Yan Gong
· Associate ProfessorVerifiedUniversity of Florida · Pharmacotherapy and Translational Research
Active 2000–2025
About
Yan Gong, Ph.D., is an Associate Professor in the Department of Pharmacotherapy and Translational Research at the University of Florida (UF) College of Pharmacy and the UF Center for Pharmacogenomics and Precision Medicine. She received her Ph.D. in Pharmaceutics in 2004 from the UF College of Pharmacy and a Master’s Degree in Statistics in 2003 from the UF Department of Statistics. Prior to joining the UF faculty in 2005, she completed a one-year post-doctoral Fellowship in Cardiovascular Pharmacogenomics at the UF Center for Pharmacogenomics. Dr. Gong's research focuses on the pharmacogenomics of efficacy and adverse responses of antihypertensive medications, as well as serious adverse drug events such as medication-related osteonecrosis of the jaw (MRONJ) and cardiotoxicities related to cancer therapies (Cardio-Oncology). She has authored over 170 peer-reviewed publications. In addition to her research activities, Dr. Gong is involved in teaching multiple graduate and professional courses at UF College of Pharmacy and College of Medicine. She is currently the course co-coordinator for Pharmacogenomic and Genomic Data Analysis (PHA6449), a required graduate course for her department.
Research topics
- Medicine
- Internal medicine
- Cardiology
- Biology
- Genetics
- Immunology
- Cancer research
- Bioinformatics
- Biochemistry
Selected publications
International Journal of Molecular Sciences · 2025-11-20
articleOpen accessSenior authorCorrespondingMedication-related osteonecrosis of the jaw (MRONJ) is a severe adverse effect of antiresorptive agents, including bisphosphonates (BPs) and denosumab (DMB). We conducted a case–control epigenome-wide association study (EWAS) of 24 cancer patients treated with BPs or BPs + DMB using the Infinium® MethylationEPIC v2.0 to explore epigenetic differences associated with MRONJ. Differentially methylated positions (DMPs) and regions (DMRs) were assessed across three analyses: MRONJ vs. controls (main), BPs-MRONJ vs. BPs-controls, and BPs/DMB-MRONJ vs. BPs/DMB-controls. Eight plasma bone biomarkers were quantified by Luminex and correlated with top methylation sites. We identified 10 DMPs and 4 DMRs at suggestive significance (p < 1 × 10−5). cg1913766 in the NOP56 promoter was hypomethylated in the main analysis (p = 2.19 × 10−7) and in BPs-MRONJ (p = 4.80 × 10−6), correlating with osteocalcin (p = 0.02 and 0.03, respectively). TNXB cg21289669 was hypermethylated in the main analyses (p = 6.31 × 10−6), and TNXB locus formed a DMR (p = 3.30 × 10−10) in the main and BPs-MRONJ analyses (p = 2.76 × 10−7). cg11392877 in PDE8A was hypomethylated in BPs/DMB-MRONJ (p = 5.35 × 10−7). TRIM15 was a significant DMR in BPs-MRONJ and the main analysis (p = 3.30 × 10−10). TRIM15, TNXB, and PDE8A regulate collagen I, while NOP56 supports ribosome biogenesis, potentially contributing to MRONJ. Given the small sample size, these findings are preliminary and validation in larger studies is warranted.
Cancers · 2025-08-30 · 1 citations
articleOpen accessBackground: This study evaluated the impact of diabetes mellitus (DM) and its treatments on cardiovascular outcomes in prostate cancer (PC) patients aged 66 years and older, with or without androgen deprivation therapy (ADT) exposure. Methods: Using the SEER-Medicare database (2009–2017), two cohorts were created: Cohort 1 included all PC patients enrolled in Medicare Parts A and B; Cohort 2 was a subset of Cohort 1 receiving ADT and enrolled in Medicare Part D. Exposures were DM and DM medications. Outcomes included cardiovascular events (CVEs), cardiovascular mortality (CVm), PC-specific mortality (PCsm), and all-cause mortality, analyzed using multivariable Fine-Gray and Cox models. Results: Cohort 1 included 150,647 PC patients (32% with DM, median age 72). DM was associated with higher risk of CVE (subdistribution hazard ratio [sHR] 1.20, 95% CI 1.17–1.22), CVm (sHR 1.35, 1.28–1.43), and all-cause mortality (adjusted HR [aHR] 1.22, 1.19–1.26) (all p < 0.001). Non-Hispanic Blacks (NHBs) and patients from lower socioeconomic (SES) and education areas experienced comparable or worse outcomes. In Cohort 2 (n = 14,938), DM patients on non-metformin therapies had higher all-cause mortality (aHR 1.33, 1.11–1.25; p = 0.002) than those on metformin, particularly in NHB and low education groups. Sensitivity analyses with follow-up limited to two years showed consistent results as overall. Conclusions: Diabetic PC patients, especially NHB, lower SES and lower education subgroups, were associated with worse cardiovascular and all-cause mortality outcomes. Metformin may be associated with better outcomes in these populations, warranting further research on the disparities in PC and diabetes, and cardioprotective effects of DM medications across different subpopulations.
