Yuanqing Ye

University of Texas MD Anderson Cancer Center, Houston, Texas, United States

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Publications (102)881.88 Total impact

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    ABSTRACT: We aimed to identify new serum biomarkers of esophageal adenocarcinoma (EAC). We performed metabolomic analyses of serum samples from 30 patients with histologically confirmed EAC (cases) from The University of Texas MD Anderson Cancer Center and 30 patients without EAC (controls). We identified metabolites whose levels differed significantly between cases and controls and validated those with the greatest difference in an analysis of 321 EAC cases and 331 controls. We generated a metabolite risk score (MRS) for the metabolites. The levels of 64 metabolites differed significantly between EAC cases and controls. The metabolites with the greatest difference were: amino acid L-proline (LP), ketone body 3-hydroxybutyrate (BHBA), and carbohydrate D-mannose (DM) different; these differences were confirmed in the validation set. Cases had lower mean levels of LP that controls (22.78±6.79 ug/ml vs 28.24±8.64 ug/ml; P<.001) and higher levels of BHBA (18.06±17.84 ug/ml vs 7.73±9.92 ug/ml; P<.001) and DM (9.87±4.28 ug/ml vs 6.28 ±3.61 ug/ml; P<.001). Levels of DM were significant higher in patients with late-stage EAC than early-stage EAC (10.61±4.79 ug/ml vs 8.97±3.36 ug/mL; P=.005). Higher levels of LP were associated with a significant decreased in risk of EAC (odds ratio [OR] =0.26; 95% confidence interval [CI], 0.18-0.38). A significant increase in risk of EAC was associated with higher levels of BHBA (OR=4.05; 95% CI, 2.84-5.78) and DM (OR=7.04; 95% CI, 4.79-10.34). Levels of all 3 metabolites associated with EAC risk in quartile analyses; the level of risk conferred by the metabolites increased with smoking status and body mass index. Individuals with a high MRS had a significant (7.76-fold) increase in risk of EAC vs those with low a MRS. Smokers with a high MRS had the greatest risk of EAC (OR=20.26; 95% CI,11.19-36.68), compared with never smokers with a low MRS. Based On A Case Vs Control Metabolic Profile analysis, levels of LP, BHBA and DM are associated with risk of EAC. These markers might be used as prognostic factors for patients with EAC. Copyright © 2015 AGA Institute. Published by Elsevier Inc. All rights reserved.
    Clinical gastroenterology and hepatology: the official clinical practice journal of the American Gastroenterological Association 05/2015; DOI:10.1016/j.cgh.2015.05.023 · 6.53 Impact Factor
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    ABSTRACT: Mitochondrial DNA (mtDNA) content has been shown to be associated with cancer susceptibility. We identified 926 bladder cancer patients and compared these to 926 healthy-controls frequency matched on age, gender, and ethnicity. Patients diagnosed with bladder cancer had significantly decreased mtDNA content when compared to control subjects (median: 0.98 vs. 1.04, p<0.001). Low mtDNA content (ie, less than the median in control subjects) was associated with a statistically significant increased risk of bladder cancer, when compared with high mtDNA content (Odds Ratio (OR) = 1.37, 95% CI = 1.13 to 1.66, p<0.001). In a trend analysis, a statistically significant dose-response relationship was detected between lower mtDNA content and increasing risk of bladder cancer (P for trend <0.001). When stratified by host characteristics, advanced age (>65 years), male/female sex and positive smoking history were all significantly associated with low mtDNA content and increased risk of bladder cancer. We identified two unique mtDNA polymorphisms significantly associated with risk of bladder cancer: mitot10464c (OR=1.39 95%CI: 1.00-1.93, p=0.048) and mitoa4918g (OR=1.40, 95% CI: 1.00-1.95, p=0.049). Analysis of the joint effect of low mtDNA content and unfavorable mtDNA polymorphisms revealed a 2.5 fold increased risk of bladder cancer (OR=2.50, 95% CI: 1.60-3.94, p<0.001). Significant interaction was observed between mitoa4918g and mtDNA content (p for interaction = 0.028). Low mtDNA content was associated with increased risk of bladder cancer and we identified new susceptibility mtDNA alleles associated with increased risk that require further investigation into the biological underpinnings of bladder carcinogenesis. Copyright © 2015, American Association for Cancer Research.
