rs62521280 C>T) remained to be significantly associated with BC risk (p = 0.0008, 0.0011, and 0.0017, respectively). Additional expression quantitative trait loci analysis revealed that the FBXO32 rs62521280 T allele was associated with decreased messenger RNA (mRNA) expression levels in breast tissue, while the FOXO6 rs61229336 T allele was found to be associated with decreased mRNA expression levels in the whole blood cells. Once replicated by other investigators, these genetic variants may serve as new biomarkers for BC risk.
Authors
Wang, H; Liu, H; Zhao, L; Luo, S; Akinyemiju, T; Hwang, S; Yue, Y; Wei, Q
MLA Citation
Wang, Haijiao, et al. “Association of genetic variants of FBXO32 and FOXO6 in the FOXO pathway with breast cancer risk.Mol Carcinog, vol. 60, no. 10, Oct. 2021, pp. 661–70. Pubmed, doi:10.1002/mc.23331.
URI
https://scholars.duke.edu/individual/pub1487619
PMID
34197655
Source
pubmed
Published In
Molecular Carcinogenesis
Volume
60
Published Date
Start Page
661
End Page
670
DOI
10.1002/mc.23331