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

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:

Association of pretreatment BMI with risk of head and neck cancer: A large-scale single-center study

Authors
Khanna, A; Sturgis, E; Xu, L; Wei, Q; Li, G; Gross, N
MLA Citation
Khanna, Anshu, et al. “Association of pretreatment BMI with risk of head and neck cancer: A large-scale single-center study.” Clinical Cancer Research, vol. 26, no. 12, 2020, pp. 45–45.
URI
https://scholars.duke.edu/individual/pub1451091
Source
wos-lite
Published In
Clinical Cancer Research : an Official Journal of the American Association for Cancer Research
Volume
26
Published Date
Start Page
45
End Page
45

Novel genetic variants in genes of the Fc gamma receptor-mediated phagocytosis pathway predict non-small cell lung cancer survival.

Background: Both antibody-dependent cellular cytotoxicity and phagocytosis activate innate immunity, and the Fc gamma receptor (FCGR)-mediated phagocytosis is an integral part of the process. We assessed associations between single-nucleotide polymorphisms (SNPs) in FCGR-related genes and survival of patients with non-small cell lung cancer (NSCLC). Methods: We evaluated associations between 24,734 (SNPs) in 97 FCGR-related genes and survival of 1,185 patients with NSCLC using a published genome-wide association study (GWAS) dataset from the Prostate, Lung, Colorectal and Ovarian (PLCO) Cancer Screening Trial and validated the results in another independent dataset of 894 NSCLC patients. Results: In the single-locus analysis with Bayesian false discovery probability (BFDP) for multiple testing correction, we found 1,084 SNPs to be significantly associated overall survival (OS) (P<0.050 and BFDP ≤0.80), of which two independent SNPs (PLCG2 rs9673682 T>G and PLPP1 rs115613985 T>A) were further validated in another GWAS dataset of 894 patients from the Harvard Lung Cancer Susceptibility (HLCS) Study, with combined allelic hazards ratios for OS of 0.87 [95% confidence interval (CI): 0.81-0.94 and P=5.90×10-4] and 1.18 (95% CI: 1.08-1.29 and 1.32×10-4, respectively). Expression quantitative trait loci analysis showed that the rs9673682 G allele was significantly correlated with increased mRNA expression levels of PLCG2 in 373 transformed lymphoblastoid cell-lines (P=7.20×10-5). Additional evidence from differential expression analysis further supported a tumor-suppressive effect of PLCG2 on OS of patients with lung cancer, with lower mRNA expression levels in both lung squamous carcinoma and adenocarcinoma than in adjacent normal tissues. Conclusions: Genetic variants in PLCG2 of the FCGR-mediated phagocytosis pathway may be promising predictors of NSCLC survival, possibly through modulating gene expression, but additional investigation of the molecular mechanisms of PLPP1 rs115613985 is warranted.
Authors
Qian, D; Liu, H; Zhao, L; Wang, X; Luo, S; Moorman, PG; Patz, EF; Su, L; Shen, S; Christiani, DC; Wei, Q
MLA Citation
Qian, Danwen, et al. “Novel genetic variants in genes of the Fc gamma receptor-mediated phagocytosis pathway predict non-small cell lung cancer survival.Transl Lung Cancer Res, vol. 9, no. 3, June 2020, pp. 575–86. Pubmed, doi:10.21037/tlcr-19-318.
URI
https://scholars.duke.edu/individual/pub1452505
PMID
32676321
Source
pubmed
Published In
Translational Lung Cancer Research
Volume
9
Published Date
Start Page
575
End Page
586
DOI
10.21037/tlcr-19-318

Novel genetic variants of KIR3DL2 and PVR involved in immunoregulatory interactions are associated with non-small cell lung cancer survival.

Immunoregulatory interactions play a pivotal role in immune surveillance, recognition, and killing, particularly its internal pathway, likely playing an important role in immune escape. By using two genotyping datasets, one from the Prostate, Lung, Colorectal and Ovarian (PLCO) Cancer screening trial (n = 1,185) as the discovery, and the other from Harvard Lung Cancer Susceptibility (HLCS) study (n = 984) as the validation, we evaluated associations between 4,713 genetic variants (338 genotyped and 4,375 imputed) in 60 genes involved in immunoregulatory interactions and survival of non-small cell lung cancer (NSCLC). We found that 115 SNPs were significantly associated with NSCLC overall survival in the discovery, of which four remained significant after validation by the HLCS dataset after multiple test correction by Bayesian false discovery probability. Final combined analysis identified two independent SNPs (KIR3DL2 rs4487030 A>G and PVR rs35385129 C>A) that predicted NSCLC survival with a combined hazards ratio of 0.84 (95% confidence interval = 0.76-0.93, P = 0.001) and 0.84 (95% confidence interval = 0.73-0.97, P = 0.021), respectively. Besides, expression quantitative trait loci analyses showed that these two survival-associated SNPs of KRI3DL2 and PVR were significantly associated with their mRNA expression levels in both normal lung tissues and whole blood cells. Additional analyses suggested an oncogenic role for KRI3DL2 and a suppressor role for PVR on the survival. Once further validated, genetic variants of KIR3DL2 and PVR may be potential prognostic markers for NSCLC survival.
Authors
Wu, Y; Yang, S; Liu, H; Luo, S; Stinchcombe, TE; Glass, C; Su, L; Shen, S; Christiani, DC; Wang, Q; Wei, Q
MLA Citation
URI
https://scholars.duke.edu/individual/pub1450626
PMID
32642289
Source
pubmed
Published In
American Journal of Cancer Research
Volume
10
Published Date
Start Page
1770
End Page
1784

Genetic variants in TKT and DERA in the nicotinamide adenine dinucleotide phosphate pathway predict melanoma survival.

