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Robert Chapkin

Chapkin , Robert
Robert Chapkin
Distinguished Professor, University Faculty Fellow, Regents Fellow & AgriLife Senior Faculty Fellow
111 Cater-Mattil
Undergraduate Education
BSc. in Nutrition and Biochemistry, University of Guelph, Ontario, Canada, 1981
Graduate Education
MSc. in Nutrition, University of Guelph, Ontario, Canada, 1983
Ph.D. in Nutrition and Physiological Chemistry, University of California, Davis, California, 1986
Post-doc, Cell Biology, University of California - Davis, 1988
2016-2023 - NCI Outstanding Investigator Awardee (R35)
2015-2016 - President Sigma Xi (Texas A&M Chapter)
2014 - Texas A&M University System Distinguished Professor
2013 - American Society for Nutrition (ASN) Osborne and Mendel Award
2011 - Texas A&M University Association of Former Students Distinguished Achievement Award in Research
2010-Present - Texas A&M University System Regents Professor
2009 - Vegetable & Fruit Improvement Center, Texas AgriLife Research Director’s Award
2008 - NASA Space Act Award
2007 - Senior Faculty Fellow, Texas A&M University
2006 - Sigma Xi Distinguished Scientist Award, Texas A&M University Chapter
2001-Present - Texas A&M University Faculty Fellow
2000 - Texas Agricultural Experimentation Station (TAES) Faculty Fellow
1996 - American Society for Nutrition (ASN) Bio Serv Award in Experimental Animal Nutrition
1995 - American Oil Chemists' Society, Outstanding Paper Presentation
1991-1992 - PEW National Nutrition Program Faculty Scholar
1989-1994 - National Institutes of Health "First Award"
Courses Taught
NUTR 203: Scientific Principles of Nutrition
NUTR 642: Nutritional Biochemistry II


Position Openings

Personal Statement

Dr. Chapkin is an expert in dietary/microbial modulators related to prevention of colon cancer and chronic inflammatory diseases. He has been continuously funded by NIH for the past 28 years and has made highly significant contributions in cancer chemoprevention and inflammation biology with specific emphasis in: (i) elucidation of signal transduction processes in intestinal stem cells, (ii) membrane biology and nutritional modulation of organ membrane structure and function, (iii) investigation of the role of inflammation as a critical factor in cancer development, and its modulation by environmental/botanical agents, (iv) establishment of models for chronic inflammation and cancer prevention studies, and (v) development of novel noninvasive Systems Biology-based methodologies to assess crosstalk between the gut microbiome and the host transcriptome and its application to translational research. These activities, together with a history of basic and translational (biomarkers) research using cutting-edge genomics and computational biology methodologies, demonstrate that Dr. Chapkin has the scientific credentials necessary to generate seminal discoveries linking microbiota and host responses to neonatal diseases. In addition, my expertise and experience in PPAR signaling with regard to colon cancer includes a collaboration with Dr. Peters (PI on this proposal) and others.

  1. J.M. Monk, W. Kim, E. Callaway, J.E. Foreman, J.M. Peters, W. He, B. Weeks, R.C. Alaniz, D.N. McMurray and R.S. Chapkin. Immunomodulatory action of dietary fish oil and targeted deletion of intestinal epithelial cell PPARδ in inflammation-induced colon carcinogenesis. American Journal of Physiology – GI Physiology 302:G153-G167, 2012. PMID: 21940900 PMCID: PMC3345959
  2. J. Vanamala, A. Glagolenko, P. Yang, R.J. Carroll, M.E. Murphy, R.A. Newman, R.S. Chapkin and J.R. Lupton. Dietary fish oil and pectin enhance colonocyte apoptosis in part through suppression of PPARdelta/PGE2 and elevation of PGE3. Carcinogenesis 29:790-796, 2008. PMID: 18022478 PMCID: PMC2659531
  3. Y.Y. Fan, T.E. Spencer, N. Wang, M.P. Moyer and R.S. Chapkin. Chemopreventive n-3 fatty acids activate RXR in colonocytes. Carcinogenesis 24:1-8, 2003. PMID:12844485

Research Interest

Molecular Mechanisms by which Dietary Bioactives Modulate Chronic Disease Risk:

Dr. Chapkin is an expert in dietary/botanical modulators related to chemoprevention of colon cancer and chronic inflammatory diseases, e.g., inflammatory bowel disease. He has been continuously funded by NIH for the past 26 years and has made highly significant contributions in cancer chemoprevention and inflammation biology with specific emphasis in:

  1. Elucidation of signal transduction processes in intestinal stem cells,
  2. Membrane biology and nutritional modulation of epithelia/immune cell membrane structure and function,
  3. Investigation of the role of inflammation as a critical factor in cancer development, and its modulation by environmental/botanical agents,
  4. Establishment of models for chronic inflammation and cancer prevention studies, and
  5. Development of novel noninvasive Systems Biology-based methodologies to assess crosstalk between the gut microbiome and the host transcriptome and its application to translational research. These activities, together with a history of basic and translational (biomarkers) research using cutting-edge genomics and computational biology methodologies, demonstrate that Dr. Chapkin has the scientific credentials necessary to generate seminal discoveries in the prevention/survivorship arena.