    Cancer Prevention Research 04/2015; 193(4). DOI:10.1158/1940-6207.CAPR-14-0414 · 5.27 Impact Factor
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    ABSTRACT: Glutathione (GSH) is an important molecule involved in cell detoxification and antioxidation and may affect cancer development or outcome. We hypothesized that genetic variation in the GSH pathway might influence the clinical outcome of patients who have non-muscle invasive bladder cancer (NMIBC). A total of 114 single nucleotide polymorphisms (SNPs) in 21 GSH pathway genes were genotyped in 414 NMIBC patients treated with transurethral resection alone (TUR) and both TUR and intravesical bacillus Calmette-Guérin instillation (BCG) therapy. The effect of each SNP on time to recurrence was estimated using the multivariate Cox proportional hazards model. Cumulative effect and survival tree analyses were performed to determine the joint effects of unfavorable genotypes and gene-gene interactions on bladder cancer prognosis. Seven SNPs showed significant associations with cancer recurrence in the TUR group and 15 SNPs showed significant associations with recurrence in the BCG group. The most significant SNP in the TUR group was rs3746162 in GPX4, whose variant genotype conferred a 5.4-fold increased risk of recurrence compared with wild-type (hazard ratio [HR] = 5.43, 95 % confidence interval [CI] = 2.19-13.46), whereas the most significant SNP in the BCG group was rs7265992 in GSS (HR 3.43, 95 % CI 1.56-7.56). The risk of recurrence increased with the number of unfavorable genotypes in both groups. Within treatment group, stratified analyses by tumor grade also indicated predictive variants. Genetic variants in GSH pathway may influence cancer recurrence in NMIBC patients receiving curative treatment.
    Annals of Surgical Oncology 04/2015; DOI:10.1245/s10434-015-4431-5 · 3.94 Impact Factor
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    ABSTRACT: Hispanic Americans comprise the largest and fastest-growing ethnic minority in the USA. In Houston, Texas, 44% of the population is of Hispanic descent, with the majority being Mexican Americans (78%). This population is under-represented in health-related research despite their high prevalence of obesity and diabetes, which may predispose them to cancer and other chronic conditions. Recognizing the need for a greater research effort into the health risks of Hispanic Americans, the population-based Mexican American (Mano a Mano) Cohort study was launched in 2001. This is an open cohort with enrolment ongoing to 2019, and as of 30 June 2014, 23 606 adult participants from over 16 600 households were enrolled. Bilingual interviewers elicit information in person on demographics, acculturation, lifestyle, occupation, medical history, family cancer history, self-reported and measured height and weight, and other exposures. Urine, blood and saliva samples have been collected at baseline from 43%, 56% and 63% of participants, respectively. DNA samples are available for about 90% of participants. Incident cancers and other chronic diseases are ascertained through annual telephone re-contact and linkage to the Texas Cancer Registry and/or medical records. Molecular data such as genetic ancestry markers, blood telomere length and HbA1c, a marker of impaired glucose tolerance, are available for a substantial proportion of the participants. Data access is provided on request [manoamano@mdanderson.org]. For further information please visit [www.mano-mano.us]. © The Author 2015; all rights reserved. Published by Oxford University Press on behalf of the International Epidemiological Association.
    International Journal of Epidemiology 03/2015; DOI:10.1093/ije/dyv016 · 9.20 Impact Factor
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    ABSTRACT: We conducted multilevel analyses to identify potential susceptibility loci for renal cell carcinoma (RCC), which may be overlooked in traditional genome-wide association studies (GWAS). A gene set enrichment analysis was performed utilizing a GWAS dataset comprised of 894 RCC cases and 1,516 controls using GenGen, SNP ratio test, and ALIGATOR. The antigen processing and presentation pathway was consistently significant (P = 0.001, = 0.004, and < 0.001, respectively). Versatile gene-based association study approach was applied to the top-ranked pathway and identified the driven genes. By comparing the expression of the genes in RCC tumor and adjacent normal tissues, we observed significant overexpression of HLA genes in tumor tissues, which was also supported by public databases. We sought to validate genetic variants in antigen processing and presentation pathway in an independent GWAS dataset comprised of 1,311 RCC cases and 3,424 control subjects from the National Cancer Institute; one SNP, rs1063355, was significant in both populations (Pmeta-analysis = 9.15 × 10-4, Pheterogeneity = 0.427). Strong correlation indicated that rs1063355 was a cis-expression quantitative trait loci which associated with HLA-DQB1 expression (Spearman's rank r = -0.59, p = 5.61 × 10-6). The correlation was further validated using a public dataset. Our results highlighted the role of immune-related pathway and genes in the etiology of RCC.
