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:

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

Potentially functional variants in nucleotide excision repair pathway genes predict platinum treatment response of Chinese ovarian cancer patients.

Acquired platinum resistance impedes successful treatment of epithelial ovarian cancer (EOC), and this resistance may be associated with inherited DNA damage-repair response. In the present study, we performed a two-phase analysis to assess associations between 8191 single-nucleotide polymorphisms (SNPs) within 127 genes of nucleotide excision repair (NER) pathway from a genome-wide association study (GWAS) dataset and platinum treatment response in 803 Han Chinese EOC patients. As a result, we identified that platinum-based chemotherapeutic response was associated with two potential functional variants MNAT1 rs2284704 T>C (TC+CC vs. TT, adjusted odds ratio (OR)=0.89, 95% confidence interval (CI)=0.83-0.95 and P=0.0005) and HUS1B rs61748571 A>G (AG+GG vs. AA, OR=1.10, 95% CI=1.03-1.18 and P=0.005). Compared to the prediction model for clinical factors only, models incorporating HUS1B rs61748571 (AUC 0.65 vs. 0.67, P=0.026) and the number of unfavorable genotypes (AUC 0.65 vs. 0.67, P=0.040) demonstrated a significant increase in the area under the curve (AUC). Further expression quantitative trait loci (eQTL) analysis suggested that MNAT1 rs2284704 T>C significantly influenced mRNA expression levels of MNAT1 (P=0.003). These results indicated that MNAT1 rs2284704 T>C and HUS1B rs61748571 A>G may serve as potential biomarkers for predicting platinum-treatment response of Chinese EOC patients, once validated by further functional studies.
Authors
Li, H; Dai, H; Shi, T; Cheng, X; Sun, M; Chen, K; Wang, M; Wei, Q
MLA Citation
URI
https://scholars.duke.edu/individual/pub1452204
PMID
32663249
Source
pubmed
Published In
Carcinogenesis
Published Date
DOI
10.1093/carcin/bgaa075

Genetic variants in the human leukocyte antigen region and survival of Chinese patients with non-small-cell lung carcinoma.

Human leukocyte antigen (HLA) is highly polymorphic, driving antigen presentation, complement cascade, and leukocyte maturation against cancer cells. Therefore, we extracted genotyping data in the HLA region from an ongoing Chinese genome-wide association study of non-small cell lung cancer (NSCLC). Using deep sequencing data of 10,689 healthy Han Chinese, we imputed the HLA region, followed by a two-stage survival analysis of 1,531 NSCLC patients. In the discovery stage of 758 patients, we identified 301 out of 15,138 single nucleotide polymorphisms (SNPs) to be independently associated with overall survival (OS) [P<0.05 and Bayesian false-discovery probability (BFDP)<0.8]. In further validation of another 773 patients, we confirmed chromosome 6p21, rs241424 (located at intron 3 of TAP2 gene) and rs6457642 as two independent survival predictors. In the combined analysis of 1,531 NSCLC patients, rs241424 G>A and rs6457642 C>T were associated with a hazards ratio of 1.26 [95% confidence interval (CI)=1.14-1.40 and P=4.04×10-6] and 0.76 (95% CI=0.66-0.87 and P=1.16×10-4), respectively. The analysis of publically available ChIP-sequencing and Hi-C data found that the rs241424 locus was involved in potential cis-regulatory element by long-range interaction with the HLA-DQA1 promoter. Additional expression quantitative trait loci analysis showed that the rs241424 G>A change decreased HLA-DQA1 mRNA expression. Furthermore, expression levels of HLA-DQA1 were lower in lung cancer tissues than in adjacent normal tissues, and the lower expression was associated with a worse prognosis for patients with lung adenocarcinoma. Collectively, HLA genetic variants may modulate OS of NSCLC patients, possibly via a mechanism of long-range promoter interaction regulating HLA-DQA1 expression.
Authors
Cheng, L; Liu, Q; Wang, M; Gu, Y; Wang, J; Wei, Q; Zhang, R
MLA Citation
Cheng, Lei, et al. “Genetic variants in the human leukocyte antigen region and survival of Chinese patients with non-small-cell lung carcinoma.Carcinogenesis, July 2020. Pubmed, doi:10.1093/carcin/bgaa066.
URI
https://scholars.duke.edu/individual/pub1450726
PMID
32614429
Source
pubmed
Published In
Carcinogenesis
Published Date
DOI
10.1093/carcin/bgaa066

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