About

Stephen D. Hursting, PhD, is the AICR/WCRF Distinguished Professor of Nutrition and Cancer in the Department of Nutrition, the Nutrition Research Institute, and the Lineberger Comprehensive Cancer Center at the University of North Carolina (UNC) at Chapel Hill. He earned his BA in biology from Earlham College, his PhD in nutritional biochemistry, and an MPH in nutritional epidemiology from UNC. He completed postdoctoral training in cancer prevention at the National Cancer Institute (NCI). Prior to joining UNC in 2014, Dr. Hursting served as Professor and Chair of the Department of Nutritional Sciences at the University of Texas at Austin, and held roles such as Chief of the NCI’s Nutrition and Molecular Carcinogenesis Laboratory Section and Deputy Director of the NCI Cancer Prevention Fellowship Program. His research focuses on the molecular, metabolic, and immunologic mechanisms linking nutrition, obesity, and cancer, with particular emphasis on energy balance modulation through lifestyle interventions, bariatric surgery, and pharmacologic agents like GLP-1 receptor agonists. His laboratory has published nearly 300 articles and book chapters establishing causal links between obesity, systemic metabolic and inflammatory factors, and cancer-related signaling pathways, and has advanced precision nutrition approaches by integrating multi-omics analyses with preclinical and clinical studies to elucidate diet–gene interactions underlying obesity-cancer associations.

Research topics

• Medicine
• Internal medicine
• Biology
• Immunology
• Sociology
• Computer Science
• Cancer research
• Art
• Chemistry
• Biochemistry
• Endocrinology
• Oncology

Selected publications

• CUP global framework for the review of the biologic pathways linking diet, nutrition, body weight, and physical activity with cancer incidence – updated to version 3

  2026-04-28

  articleOpen accessSenior author

  <ns3:p>This current framework (version 3) updates the previous one published within the WCRF Gateway on Health Open Research (publication data of version 2: 23 September 2025).</ns3:p> <ns3:p/> <ns3:p> The purpose of the Framework is to provide guidance on how to: <ns3:list list-type="bullet"> <ns3:list-item> <ns3:p>identify, review, and summarise the biological mechanisms that underpin the associations between diet, nutrition, body weight, and physical activity and cancer incidence found within CUP Global</ns3:p> </ns3:list-item> <ns3:list-item> <ns3:p>assess the strength of evidence that a given biological mechanism operates between an exposure and outcome of interest</ns3:p> </ns3:list-item> </ns3:list> These biological plausibility investigations apply to 1) exposures with an established link to cancer (strong evidence in CUP/CUP Global) and for which there are strong mechanistic data, but further work is needed (for example, a poorer understanding of the evidence for certain cancer sites); 2) exposures with a strong epidemiological link to cancer (strong evidence in CUP/CUP Global) but with limited mechanistic understanding; 3) exposures with a putative epidemiological link to cancer (limited suggestive evidence in the CUP/CUP Global) for which more robust mechanistic data would strengthen conclusions. </ns3:p> <ns3:p/> <ns3:p> Note that mechanisms evaluated using this Framework are defined as <ns3:italic>biological</ns3:italic> processes linking diet, nutrition, body weight, and physical activity and cancer incidence. <ns3:bold> The focus is primarily on molecular mechanisms but may expand to physiological mechanisms depending on the research question.</ns3:bold> </ns3:p>

  PublisherOA PDFDOI

• Abstract 2020: Fatty acid metabolism supports survival in normoxia and migration upon reoxygenation in lung-metastasizing breast cancer cells.