    Oncotarget 02/2015; 6(6):4097-109. · 6.63 Impact Factor
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    ABSTRACT: Marginal zone lymphoma (MZL) is the third most common subtype of B-cell non-Hodgkin lymphoma. Here we perform a two-stage GWAS of 1,281 MZL cases and 7,127 controls of European ancestry and identify two independent loci near BTNL2 (rs9461741, P=3.95 × 10(-15)) and HLA-B (rs2922994, P=2.43 × 10(-9)) in the HLA region significantly associated with MZL risk. This is the first evidence that genetic variation in the major histocompatibility complex influences MZL susceptibility.
    Nature Communications 01/2015; 6:5751. DOI:10.1038/ncomms6751 · 10.74 Impact Factor
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    ABSTRACT: Liver function tests (LFTs) have been reported as independent predictors of non-liver disease-related morbidity and mortality in general population and cancer patients. In this study, we evaluated the relationship between pretreatment serum LFTs and overall survival (OS) in non-metastatic Caucasian breast cancer patients. Seven LFTs, including albumin, alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP), lactate dehydrogenase (LDH), total bilirubin, and total protein, were measured in pretreatment serum from 2,425 female Caucasian patients with newly diagnosed, histologically confirmed non-metastatic invasive breast cancer. Multivariate Cox model was used to estimate hazard ratio (HR) and 95% confidence interval (CI) for the association of individual LFTs with 5-year OS while adjusting for age, smoking status, pathological characteristics and treatment regimen. We found that serum albumin, LDH, and total bilirubin were significantly associated with 5-year OS in multivariate Cox analyses. Patients with higher albumin level exhibited 45% reduced risk of death (HR=0.55, 95% CI, 0.40-0.75) compared to those with lower albumin level. Patients with higher total bilirubin level had a nearly 40% reduction in the risk of death (HR=0.62, 95% CI, 0.45-0.85) and patients with higher LDH levels had a 1.42-fold increased risk of death (HR=1.42, 95% CI, 1.08-1.88). Furthermore, cumulative analysis showed a significant dose-response trend of significantly increasing risk of death with increasing number of unfavorable LFT levels. Our result highlighted the potential of using pretreatment serum levels of albumin, LDH and total bilirubin as prognostic factors for overall survival in patients with non-metastatic breast cancer. © The Author 2014. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oup.com.
    Carcinogenesis 12/2014; DOI:10.1093/carcin/bgu247 · 5.27 Impact Factor
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    ABSTRACT: BACKGROUND In the current study we present a validated miRNA signature to predict pathologic complete response (pCR) to neoadjuvant chemoradiation in esophageal adenocarcinoma.METHODS Three patient cohorts (discovery, n = 10; model, n = 43; and validation, n = 65) with locally advanced esophageal adenocarcinoma were analyzed. In the discovery cohort 754 miRNAs were examined in pretreatment tumor biopsy specimens using a TaqMan array. Of these, the 44 most significantly altered between tumors with pCR and non-pCR were examined in an additional 43 tumors using a Fluidigm 48.48 array. The 4 miRNAs (mir-505*, mir-99b, mir-451, and mir-145*) significantly predicting pCR in both cohorts were examined in an additional validation cohort (n = 65) using an Illumina array. These 4 miRNAs were used to generate an miRNA expression profile (MEP) score.RESULTSThe 4 miRNAs profiled are highly significantly associated with pCR in the model cohort (Ptrend = .008), the validation cohort (Ptrend = .025), and the combined cohort (Ptrend = 4.6 × 10−4). The receiver-operator characteristic areas under the curves (AUCs) for the MEP score were 0.78 for the model cohort, 0.71 for the validation cohort, and 0.72 for the combined cohort. When combined with clinical variables, the MEP score AUCs increased to 0.89, 0.77, and 0.81, respectively Estimates from logistic regression based on the MEP were determined and used to generate a probability of pCR plot, which identifies a group of patients with very high (≥80%) and very low (≤10%) probability of pCR.CONCLUSIONS The MEP score provides a validated means of predicting pCR to neoadjuvant chemoradiotherapy in esophageal adenocarcinoma that is robust across several analysis platforms. Cancer 2014. © 2014 The Authors. Cancer published by Wiley Periodicals, Inc. on behalf of American Cancer Society.