BACKGROUND: Cutaneous melanoma (CM) is the most lethal type of skin cancers. Nicotinamide adenine dinucleotide phosphate (NADPH) plays an important role in anabolic reactions and tumorigenesis, but many genes are involved in the NADPH system. METHODS: We used 10,912 single-nucleotide polymorphisms (SNPs) (2018 genotyped and 8894 imputed) in 134 NADPH-related genes from a genome-wide association study (GWAS) of 858 patients from The University of Texas MD Anderson Cancer Center (MDACC) in a single-locus analysis to predict CM survival. We then replicated the results in another GWAS data set of 409 patients from the Nurses' Health Study (NHS) and the Health Professionals Follow-up Study (HPFS). RESULTS: There were 95 of 858 (11.1%) and 48 of 409 (11.7%) patients who died of CM, respectively. In multivariable Cox regression analyses, we identified two independent SNPs (TKT rs9864057 G > A and deoxyribose phosphate aldolase (DERA) rs12297652 A > G) to be significantly associated with CM-specific survival [hazards ratio (HR) of 1.52, 95% confidence interval (CI) = 1.18-1.96, P = 1.06 × 10-3 and 1.51 (1.19-1.91, 5.89 × 10-4)] in the meta-analysis, respectively. Furthermore, an increasing number of risk genotypes of these two SNPs was associated with a higher risk of death in the MDACC, the NHS/HPFS, and their combined data sets (Ptrend<0.001, = 0.004 and <0.001, respectively). In the expression quantitative trait loci analysis, TKT rs9864057 G > A and DERA rs12297652 A > G were also significantly associated with higher mRNA expression levels in sun-exposed lower-leg skin (P = 0.043 and 0.006, respectively). CONCLUSIONS: These results suggest that these two potentially functional SNPs may be valuable prognostic biomarkers for CM survival, but larger studies are needed to validate these findings.
Authors
Gu, N; Dai, W; Liu, H; Ge, J; Luo, S; Cho, E; Amos, CI; Lee, JE; Li, X; Nan, H; Yuan, H; Wei, Q
MLA Citation
Gu, Ning, et al. “Genetic variants in TKT and DERA in the nicotinamide adenine dinucleotide phosphate pathway predict melanoma survival.Eur J Cancer, vol. 136, Sept. 2020, pp. 84–94. Pubmed, doi:10.1016/j.ejca.2020.04.049.
URI
https://scholars.duke.edu/individual/pub1450777
PMID
32659474
Source
pubmed
Published In
Eur J Cancer
Volume
136
Published Date
Start Page
84
End Page
94
DOI
10.1016/j.ejca.2020.04.049

Novel Variants of ELP2 and PIAS1 in the Interferon Gamma Signaling Pathway Are Associated with Non-Small Cell Lung Cancer Survival.

BACKGROUND: IFNγ is a pleiotropic cytokine that plays critical immunomodulatory roles in intercellular communication in innate and adaptive immune responses. Despite recognition of IFNγ signaling effects on host defense against viral infection and its utility in immunotherapy and tumor progression, the roles of genetic variants of the IFNγ signaling pathway genes in survival of patients with cancer remain unknown. METHODS: We used a discovery genotyping dataset from the Prostate, Lung, Colorectal and Ovarian Cancer Screening Trial (n = 1,185) and a replication genotyping dataset from the Harvard Lung Cancer Susceptibility Study (n = 984) to evaluate associations between 14,553 genetic variants in 150 IFNγ pathway genes and survival of non-small cell lung cancer (NSCLC). RESULTS: The combined analysis identified two independent potentially functional SNPs, ELP2 rs7242481G>A and PIAS1 rs1049493T>C, to be significantly associated with NSCLC survival, with a combined HR of 0.85 (95% confidence interval, 0.78-0.92; P < 0.0001) and 0.87 (0.81-0.93; P < 0.0001), respectively. Expression quantitative trait loci analyses showed that the survival-associated ELP2 rs7242481A allele was significantly associated with increased mRNA expression levels of elongator acetyltransferase complex subunit 2 (ELP2) in 373 lymphoblastoid cell lines and 369 whole-blood samples. The PIAS1 rs1049493C allele was significantly associated with decreased mRNA expression levels of PIAS1 in 383 normal lung tissues and 369 whole-blood samples. CONCLUSIONS: Genetic variants of IFNγ signaling genes are potential prognostic markers for NSCLC survival, likely through modulating the expression of key genes involved in host immune response. IMPACT: Once validated, these variants could be useful predictors of NSCLC survival.
Authors
Zhao, YC; Tang, D; Yang, S; Liu, H; Luo, S; Stinchcombe, TE; Glass, C; Su, L; Shen, S; Christiani, DC; Wei, Q
MLA Citation
Zhao, Yu Chen, et al. “Novel Variants of ELP2 and PIAS1 in the Interferon Gamma Signaling Pathway Are Associated with Non-Small Cell Lung Cancer Survival.Cancer Epidemiol Biomarkers Prev, vol. 29, no. 8, Aug. 2020, pp. 1679–88. Pubmed, doi:10.1158/1055-9965.EPI-19-1450.
URI
https://scholars.duke.edu/individual/pub1446736
PMID
32493705
Source
pubmed
Published In
Cancer Epidemiol Biomarkers Prev
Volume
29
Published Date
Start Page
1679
End Page
1688
DOI
10.1158/1055-9965.EPI-19-1450