  Cancer Research · 2026-04-03

  article

  Abstract Breast cancer is the most common cancer among women, and metastasis remains the leading cause of mortality. While fatty acid metabolism plays a critical role in cancer progression, its specific contribution to supporting breast cancer metastasis to distinct organs, particularly the lungs and liver, remains poorly understood. This study aims to characterize the lipid metabolic profiles of breast cancer cells with preferential metastasis to the lung versus the liver, and to determine how lipid metabolism supports cell survival under normoxia and drives migration upon reoxygenation after exposure to hypoxia. We utilized a unique murine breast cancer cell model with preferential metastasis to either lung (metM-WntLung; MLg) or liver (metM-WntLiver; MLr). The metastatic cells were exposed to normoxia or hypoxia (1% O2, 48 hrs) and reoxygenation to mimic dynamic tumor microenvironmental stress. Fatty acid metabolism was assessed using 13C isotopic tracing, and cell viability and migration were evaluated following inhibition of key metabolic enzymes. Results showed that 13C6-glucose and 13C5-glutamine were significantly incorporated into the synthesis of both saturated (16:0 and 18:0) and unsaturated (16:1 and 18:0) fatty acids, indicating higher de novo fatty acid synthesis in MLg cells compared to MLr cells. Despite this, both cell lines exhibited similar triacylglycerol levels without evident lipid accumulation. A pulse-chase experiment showed that 13C6-glucose-labeled fatty acids declined more rapidly in MLg than in MLr cells at 24 and 48 hrs (48.8% vs 30.3%, and 58.5% vs 48.3%, respectively), indicating more rapid fatty acid turnover in MLg than MLr cells. Inhibition of key enzymes in fatty acid metabolism, including de novo fatty acid synthesis (FASN via TVB-3166), esterification (DGAT2 via PF-06424439), lipolysis (ATGL via ATGListatin), and β-oxidation (CPT1A via etomoxir), induced a significantly greater reduction in cell viability of MLg than MLr cells, indicating that dynamic fatty acid synthesis, storage, lipolysis and oxidation are necessary to support survival in MLg cells. Under hypoxic conditions, MLg cells sustained higher de novo fatty acid synthesis accompanied by lipid accumulation. Upon reoxygenation following hypoxia, inhibition of either lipolysis or β-oxidation reduced MLg cell migration by 57% and 42%, respectively, an effect not observed in MLr cells. Overall, these results support that dynamic and rapid fatty acid turnover in lung-metastatic breast cancer cells is necessary to support survival, with lipids accumulated during hypoxia subsequently mobilized and oxidized to fuel migration upon reoxygenation. These findings identify lipid metabolism as a critical driver of lung-specific metastasis and a promising therapeutic target to reduce metastatic spread and improve outcomes for patients with breast cancer. Citation Format: Marjorie Anne Layosa, Morgan Conrad, Chaylen Jade Andolino, Michael K. Wendt, Stephen D. Hursting, Dorothy Teegarden. Fatty acid metabolism supports survival in normoxia and migration upon reoxygenation in lung-metastasizing breast cancer cells [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2026; Part 1 (Regular Abstracts); 2026 Apr 17-22; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2026;86(7 Suppl):Abstract nr 2020.

  PublisherDOI

• Weight Loss and Omega-3 Supplementation Modulate the Microbiome in Women with Increased Breast Cancer Risk

  Cancer Prevention Research · 2026-04-18

  articleOpen access

  Abstract Obesity is associated with gut dysbiosis, chronic inflammation, and insulin resistance. We assessed the proportional change in fecal microbial populations in a pilot study (n = 34) of peri/postmenopausal women with a body mass index ≥28 kg/m2 who were randomized to receive either 3.25 g/day of omega-3 fatty acids or a placebo during a weight loss intervention. Body composition was assessed using dual X-ray absorptiometry, and fecal and blood samples were collected. The median weight change was −10%. Among participants who lost ≥10% of their weight, those assigned to omega-3 fatty acids showed the greatest decrease in the Firmicutes:Bacteroidetes ratio and displayed favorable changes in systemic biomarkers. Notable increases in the proportional abundance of short-chain fatty acid (SCFA)–producing microbes including Phocaeicola vulgatus and Alistipes putredinis were observed in women receiving omega-3, which correlated with improvements in breast cancer biomarkers such as bioavailable estradiol, adiponectin:leptin ratio, and C-reactive protein levels. Women administered omega-3 fatty acids displayed increased % change in plasma SCFA propionate and decreased butyrate, suggesting that intervention differentially modulated circulating bacteria-derived SCFA metabolites. High-dose omega-3 fatty acids, when added to a behavioral weight loss intervention, promoted beneficial shifts in the gut microbiome and associated with improved breast cancer risk factor biomarkers. Prevention Relevance: Obesity is a modifiable risk factor for breast cancer, characterized by chronic inflammation and altered adipokines. This trial addresses the need to enhance weight loss by targeting underlying metabolic and inflammatory drivers. We show that omega-3 polyunsaturated fatty acids (eicosapentaenoic acid/docosahexaenoic acid) shift SCFA-producing microbiota, increase propionate, and correlate with improved breast cancer risk factor biomarkers.