    Cancer 12/2014; 120(23). DOI:10.1002/cncr.28911 · 4.90 Impact Factor
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    ABSTRACT: Background: Depression is associated with an increased risk of mortality in cancer patients; it has been hypothesized that depression-associated alterations in cell aging mechanisms in particular, the telomere/telomerase maintenance system, may underlie this increased risk. We evaluated the association of depressive symptoms and telomere length to mortality and recurrence/progression in 464 bladder cancer patients. Methods: We used the CES-D and SCID to assess current depressive symptoms and lifetime MDD, respectively, and telomere length was assessed from peripheral blood lymphocytes. Multivariate Cox regression was used to assess the association of depression, and telomere length to outcomes and the joint effect of both. Kaplan-Meier plots and log rank tests were used to compare survival time of subgroups by depression variables and telomere length. Results: Patients with depressive symptoms (CES-D ≥16) had a 1.83-fold (95%CI= 1.08 to 3.08, P=0.024) increased risk of mortality compared to patients without depressive symptoms (CES-D < 16) and shorter disease-free survival time (P=0.004). Patients with both depressive symptoms and lifetime history of MDD were at 4.88-fold (95%CI=1.40 to 16.99; P=0.013) increased risk compared to patients with neither condition. Compared to patients without depressive symptoms and long telomere length, patients with depressive symptoms and short telomeres exhibited a 4-fold increased risk of mortality (HR=3.96, 95% CI=1.86 to 8.41, P=0.0003) and significantly shorter disease-free survival time (P<0.001). Conclusion: Short telomere length and depressive symptoms are associated with bladder cancer mortality individually and jointly. Impact: Further investigation of interventions that impact depression and telomere length may be warranted in cancer patients. Copyright © 2014, American Association for Cancer Research.
    Cancer Epidemiology Biomarkers & Prevention 11/2014; 24(2). DOI:10.1158/1055-9965.EPI-14-0992 · 4.32 Impact Factor
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    ABSTRACT: We investigated genetic variation in CYP2A6 in relation to lung cancer risk among African American smokers, a high-risk population. Previously, we found that CYP2A6, a nicotine/nitrosamine metabolism gene, was associated with lung cancer risk in European Americans, but smoking habits, lung cancer risk, and CYP2A6 gene variants differ significantly between European and African ancestry populations. Herein, African American ever-smokers, drawn from two independent lung cancer case control studies, were genotyped for reduced activity CYP2A6 alleles and grouped by predicted metabolic activity. Lung cancer risk in the Southern Community Cohort Study (n = 494) was lower among CYP2A6 reduced versus normal metabolizers, as estimated by multivariate conditional logistic regression (OR = 0.44; 95% confidence interval [CI] = 0.26 to 0.73) and by unconditional logistic regression (OR = 0.62; 95% confidence interval [CI] = 0.41 to 0.94). The association was replicated in an independent study from MD Anderson Cancer Center (n = 407) (OR = 0.64; 95% CI = 0.42 to 0.98), and pooling the studies yielded an odds ratio of 0.64 (95% CI = 0.48 to 0.86). Exploratory analyses revealed a significant interaction between CYP2A6 genotype and sex on the risk for lung cancer (Southern Community Cohort Study: P=.03; MD Anderson: P=.03; Pooled Studies: P=.003) with a CYP2A6 effect in men only. These findings support a contribution of genetic variation in CYP2A6 to lung cancer risk among African American smokers, particularly men, whereby CYP2A6 genotypes associated with reduced metabolic activity confer a lower risk of developing lung cancer. © The Author 2014. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oup.com.
    Carcinogenesis 11/2014; 36(1). DOI:10.1093/carcin/bgu235 · 5.27 Impact Factor
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    ABSTRACT: Purpose: We aimed to identify serum metabolites as potential valuable biomarkers for lung cancer and to improve risk stratification in smokers. Experimental Design: We performed global metabolomic profiling followed by targeted validation of individual metabolites in a case-control design of 386 lung cancer cases and 193 matched controls. We then validated the most significant metabolite bilirubin as a risk marker for lung cancer incidence and mortality in a large prospective cohort comprised of 425,660 participants. Results: Through global metabolomic profiling and following targeted validation, bilirubin levels consistently showed a statistically significant difference among healthy controls and lung cancer cases. In the prospective cohort, the inverse association was only seen in male smokers, regardless of smoking pack-years and intensity. Compared with male smokers in the highest bilirubin group (>1 mg/dL), those in the lowest bilirubin group (<0.75 mg/dL) had 55% and 66% increase in risks of lung cancer incidence and mortality, respectively. For every 0.1 mg/dL decrease of bilirubin, the risks for lung cancer incidence and mortality increased by 5% and 6% in male smokers, respectively (both P < 0.001). There was a significant interaction between low serum bilirubin level and smoking on lung cancer risk (P for interaction = 0.001). Conclusions: Low levels of serum bilirubin are associated with higher risks of lung cancer incidence and mortality in male smokers and can be used to identify higher risk smokers for lung cancer.
