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:

Association of pretreatment body mass index with risk of head and neck cancer: a large single-center study.

Smoking and alcohol exposure continue to be the dominant risk factors for the development of head and neck squamous cell carcinoma (SCCHN) worldwide. Moreover, human papillomavirus (HPV) is associated with SCCHN, particularly SCC of the oropharynx (SCCOP). Body mass index (BMI) has been reported as a possible risk factor for SCCHN, yet the data available so far about the relationship between BMI and SCCHN risk have been mixed. We sought to clarify this relationship. BMI and demographic, clinical, and epidemiological information at diagnosis were collected from 2310 SCCHN cases and 1915 controls (who were cancer-free) from October 2001 through May 2013. The odds ratios (ORs) and 95 percent confidence intervals (95% CI) were determined using the logistic regression process. Multivariable models were used to evaluate the strength of the relation between BMI and SCCHN risk. At diagnosis, 64 (2.8%) of the cases were underweight (BMI <18.5 kg/m2), 661 (28.6%) were normal weight (BMI 18.5<25 kg/m2), 833 (36.1%) were overweight (BMI 25<30 kg/m2), and 752 (32.6%) were obese (BMI ≥30 kg/m2). Comparatively, the ORs (95% CIs) for SCCHN associated with being underweight, overweight, and obese were 2.6 (1.54.7), 0.7 (0.6-0.8), and 0.8 (0.7-0.9), respectively, after adjusting for age, gender, race/ethnicity, smoking, and alcohol consumption. On analysis stratified by tumor sites, the risk of SCCOP among patients seropositive for HPVE6 and/or HPVE7 was higher among the overweight (OR, 5.4, 95% CI, 1.3-23.1) and obese patients (OR, 2.4, 95% CI, 1.1-7.6) compared to the normal weight patients. These findings suggest that pretreatment BMI could be a major risk factor for SCCHN, and the association between BMI and HPV may increase the risk of SCCOP.
Authors
Khanna, A; Sturgis, EM; Dahlstrom, KR; Xu, L; Wei, Q; Li, G; Gross, ND
MLA Citation
Khanna, Anshu, et al. “Association of pretreatment body mass index with risk of head and neck cancer: a large single-center study.Am J Cancer Res, vol. 11, no. 5, 2021, pp. 2343–50.
URI
https://scholars.duke.edu/individual/pub1484764
PMID
34094690
Source
pubmed
Published In
American Journal of Cancer Research
Volume
11
Published Date
Start Page
2343
End Page
2350

FUNCTIONAL POLYMORPHISMS IN CANCER STEM CELL MARKER GENE CD133 PREDICT LOCAL RECURRENCE AND DISTANT METASTASIS IN NON-SMALL CELL LUNG CANCER PATIENTS TREATED WITH DEFINITIVE RADIOTHERAPY

Authors
Wang, Q; Li, P; Liu, H; Xiong, H; Qian, J; Gomez, D; Liu, Z; Wang, L-E; Liao, Z; Wei, Q
URI
https://scholars.duke.edu/individual/pub1498218
Source
wos-lite
Published In
Asia Pacific Journal of Clinical Oncology
Volume
10
Published Date
Start Page
194
End Page
194

Genetic variants of EML1 and HIST1H4E in myeloid cell-related pathway genes independently predict cutaneous melanoma-specific survival.

Both in vivo and in vitro evidence has supported a key role of myeloid cells in immune suppression in melanoma and in promoting melanocytic metastases. Some single-nucleotide polymorphisms (SNPs) have been shown to predict cutaneous melanoma-specific survival (CMSS), but the association between genetic variation in myeloid cell-related genes and cutaneous melanoma (CM) patient survival remains unknown. METHODS: we investigated associations between SNPs in myeloid cell-related pathway genes and CMSS in a discovery dataset of 850 CM patients and replicated the findings in another dataset of 409 CM patients. RESULTS: we identified two SNPs (EML1 rs10151787 A>G and HIST1H4E rs2069018 T>C) as independent prognostic factors for CMSS, with adjusted allelic hazards ratios of 1.56 (95% confidence interval =1.19-2.05, P=0.001) and 1.66 (1.22-2.26, P=0.001), respectively; so were their combined unfavorable alleles in a dose-response manner in both discovery and replication datasets (P trend<0.001 and 0.002, respectively). Additional functional analysis revealed that both EML1 rs10151787 G and HIST1H4E rs2069018 C alleles were associated with elevated mRNA expression levels in normal tissues. CONCLUSIONS: Our findings suggest that EML1 rs10151787 A>G and HIST1H4E rs2069018 T>C are independent prognostic biomarkers for CMSS.
Authors
He, Y; Liu, H; Luo, S; Amos, CI; Lee, JE; Yang, K; Qureshi, AA; Han, J; Wei, Q
MLA Citation
URI
https://scholars.duke.edu/individual/pub1488885
PMID
34249459
Source
pubmed
Published In
American Journal of Cancer Research
Volume
11
Published Date
Start Page
3252
End Page
3262

Genetic Variants of CLPP and M1AP Are Associated With Risk of Non-Small Cell Lung Cancer.

Background: Single nucleotide polymorphisms (SNPs) are often associated with distinct phenotypes in cancer. The present study investigated associations of cancer risk and outcomes with SNPs discovered by whole exome sequencing of normal lung tissue DNA of 15 non-small cell lung cancer (NSCLC) patients, 10 early stage and 5 advanced stage. Methods: DNA extracted from normal lung tissue of the 15 NSCLC patients was subjected to whole genome amplification and sequencing and analyzed for the occurrence of SNPs. The association of SNPs with the risk of lung cancer and survival was surveyed using the OncoArray study dataset of 85,716 patients (29,266 cases and 56,450 cancer-free controls) and the Prostate, Lung, Colorectal and Ovarian study subset of 1,175 lung cancer patients. Results: We identified 4 SNPs exclusive to the 5 patients with advanced stage NSCLC: rs10420388 and rs10418574 in the CLPP gene, and rs11126435 and rs2021725 in the M1AP gene. The variant alleles G of SNP rs10420388 and A of SNP rs10418574 in the CLPP gene were associated with increased risk of squamous cell carcinoma (OR = 1.07 and 1.07; P = 0.013 and 0.016, respectively). The variant allele T of SNP rs11126435 in the M1AP gene was associated with decreased risk of adenocarcinoma (OR = 0.95; P = 0.027). There was no significant association of these SNPs with the overall survival of lung cancer patients (P > 0.05). Conclusions: SNPs identified in the CLPP and M1AP genes may be useful in risk prediction models for lung cancer. The previously established association of the CLPP gene with cancer progression lends relevance to our findings.
Authors
Li, X; Zou, Y; Li, T; Wong, TKF; Bushey, RT; Campa, MJ; Gottlin, EB; Liu, H; Wei, Q; Rodrigo, A; Patz, EF
MLA Citation
Li, Xianghan, et al. “Genetic Variants of CLPP and M1AP Are Associated With Risk of Non-Small Cell Lung Cancer.Front Oncol, vol. 11, 2021, p. 709829. Pubmed, doi:10.3389/fonc.2021.709829.
URI
https://scholars.duke.edu/individual/pub1498093
PMID
34604049
Source
pubmed
Published In
Frontiers in Oncology
Volume
11
Published Date
Start Page
709829
DOI
10.3389/fonc.2021.709829

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