  PublisherDOI

• Abstract 3627: Metabolomic signatures of physical activity in treatment-naive patients with early-onset vs. late-onset colorectal cancer: Results from the ColoCare Study

  Cancer Research · 2026-04-03

  article

  Abstract Introduction: Emerging studies link physical inactivity to early-onset colorectal cancer (EOCRC), but most rely on subjective measures of physical activity (PA). Metabolite signatures may offer an objective measure of PA that also captures the systemic metabolic response to activity. We assessed a previously validated PA metabolomic signature in patients with recently diagnosed colorectal cancer (CRC) and compared profile scores between patients with EOCRC (&amp;lt;50 yrs) vs. non-EOCRC (&amp;gt;50 yrs). Methods: We examined baseline (pre-surgery) data from 122 stage I-III patients with CRC in the ColoCare Study at Huntsman Cancer Institute (Utah) and Heidelberg University Hospital (Germany). PA for the previous year was measured with the International Physical Activity Questionnaire-Short Form. Untargeted serum metabolites and complex lipids were profiled at the West Coast Metabolomics Center. We calculated a 24-metabolite PA signature developed in &amp;gt;6,000 cancer-free individuals (Papadimitriou et al., CEBP, 2025) consisting of acylcarnitines, glycerophospholipids, monosaccharides, amino acids, and sphingolipids. Following metabolite pre-processing, normalization, and scaling, we performed multivariable linear regression on 20 metabolites available in our dataset, adjusting for age, sex, tumor stage, and body mass index (BMI). Metabolite scores were calculated for each participant by multiplying normalized metabolite concentrations by the previously developed PA metabolite signature coefficients and were then compared between EOCRC vs. non-EOCRC survivors. Results: Compared to patients with non-EOCRC (67±9 years, N=102), those with EOCRC (39±10 years, N=20) were diagnosed with higher stages (55% vs. 43% stage III), had lower prevalence of obese BMI (25% vs. 37%), and were more physically active (16±17 metabolic equivalent (MET) hrs/week vs. 11±17 MET hrs/week), p&amp;gt;0.05. Patients with EOCRC were more likely to meet PA guidelines (&amp;gt;150 min/week of moderate to vigorous PA; 60% vs. 38%) compared to those with non-EOCRC, p&amp;gt;0.05. Among the 20 metabolites investigated in our data, 15 showed a consistent direction of association with the previously developed PA signature. Patients with EOCRC had higher scores of the PA metabolite signature (0.04±0.09) than older patients (-0.01±0.10), t=2.3, p=0.03. This modest association remained significant after adjustment for stage, sex, and BMI (β=0.05, p=0.048). Conclusions: A PA metabolite signature showed comparable associations to questionnaire-derived PA measures in our CRC survivor cohort, consistent with findings in healthy individuals. Patients with EOCRC reported a higher level of PA compared to those with non-EOCRC and had a significantly higher PA metabolite signature score. The metabolite response to PA may clarify how physical inactivity influences EOCRC risk and outcomes. Citation Format: Victoria Maria Bandera, Tengda Lin, Patricia Erickson, Caroline Himbert, Aik Choon Tan, Mary C. Playdon, Alan Maschek, Paul Stewart, Sheetal Hardikar, Elaine M. Glenny, Jennifer Ose, Victoria Damerell, Christy A. Warby, Olena Aksonova, Oliver Fiehn, Kenneth Boucher, Peter Schirmacher, Ildiko Strehli, Megan Mclaws, Alejandro Sanchez, Jolanta Jedrzkiewicz, Lyen C. Huang, Vaia Florou, Jessica N. Cohan, Alexander Brobeil, Hans-Ulrich Kauczor, Christoph Kahlert, Meghana Karchi, Elizabeth H. Wood, Doratha A. Byrd, Erin M. Siegel, Adetunji T. Toriola, David Shibata, Christopher I. Li, Jane C. Figueiredo, Biljana Gigic, Jatin Roper, Stephen Hursting, Cornelia M. Ulrich. Metabolomic signatures of physical activity in treatment-naive patients with early-onset vs. late-onset colorectal cancer: Results from the ColoCare Study [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2026; Part 1 (Regular Abstracts); 2026 Apr 17-22; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2026;86(7 Suppl):Abstract nr 3627.

