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 Risk for Overall Cancer and the Benefit of Adherence to a Healthy Lifestyle.

Cancer site-specific polygenic risk scores (PRS) effectively identify individuals at high risk of individual cancers, but the effectiveness of PRS on overall cancer risk assessment and the extent to which a high genetic risk of overall cancer can be offset by a healthy lifestyle remain unclear. Here, we constructed an incidence-weighted overall cancer polygenic risk score (CPRS) based on 20 cancer site-specific PRSs. Lifestyle was determined according to smoking, alcohol consumption, physical activity, body mass index, and diet. Cox regression by sex was used to analyze associations of genetic and lifestyle factors with cancer incidence using UK Biobank data (N = 442,501). Compared with participants at low genetic risk (bottom quintile of CPRS), those at intermediate (quintiles 2 to 4) or high (top quintile) genetic risk had HRs of 1.27 (95% confidence interval, 1.21-1.34) or 1.91 (1.81-2.02) for overall cancer, respectively, for men, and 1.21 (1.16-1.27) or 1.62 (1.54-1.71), respectively, for women. A joint effect of genetic and lifestyle factors on overall cancer risk was observed, with HRs reaching 2.99 (2.45-3.64) for men and 2.38 (2.05-2.76) for women with high genetic risk and unfavorable lifestyle compared with those with low genetic risk and favorable lifestyle. Among participants at high genetic risk, the standardized 5-year cancer incidence was significantly reduced from 7.23% to 5.51% for men and from 5.77% to 3.69% for women having a favorable lifestyle. In summary, individuals at high genetic risk of overall cancer can be identified by CPRS, and risk can be attenuated by adopting a healthy lifestyle. SIGNIFICANCE: A new indicator of cancer polygenic risk score measures genetic risk for overall cancer, which could identify individuals with high cancer risk to facilitate decision-making about lifestyle modifications for personalized prevention.
Authors
Zhu, M; Wang, T; Huang, Y; Zhao, X; Ding, Y; Zhu, M; Ji, M; Wang, C; Dai, J; Yin, R; Xu, L; Ma, H; Wei, Q; Jin, G; Hu, Z; Shen, H
MLA Citation
Zhu, Meng, et al. “Genetic Risk for Overall Cancer and the Benefit of Adherence to a Healthy Lifestyle.Cancer Res, vol. 81, no. 17, Sept. 2021, pp. 4618–27. Pubmed, doi:10.1158/0008-5472.CAN-21-0836.
URI
https://scholars.duke.edu/individual/pub1492878
PMID
34321244
Source
pubmed
Published In
Cancer Res
Volume
81
Published Date
Start Page
4618
End Page
4627
DOI
10.1158/0008-5472.CAN-21-0836

Analyses of Copy Number Variation in Cutaneous Melanoma Implicates its Functional Role in Gene Expression Regulation

Authors
Xiao, F; Luo, X; Lee, JE; Wei, Q; Cai, G; Amos, CI
MLA Citation
Xiao, Feifei, et al. “Analyses of Copy Number Variation in Cutaneous Melanoma Implicates its Functional Role in Gene Expression Regulation.” Genetic Epidemiology, vol. 41, no. 7, 2017, pp. 654–55.
URI
https://scholars.duke.edu/individual/pub1498210
Source
wos-lite
Published In
Genetic Epidemiology
Volume
41
Published Date
Start Page
654
End Page
655

Common genetic polymorphisms contribute to the association between chronic lymphocytic leukaemia and non-melanoma skin cancer.