<i>CYP2D6</i> Phenotypes and Emergency Department Visits Among Patients Receiving Opioid Treatment
JAMA Network Open · 2025-07-28 · 4 citations
articleOpen accessImportance: Cytochrome P450 2D6 (CYP2D6) bioactivates hydrocodone, tramadol, codeine, and oxycodone to active metabolites that primarily provide analgesic activity. Reduced CYP2D6 activity may be associated with poor pain control. Objective: To evaluate associations of impaired CYP2D6 activity based on genotype or CYP2D6 inhibitors, alone and together, with analgesic activity of CYP2D6-metabolized opioids among patients with pain. Design, Setting, and Participants: This retrospective national, community-based cohort study used electronic health records and genetics data from the All of Us Research Program. Participants included adults prescribed at least 1 CYP2D6-metabolized opioid for more than 7 days between January 1, 2014, and December 31, 2022, with whole-genome sequencing data available. Analysis groups were defined by CYP2D6 phenotype, which was determined based on CYP2D6 genotype or CYP2D6 inhibitor-mediated phenoconversion. Statistical analysis was performed from July 1, 2023, to January 15, 2025. Exposures: CYP2D6-metabolized opioids, with or without concomitant CYP2D6 inhibitor exposure, based on prescription records and overlap with opioids. Main Outcomes and Measures: The primary outcome was occurrence of any pain-related emergency department (ED) visits during opioid treatment, up to 60 days after opioid initiation. The association between ED visits and CYP2D6 phenotype was assessed using inverse probability treatment weighting-adjusted logistic regression. Additional analyses were conducted by drug and isolating CYP2D6 genotype and inhibitors. Results: Among 31 669 patients (mean [SD] age, 51.2 [15.4] years; 66.5% women) prescribed CYP2D6-metabolized opioids, 15 960 had reduced CYP2D6 activity, and 15 709 had normal or high CYP2D6 activity based on genotype and inhibitors. A higher percentage of patients with reduced CYP2D6 activity (hereafter referred to as phenotypic intermediate metabolizers [pIMs] or phenotypic poor metabolizers [pPMs]) had experienced pain-related ED visits compared with patients with normal or high CYP2D6 activity (phenotypic normal metabolizers [pNMs] and phenotypic ultrarapid metabolizers [pUMs]) (2.1% vs 1.8%; inverse probability-weighted odds ratio, 1.19; 95% CI, 1.06-1.33). There were no significant differences in ED visits among CYP2D6 genotypic IMs or PMs vs NMs or UMs when testing all 4 drugs together. Among genotypic NMs, ED visits were more frequent among the individuals prescribed CYP2D6 inhibitors (inverse probability-weighted odds ratio, 1.49; 95% CI, 1.32-1.68). In analyses by medication, drug interactions were important for all 4 medications, while genotype associations were significant only for hydrocodone, tramadol, and codeine. Conclusions and Relevance: In this cohort study, reduced CYP2D6 activity was associated with increased ED visits among individuals treated with CYP2D6-metabolized opioids. This finding suggests that incorporating data on CYP2D6 genotype and accounting for drug interactions in opioid prescribing may improve pain management and reduce ED visits.