  PublisherDOI

• Sex-specific systemic metabolic predictors of resistance to calorie restriction-induced weight loss in obese Diversity Outbred mice

  UNC Libraries · 2026-03-10

  articleOpen access

  Calorie restriction (CR) is a well-established weight loss strategy, albeit with variation in response. Using genetically heterogeneous mice, we sought to identify metabolic predictors of resistance to CR-induced weight loss. Diversity Outbred mice (150 males, 150 females) were fed a high-fat diet for 12 weeks to generate diet-induced obesity (DIO), then underwent CR for 8 weeks. Body weight and composition, blood glucose, and plasma levels of 9 metabolic hormones were assessed at baseline, following DIO, and following CR. In response to each dietary intervention, the mice displayed substantial heterogeneity across all outcomes, often with sexual dimorphism. Among the metabolic markers, leptin changed the most in response to each dietary intervention. Logistic regression found that resistance to CR-induced weight loss in obese mice was associated with lower glucose levels in males, and with lower levels of insulin, resistin, homeostatic model assessment for insulin resistance (HOMA-IR), and plasminogen activator inhibitor-1, and higher levels of ghrelin in females. Moreover, lower leptin levels predicted resistance to CR-induced weight loss in obese mice, regardless of sex. These preclinical findings provide proof-of-principle that the genetic and phenotypic heterogeneity of DO mice can be leveraged to identify mechanistic predictors that may enhance the personalization of weight loss interventions.

  PublisherDOI

• Adaptability of lung and liver metastatic breast cancer cells to glucose

  UNC Libraries · 2025-12-11

  articleOpen access1st authorCorresponding
  PublisherDOI

• Abstract PR007: Tumor-adjacent visceral adipose tissue displays an altered transcriptomic landscape in early-onset colorectal cancer patients: Results from the ColoCare Study

  Clinical Cancer Research · 2025-12-10

  article

  Abstract Introduction: Obesity is commonly characterized by high levels of internal (visceral) adiposity. Visceral adipose tissue (VAT) is highly metabolically active and secretes proteins and metabolites in paracrine and endocrine signaling pathways. The phenotype of tumor-adjacent VAT may be an unexplored factor for risk and progression of early-onset colorectal cancer (EOCRC). Thus, we aimed to identify transcriptomic differences in tumor-adjacent visceral adipose tissue (VAT) in patients with EOCRC (&amp;lt;50 years at diagnosis) vs. those diagnosed with later-onset colorectal cancer (LOCRC; &amp;gt;50 years at diagnosis). Methods: VAT samples were collected from 332 patients with stage 0-III colorectal cancer enrolled in the ColoCare Study and recruited at Huntsman Cancer Institute (Utah), Heidelberg University Hospital (Germany), University of Tennessee Health Science Center (Tennessee), and Moffitt Cancer Center (Florida). Patients in our study were treatment naïve. VAT tissue was collected 1-3 cm from the colorectal tumor during surgery. VAT transcriptomes were measured with bulk RNA sequencing. Participants were classified as EOCRC vs. LOCRC. Normalized differentially expressed genes were identified (DESeq2), with analyses adjusted for sex, body mass index (BMI), study site, and tumor stage. Gene set enrichment analysis (GSEA) identified enriched pathways within the 2025 Hallmark gene sets. Significance was assessed using false discovery rate (FDR) p-adj&amp;lt;0.05. We replicated our analyses, adjusting for tumor site (colon vs. rectal), to account for potential differences by anatomical subgroup. Results: Patients with EOCRC (n=45, average age: 41±9 years) had higher disease stages compared to LOCRC patients (n=287, average age: 66±10 years) (EOCRC: 64% Stage III vs LOCRC: 39% Stage III) and similar BMI (EOCRC: 28.8±7.0 kg/m2 vs. LOCRC: 28.5±5.9 kg/m2). GSEA revealed 5 significantly enriched gene sets (FDR p-adj&amp;lt;0.05) in VAT when comparing EOCRC to LOCRC patients. VAT of EOCRC patients exhibited upregulation of immune pathways (Interferon Alpha Response, Interferon Gamma Response, TNFA Signaling via NF- κB), and fibrosis Hallmark pathways (Epithelial Mesenchymal Transition) (Normalized Enrichment Score (NES) &amp;gt;1.5, p-adj&amp;lt;0.05). Additionally, the VAT of patients with EOCRC showed upregulation of the glycolysis gene set relative to LOCRC (NES&amp;gt;1.5, p-adj&amp;lt;0.05). These pathways remained significantly enriched regardless of tumor site adjustment. Conclusions: VAT of patients with EOCRC displays a differential gene expression landscape relative to LOCRC patients, suggesting enhanced immune, fibrotic, and metabolic activity. These findings suggest that tumor-adjacent VAT physiology may be a relevant factor of the tumor-microenvironment in EOCRC progression. Citation Format: Victoria M. Bandera, Patricia Erickson, Caroline Himbert, Elaine M. Glenny, Tengda Lin, Sheetal Hardikar, Aik Choon Tan, Jennifer Ose, Victoria Damerell, Christy Warby, Olena Aksonova, Chris Stubben, David Nix, Kenneth Boucher, Peter Schirmacher, Ildiko Strehli, Megan Mclaws, Alejandro Sanchez, Jolanta Jedrzkiewicz, Lyen C. Huang, Vaia Florou, Jessica N. Cohan, Alexander Brobeil, Hans-Ulrich Kauczor, Christoph Kahlert, Meghana Karchi, Elizabeth H. Wood, Doratha A. Byrd, Erin M. Siegel, Adetunji T. Toriola, David Shibata, Christopher I. Li, Jane C. Figueiredo, Biljana Gigic, Jatin Roper, Stephen Hursting, Cornelia M. Ulrich. Tumor-adjacent visceral adipose tissue displays an altered transcriptomic landscape in early-onset colorectal cancer patients: Results from the ColoCare Study [abstract]. In: Proceedings of the AACR Special Conference in Cancer Research: The Rise in Early-Onset Cancers—Knowledge Gaps and Research Opportunities; 2025 Dec 10-13; Montreal, QC, Canada. Philadelphia (PA): AACR; Clin Cancer Res 2025;31(23_Suppl):Abstract nr PR007.