    Clinical Cancer Research 10/2014; 21(1). DOI:10.1158/1078-0432.CCR-14-0748 · 8.19 Impact Factor
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    ABSTRACT: Cancers are composed of populations of cells with distinct molecular and phenotypic features, a phenomenon termed intratumor heterogeneity (ITH). ITH in lung cancers has not been well studied. We applied multiregion whole-exome sequencing (WES) on 11 localized lung adenocarcinomas. All tumors showed clear evidence of ITH. On average, 76% of all mutations and 20 out of 21 known cancer gene mutations were identified in all regions of individual tumors, which suggested that single-region sequencing may be adequate to identify the majority of known cancer gene mutations in localized lung adenocarcinomas. With a median follow-up of 21 months after surgery, three patients have relapsed, and all three patients had significantly larger fractions of subclonal mutations in their primary tumors than patients without relapse. These data indicate that a larger subclonal mutation fraction may be associated with increased likelihood of postsurgical relapse in patients with localized lung adenocarcinomas.
    Science 10/2014; 346(6206):256-9. DOI:10.1126/science.1256930 · 31.48 Impact Factor
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    ABSTRACT: We hypothesized that telomere length in peripheral blood would have significant predictive value for risk of recurrence after curative resection in non-small cell lung cancer (NSCLC).
    Journal of thoracic oncology: official publication of the International Association for the Study of Lung Cancer 10/2014; DOI:10.1097/JTO.0000000000000398 · 5.80 Impact Factor
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    ABSTRACT: Genome-wide association studies (GWASs) of follicular lymphoma (FL) have previously identified human leukocyte antigen (HLA) gene variants. To identify additional FL susceptibility loci, we conducted a large-scale two-stage GWAS in 4,523 case subjects and 13,344 control subjects of European ancestry. Five non-HLA loci were associated with FL risk: 11q23.3 (rs4938573, p = 5.79 × 10(-20)) near CXCR5; 11q24.3 (rs4937362, p = 6.76 × 10(-11)) near ETS1; 3q28 (rs6444305, p = 1.10 × 10(-10)) in LPP; 18q21.33 (rs17749561, p = 8.28 × 10(-10)) near BCL2; and 8q24.21 (rs13254990, p = 1.06 × 10(-8)) near PVT1. In an analysis of the HLA region, we identified four linked HLA-DRβ1 multiallelic amino acids at positions 11, 13, 28, and 30 that were associated with FL risk (pomnibus = 4.20 × 10(-67) to 2.67 × 10(-70)). Additional independent signals included rs17203612 in HLA class II (odds ratio [ORper-allele] = 1.44; p = 4.59 × 10(-16)) and rs3130437 in HLA class I (ORper-allele = 1.23; p = 8.23 × 10(-9)). Our findings further expand the number of loci associated with FL and provide evidence that multiple common variants outside the HLA region make a significant contribution to FL risk.
    The American Journal of Human Genetics 10/2014; 95(4):462-71. DOI:10.1016/j.ajhg.2014.09.004 · 10.99 Impact Factor
  • Cancer Research 10/2014; 74(19 Supplement):5077-5077. DOI:10.1158/1538-7445.AM2014-5077 · 9.28 Impact Factor
  • Cancer Research 10/2014; 74(19 Supplement):5146-5146. DOI:10.1158/1538-7445.AM2014-5146 · 9.28 Impact Factor
  • Cancer Research 10/2014; 74(19 Supplement):5038-5038. DOI:10.1158/1538-7445.AM2014-5038 · 9.28 Impact Factor
  • Cancer Research 10/2014; 74(19 Supplement):296-296. DOI:10.1158/1538-7445.AM2014-296 · 9.28 Impact Factor
  • Cancer Research 10/2014; 74(19 Supplement):2915-2915. DOI:10.1158/1538-7445.AM2014-2915 · 9.28 Impact Factor
  • Cancer Research 10/2014; 74(19 Supplement):4149-4149. DOI:10.1158/1538-7445.AM2014-4149 · 9.28 Impact Factor

Publication Stats

1k Citations
881.88 Total Impact Points


  • 2008–2015
    • University of Texas MD Anderson Cancer Center
      • • Department of Epidemiology
      • • Division of Cancer Prevention & Population Sciences
      Houston, Texas, United States
  • 2008–2013
    • University of Houston
      Houston, Texas, United States
  • 2012
    • University of Texas Southwestern Medical Center
      • Hamon Center for Therapeutic Oncology Research
      Dallas, Texas, United States