Phytomedicine · 2025-04-22 · 3 citations
articleClinical Pharmacology & Therapeutics · 2025-12-08 · 1 citations
articleOpen accessHypertension is a known modifiable risk factor for Alzheimer's disease and related dementia (ADRD). However, it is unknown how variance in hypertension control, antihypertensive medications, and social determinants of health, such as social deprivation index (SDI), influence the risk of developing ADRD. Validated hypertension computable phenotype algorithms were applied to electronic health record data from the OneFlorida Data Trust (1/1/2013-12/31/2016), to identify apparent treatment-resistant hypertension (aTRH), and hypertension-control levels (well-controlled hypertension, intermediate-controlled hypertension, uncontrolled hypertension). The primary outcome was a new ADRD diagnosis using validated ICD-9/10 codes. Multiple adjusted stepwise logistic regression models were used to identify factors associated with ADRD development. ADRD cumulative hazard incidence per hypertension control levels was assessed using the Nelson-Aalen estimator and log-rank test. A total of 57,273 hypertension patients with 6401 (11%) incident ADRD cases were included in the analysis. The average age was 67 years, with 57% females and 32% identifying as Black or African American. aTRH was a significant ADRD predictor (OR: 1.327, 95% CI: 1.234-1.427), compared to other hypertension phenotypes. aTRH was also significantly associated with a higher incidence of ADRD over time (P < 0.0001). Patients prescribed thiazide diuretics (OR: 0.894, 95% CI: 0.837-0.956) and fixed-dose combination medications (OR: 0.804, 95% CI: 0.732-0.882) had a lower risk of ADRD. A linear relationship between SDI quartiles and ADRD risk was found. aTRH was significantly associated with the development of ADRD. Our study also highlights the importance of comprehensive hypertension control and socioeconomic interventions in preventing or reducing ADRD risk in hypertension patients.
Genes · 2025-02-11 · 4 citations
articleOpen accessCYP2C9 metabolizes approximately 20% of clinically administered drugs. Several single-nucleotide polymorphisms (SNPs) of CYP2C9 (e.g., *2, *3, *8, and rs12777823) are used as biomarkers to predict CYP2C9 activity. However, a large proportion of variability in CYP2C9 expression remains unexplained. BACKGROUND/OBJECTIVES: We previously identified a variable number tandem repeat (pVNTR) polymorphism in the CYP2C9 promoter. The short repeat (pVNTR-S) showed reduced transcriptional activity in reporter gene assays and was associated with decreased CYP2C9 mRNA expression. However, because pVNTR-S is in high linkage disequilibrium (LD) with CYP2C9*3 in the European population, whether pVNTR-S directly impacts CYP2C9 expression remains unclear. The objective of this study was to clarify the association between the pVNTR-S and CYP2C9 mRNA expression in human liver samples and to assess its impact on CYP2C9 expression independently of known CYP2C9 biomarkers. METHODS: Gene expression was measured by real-time qPCR. SNPs and pVNTRs were genotyped using SNapShot assays and fragment analysis, respectively. Associations between CYP2C9 and the pVNTR-S or SNPs were analyzed using multiple linear regression. RESULTS: = 247), while the known CYP2C9 biomarkers (CYP2C9*2, *3, *8, or rs12777823) were not. These results suggest that pVNTR-S reduces CYP2C9 expression independently of known biomarkers. Therefore, pVNTR-S may explain additional variability in CYP2C9 expression when present alone or in conjunction with other CYP2C9 alleles.