  PublisherDOI

• Supplementary Table from Obesity and Breast Cancer Metastasis across Genomic Subtypes

  2025-11-26

  articleOpen access

  Supplementary Table from Obesity and Breast Cancer Metastasis across Genomic Subtypes

  PublisherDOI

• Adaptability of lung and liver metastatic breast cancer cells to glucose

  Cancer Cell International · 2025-10-24

  articleOpen access

  Abstract Background Breast cancer is the most common cancer among women, and metastasis is the leading cause of mortality. It is still unknown how breast cancer cells metabolically adapt to successfully metastasize to different organs to survive adverse conditions, including varying nutrient availability. The purpose of this study is to elucidate the metabolic characteristics and glucose adaptation mechanisms of breast cancer cells that preferentially metastasize to the lungs or the liver. Methods Using a Wnt-driven breast cancer model with preferential metastasis to lung (metM-Wnt Lung ) or liver (metM-Wnt Liver ), we measured 14 C-glucose uptake, 13 C 6 -glucose metabolic flux, metabolic enzyme levels, and cell viability under normal (5 mM), high (25 mM), and low (1 or 0 mM) glucose conditions. Results Under normal glucose conditions, metM-Wnt Lung cells were more glycolytic, exhibiting greater flux of 13 C 6 -glucose-derived carbons into glycolytic intermediates, such as pyruvate and lactate. In contrast, metM-Wnt Liver cells favored oxidative phosphorylation, with higher levels of 13 C 6 -glucose-derived carbons in tricarboxylic acid (TCA) cycle metabolites such as oxaloacetate indicative of higher pyruvate carboxylase (PC) activity. Exposure to high glucose reduced metM-Wnt Liver cell viability, with no effect on metM-Wnt Lung cells, suggesting better adaptability of metM-Wnt Lung cells to glucose excess. This was accompanied by increased PC activity and oxidative phosphorylation in metM-Wnt Lung cells, whereas metM-Wnt Liver cells shifted to a more glycolytic phenotype. Under glucose deprivation, metM-Wnt Lung cells were more viable than metM-Wnt Liver cells, suggesting that metM-Wnt Lung cells have better adaptability to glucose deprivation. Inhibiting phosphoenolpyruvate carboxykinase, a key enzyme in gluconeogenesis, reduced metM-Wnt Lung cell viability compared to metM-Wnt Liver cells. Similarly, inhibiting catabolism of glutamine, a gluconeogenic substrate, decreased metM-Wnt Lung cell viability compared to metM-Wnt Liver cells, indicating that metM-Wnt Lung cells rely on more on gluconeogenesis and glutamine metabolism under glucose deprivation. Conclusion Our findings reveal that metM-Wnt Lung cells exhibit greater metabolic flexibility to glucose than metM-Wnt Liver cells by shifting from glycolysis to oxidative phosphorylation under high glucose conditions while utilizing gluconeogenesis and glutamine under glucose deprivation conditions.