BACKGROUND: Epidemiological studies have demonstrated a positive association between chronic lymphocytic leukaemia (CLL) and non-melanoma skin cancer (NMSC). We hypothesized that shared genetic risk factors between CLL and NMSC could contribute to the association observed between these diseases. METHODS: We examined the association between (i) established NMSC susceptibility loci and CLL risk in a meta-analysis including 3100 CLL cases and 7667 controls and (ii) established CLL loci and NMSC risk in a study of 4242 basal cell carcinoma (BCC) cases, 825 squamous cell carcinoma (SCC) cases and 12802 controls. Polygenic risk scores (PRS) for CLL, BCC and SCC were constructed using established loci. Logistic regression was used to estimate odds ratios (ORs) and 95% confidence intervals (CIs). RESULTS: Higher CLL-PRS was associated with increased BCC risk (OR4th-quartile-vs-1st-quartile = 1.13, 95% CI: 1.02-1.24, Ptrend = 0.009), even after removing the shared 6p25.3 locus. No association was observed with BCC-PRS and CLL risk (Ptrend = 0.68). These findings support a contributory role for CLL in BCC risk, but not for BCC in CLL risk. Increased CLL risk was observed with higher SCC-PRS (OR4th-quartile-vs-1st-quartile = 1.22, 95% CI: 1.08-1.38, Ptrend = 1.36 × 10-5), which was driven by shared genetic susceptibility at the 6p25.3 locus. CONCLUSION: These findings highlight the role of pleiotropy regarding the pathogenesis of CLL and NMSC and shows that a single pleiotropic locus, 6p25.3, drives the observed association between genetic susceptibility to SCC and increased CLL risk. The study also provides evidence that genetic susceptibility for CLL increases BCC risk.
Authors
Besson, C; Moore, A; Wu, W; Vajdic, CM; de Sanjose, S; Camp, NJ; Smedby, KE; Shanafelt, TD; Morton, LM; Brewer, JD; Zablotska, L; Engels, EA; Cerhan, JR; Slager, SL; Han, J; Berndt, SI; InterLymph Consortium. Full authors list is given at the end of the manuscript,
MLA Citation
Besson, Caroline, et al. “Common genetic polymorphisms contribute to the association between chronic lymphocytic leukaemia and non-melanoma skin cancer.Int J Epidemiol, vol. 50, no. 4, Aug. 2021, pp. 1325–34. Pubmed, doi:10.1093/ije/dyab042.
URI
https://scholars.duke.edu/individual/pub1498167
PMID
33748835
Source
pubmed
Published In
Int J Epidemiol
Volume
50
Published Date
Start Page
1325
End Page
1334
DOI
10.1093/ije/dyab042

POTENTIALLY FUNCTIONAL SINGLE NUCLEOTIDE POLYMORPHISMS IN CD133 PREDICT LOCAL RECURRENCE AND DISTANT METASTASIS AFTER RADIOTHERAPY FOR NON-SMALL CELL LUNG CANCER

Authors
Wang, Q; Li, P; Liu, H; Xiong, H; Qian, J; Xu, T; Liu, Z; Liao, Z; Wei, Q
URI
https://scholars.duke.edu/individual/pub1498219
Source
wos-lite
Published In
Journal of Thoracic Oncology
Volume
9
Published Date
Start Page
S33
End Page
S33

Genetic variants of DOCK2, EPHB1 and VAV2 in the natural killer cell-related pathway are associated with non-small cell lung cancer survival.

Although natural killer (NK) cells are a known major player in anti-tumor immunity, the effect of genetic variation in NK-associated genes on survival in patients with non-small cell lung cancer (NSCLC) remains unknown. Here, in 1,185 with NSCLC cases of a discovery dataset, we evaluated associations of 28,219 single nucleotide polymorphisms (SNPs) in 276 NK-associated genes with their survival. These patients were from the reported genome-wide association study (GWAS) from the Prostate, Lung, Colorectal and Ovarian (PLCO) Cancer Screening Trial. We further validated the findings in an additional 984 cases from the Harvard Lung Cancer Susceptibility (HLCS) Study. We identified three SNPs (i.e., DOCK2 rs261083 G>C, VAV2 rs2519996 C>T and EPHB1 rs36215 A>G) to be independently associated with overall survival (OS) in NSCLC cases with adjusted hazards ratios (HRs) of 1.16 (95% confidence interval [CI] = 1.07-1.26, P = 3.34×10-4), 1.28 (1.12-1.47, P = 4.57×10-4) and 0.75 (0.67-0.83, P = 1.50×10-7), respectively. Additional joint assessment of the unfavorable genotypes of the three SNPs showed significant associations with OS and disease-specific survival of NSCLC cases in the PLCO dataset (P trend<0.0001 and <0.0001, respectively). Moreover, the survival-associated DOCK2 rs261083 C allele had a significant correlation with reduced DOCK2 transcript levels in lung adenocarcinoma (LUAD), while the rs36215 G allele was significantly correlated with reduced EPHB1 transcript levels in lymphoblastoid cell lines in the 1000 Genomes Project. These results revealed that DOCK2 and EPHB1 genetic variants may be prognostic biomarkers of NSCLC survival, likely via transcription regulation of respective genes.
Authors
Du, H; Liu, L; Liu, H; Luo, S; Patz, EF; Glass, C; Su, L; Du, M; Christiani, DC; Wei, Q
MLA Citation
URI
https://scholars.duke.edu/individual/pub1484578
PMID
34094683
Source
pubmed
Published In
American Journal of Cancer Research
Volume
11
Published Date
Start Page
2264
End Page
2277