Colloids and Surfaces B Biointerfaces · 2025-01-25 · 5 citations
articleRegular and Young Investigator Award Abstracts · 2025-11-01
articleOpen accessEuropean Heart Journal · 2024-10-01
articleAbstract Background Prostate cancer (PC) patients on androgen deprivation therapy (ADT) with diabetes mellitus (DM) are at increased risk of cardiovascular events (CVE) and all-cause mortality (ACM), with metformin use linked to lower ACM. Purpose To analyze the impact of low socioeconomic status (SES), low educational levels, and Non-Hispanic Black (NHB) race on the relationship between DM, and its treatments, and CVE, cardiovascular mortality (CVm), prostate cancer-specific mortality (PCsm), and ACM within 2 years of PC diagnosis in patients ± ADT. Methods We utilized SEER-Medicare (national database for individuals 65 or older covered under US federal health insurance program merged with multiple state cancer registries with ~50% US cancers covered) to study a cohort of PC patients diagnosed from 2009 to 2017, identifying PC cases with ICD-10 - C61 and DM via the Medicare chronic condition file. CVE included Afib, AMI, peripheral artery disease, ischemic stroke, and heart failure. Two patient cohorts were analyzed: those enrolled in Medicare Parts A and B with PC (cohort 1), and those exclusively on ADT (± diabetic medications) and enrolled in Medicare Part D (cohort 2). Outcomes were evaluated using Fine-Gray and Cox models, with further analysis by subgroups: NHB, SES, and education. Results We analyzed 74,052 PC patients, with 6,682 having comprehensive Part D data. Of these, 35% in cohort 1 and 16% in cohort 2 had DM, with median ages of 73 and 72, respectively. Diabetes was more prevalent among NHB men than Non-Hispanic White (NHW), 49% vs 33% in cohort 1 and 25% vs 15% in cohort 2. In cohort 1, 9% and 8.5% of overall and DM individuals were on ADT. Risk factor details are in Table 1, and CVE, CVm, PCsm, and ACM are included in Table 2, showing higher risks of various cardiovascular outcomes for DM patients, particularly for those with low-education levels. In cohort 1, we demonstrated a higher risk of all outcomes across all subgroups with DM (p&lt;0.001). No significant interaction with race was present except in those with lower education levels, where NHW men with lower education showed an increased risk of CVE (sHR 1.15, 95%CI 1.10-1.21, P&lt;0.001). In cohort 2, compared to metformin, the use of all other DM medications was associated with higher ACM. Additionally, those on other DM medications with lower education levels had higher CVE rates. Non-DM individuals with low SES had lower CVE rates, while NHB non-DM individuals had higher PCsm. Conclusion Our study highlights disparities in PC patients with DM in relation to cardiovascular and ACM, with NHB men and those with lower SES and educational status having worse outcomes. Metformin use in patients with low education levels was associated with reduced ACM and CVE risk, indicating its potential protective effect. These findings emphasize the need for further research on the disparities in PC and effects of diabetes medications across different subpopulations.
Antimicrobial Agents and Chemotherapy · 2024-07-30 · 4 citations
articleOpen accessABSTRACT The nucleos(t)ide analogs require phosphorylation to the pharmacologically active anabolites in cells. We investigated the hypothesis that single-nucleotide polymorphisms (SNPs) in genes that encode transporters and phosphodiesterase (PDE) enzymes involved in tenofovir (TFV), disoproxil fumarate (TDF), and lamivudine (3TC) disposition will be associated with concentrations of their phosphate anabolites and virologic response. Individuals with human immunodeficiency virus (HIV) and hepatitis B virus (HBV) coinfection receiving TDF/3TC-containing antiretroviral therapy were enrolled. Steady-state TFV diphosphate (TFV-DP) and 3TC triphosphate (3TC-TP) concentrations in peripheral blood mononuclear cells (PBMCs) and dried blood spot samples were quantified. The relationship between genetic variants and TFV-DP and 3TC-TP concentrations as well as with virologic response were examined using multivariable linear regression. Of the 136 participants (median age 43 years; 63% females), 6.6% had HBV non-suppression, and 7.4% had HIV non-suppression. The multidrug resistance protein 2 (encoded by ABCC2 rs2273697) SNP was associated with 3TC-TP concentrations in PBMCs. The human organic anion transporter-1 (encoded by SLC28A2 ) rs11854484 SNP was associated with HIV non-suppression, and when evaluated together with SNPs with marginal associations ( ABCC2 rs717620 and PDE1C rs30561), participants with two or three variants compared to those with none of these variants had an adjusted odds ratio of 48.3 (confidence interval, 4.3–547.8) for HIV non-suppression. None of the SNPs were associated with HBV non-suppression. Our study identified ABCC2 SNP to be associated with 3TC-TP concentrations in PBMCs. Also, a combination of genetic variants of drug transporters and PDE was associated with HIV non-suppression.
Frequent coauthors
- 745 shared
Julie A. Johnson
University of North Carolina at Chapel Hill
- 708 shared
Rhonda M. Cooper‐DeHoff
University of Florida
- 530 shared
Amber L. Beitelshees
University of Maryland, Baltimore
- 504 shared
John G. Gums
University of Florida
- 496 shared
Eric Boerwinkle
The University of Texas Health Science Center at Houston
- 475 shared
Stephen T. Turner
Australian Regenerative Medicine Institute
- 316 shared
Caitrin W. McDonough
University of Florida
- 310 shared
Carl J. Pepine
University of Florida
Education
- 2004
Ph.D., Pharmaceutics
University of Florida
- 2003
M.S., Statistics
University of Florida
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