  PublisherOA PDFDOI

• Data from Obesity and Breast Cancer Metastasis across Genomic Subtypes

  2025-11-26

  articleOpen access

  &lt;div&gt;AbstractBackground:&lt;p&gt;Obese women have higher risk of aggressive breast tumors and distant metastasis. However, obesity has rarely been assessed in association with metastasis in diverse populations.&lt;/p&gt;Methods:&lt;p&gt;In the Carolina Breast Cancer Study Phase 3 (2008–2013), waist-to-hip ratio (WHR), body mass index (BMI), and molecular subtype [PAM50 risk-of-recurrence (ROR) score] were assessed. Obesity measures were evaluated in association with metastasis within five years of diagnosis, overall and stratified by race and ROR score. Absolute risk of metastasis and risk differences between strata were calculated using the Kaplan–Meier estimator, adjusted for age, grade, stage, race, and ER status. Relative frequency of metastatic site and multiplicity were estimated in association with obesity using generalized linear models.&lt;/p&gt;Results:&lt;p&gt;High-WHR was associated with higher risk of metastasis (5-year risk difference, RD, 4.3%; 95% confidence interval, 2.2–6.5). It was also associated with multiple metastases and metastases at all sites except brain. The 5-year risk of metastasis differed by race (11.2% and 6.9% in Black and non-Black, respectively) and ROR score (19.5% vs. 6.6% in high vs. low-to-intermediate ROR-PT). Non-Black women and those with low-to-intermediate ROR scores had similar risk in high- and low-WHR strata. However, among Black women and those with high ROR, risk of metastasis was elevated among high-WHR (RD&lt;sub&gt;Black/non-Black&lt;/sub&gt; = 4.6%, RD&lt;sub&gt;High/Low-Int&lt;/sub&gt; = 3.1%). Patterns of metastasis were similar by BMI.&lt;/p&gt;Conclusions:&lt;p&gt;WHR is associated with metastatic risk, particularly among Black women and those with high-risk tumors.&lt;/p&gt;Impact:&lt;p&gt;Understanding how risk factors for metastasis interact may help in tailoring care plans and surveillance among patients with breast cancer.&lt;/p&gt;&lt;/div&gt;

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Recent grants

• Obesity, Metabolism and Breast Cancer Metastasis

  NIH · $2.6M · 2019–2025

• Animal Metabolism Phenotyping Core

  NIH · $11.3M · 1999–2027

• Akt/mTOR Signaling in Energy Balance Modulation of Epithelial Carcinogenesis

  NIH · $1.6M · 2009–2014

• Breaking the Obesity-Cancer Link: New Targets and Strategies

  NIH · $6.0M · 2015–2023

• Adipose tissue-colorectal tumor cross-talk: new targets for breaking the obesity-cancer link

  NIH · $3.2M · 2021–2026

Frequent coauthors

• Susan N. Perkins

  Frederick National Laboratory for Cancer Research

  169 shared

• Michael F. Coleman

  University of North Carolina at Chapel Hill

  146 shared

• Laura W. Bowers

  120 shared

• J. Carl Barrett

  98 shared

• Emily L. Rossi

  National Cancer Institute

  91 shared

• Jackie A. Lavigne

  Virginia Mason Medical Center

  85 shared

• Nomelí P. Núñez

  80 shared

• John DiGiovanni

  Livestrong Foundation

  66 shared

Education

• PhD, Nutrition

  University of North Carolina at Chapel Hill

  1992

Awards & honors

• Jean Andrews Award and Visiting Professorship 2024, Universi…
• Impact Award 2022, UNC-Chapel Hill Department of Nutrition
• Outstanding Investigator 7-Year Award 2015-2022, NCI
• Distinguished Service Award 2022, American Institute for Can…
• Outstanding Service Award for Excellence as Vice-Chair of th…