Our central goal is to (1) understand dietary chemoprevention at a fundamental level, and (2) to test pharmaceutical agents in combination with dietary (countermeasures to the Western diet) to more effectively improve gut health and reduce systemic chronic inflammation. Since diet influences gut microbiota composition and metabolite production, to unravel the interrelationships among gut health and the structure of the gut microbial ecosystem, we are in the process of evaluating (using preclinical models and humans) how the gut microbiome modulates intestinal cells, innate immune cells and tumors. As part of this endeavor, we are modeling, at the molecular level, the dynamic relationship between diet and gut microbe-derived metabolites which modulate chronic inflammation and the hierarchical cellular organization of the intestine, e.g., stem cell niche. Work in the lab related to intestinal “phenotypic flexibility” falls into four specific areas:

  1. Synergistic effects of systemic and lumenal metabolites on intestinal stem cells and differentiated colonocytes.
    Projects in this research area are designed to assess how the chemoprotective properties of dietary lipid are altered when a highly fermentable fiber, pectin, rather than a poorly fermentable fiber, cellulose, is added to the diet. This protective effect is mediated in part by the up-regulation of targeted apoptosis of DNA adducts during tumor initiation. Our findings indicate that highly fermentable fiber, which generates butyrate in the colon, only has chemotherapeutic value when n-3 PUFA is the lipid source. With respect to a molecular mechanism of action, n-3 PUFA and butyrate (a microbial fermentation product), in combination, synergistically induce a novel p53-independent, oxidation-sensitive, mitochondrial Ca2+-dependent (intrinsic) pathway. This critical observation emphasizes the need to examine both the lipid and fiber composition of diets. The lab is now focusing on the impact of gut-related metabolites on intestinal stem cell biology in vivo and ex vivo using a colonic organoid model system.

    1. E.J. Kim, L.A. Davidson, R.S. Zoh, B.S. Patil, G.K. Jayaprakasha, E.S. Callaway, C.D. Allred, N.D. Turner and R.S. Chapkin. Homeostatic responses of colonic LGR5 stem cells following acute in vivo exposure to a genotoxic carcinogen. Carcinogenesis 37:206-214, 2016. PMID:26717997.
    2. M. Shah, E. Kim, L.A. Davidson, J.M. Knight, R. Zoh, J.S. Goldsby, E.S. Callaway, B. Zhou, I. Ivanov and R.S. Chapkin. Comparative effects of diet and carcinogen on mircoRNA expression in the stem cell niche of the mouse colonic crypt. Biochimica et Biophysica – Molecular Basis for Disease 1862:121-134, 2015. PMID:26493444; Data in Brief: 6:398-404, 2015.
    3. L.A. Davidson, E. Callaway, E. Kim, B. Weeks, Y.Y. Fan, C.D. Allred and R.S. Chapkin. Targeted deletion of p53 in Lgr5-expressing intestinal stem cells promotes colon tumorigenesis in a preclinical model of colitis-associated cancer. Cancer Research 75:5392-5397, 2015. PMID:26631266.
    4. Y.Y. Fan, L.A. Davidson, E.S. Callaway, J.S. Goldsby and R.S. Chapkin. Differential effects of 2 and 3-series prostaglandins on in vitro expansion of Lgr5+ intestinal stem cells. Carcinogenesis 35:606-612, 2014. PMID:24336194
  2. Investigation of the role of dietary and microbial ligands as modifiers of inflammation and colon cancer development.
    Projects in this research area are designed to assess how microbiota-derived tryptophan metabolites mediate AhR-dependent intestinal function. Since transformation of adult stem cells is an extremely important route towards initiating intestinal cancer, we have interrogated the effect of diet and microbiota-derived AhR ligands on intestinal stem cell homeostasis and colon tumorigenesis using tissue and stem cell-specific AhR knock out and control compound mice. This objective is supported by our novel preliminary data indicating that microbial-derived AhR ligands have a direct effect on the intestinal epithelium (without the contribution of the mesenchymal niche) and modulate stemness. In addition, we have demonstrated that microbiota-derived AhR ligand levels are decreased under high fat diet (obesogenic) conditions. This is noteworthy, because a growing body of preclinical and epidemiological data indicate that the risk of colon cancer is strongly associated with obesity. Collectively, our results provide a critical new paradigm in understanding the molecular mechanisms through which microbes modulate colon cancer risk.

    1. Y. Cheng, U.H. Jin, C.D. Allred, A. Jayraman, R.S. Chapkin and S. Safe. Aryl hydrocarbon receptor activity of tryptophan metabolites in Young Adult Mouse Colonocytes. Drug Metabolism & Disposition 43:1536-1543, 2015. PMID: 25873348
    2. Y.Y. Fan, L.A. Davidson, E.S. Callaway, G.A. Wright, S. Safe and R.S. Chapkin. A bioassay to measure energy metabolism in mouse colonic crypts, organoids and sorted stem cells. American Journal of Physiology-GI 309:G1-9, 2015. PMID: 25977509
    3. U.H. Jin, S.O. Lee, G. Sridharan, K. Lee, L.A. Davidson, A. Jayaraman, R.S. Chapkin, R. Alaniz and S. Safe. Microbiome-derived tryptophan metabolites and their aryl hydrocarbon receptor-dependent agonist and antagonist activities. Molecular Pharmacology 85:777-788, 2014. PMID:24563545.
    4. V. DeClercq, D.N. McMurray and R.S. Chapkin. Obesity promotes colonic stem cell expansion during cancer initiation. Cancer Letters 369:336-343, 2015. PMID:26455770
  3. Development of a novel noninvasive methodology to monitor host/microbe interaction.
    Early detection can be considered a method for prevention in the sense that it can prevent serious morbidity and mortality. To address this need, our team has identified novel early detection biomarkers, e.g., genomic signals, to classify/predict chronic inflammation, metabolic profiling, immune status, and gut barrier function on a molecular level in mouse models and humans. For this purpose, we mathematically model dynamical system behavior for the purpose of deriving therapeutic strategies to alter undesirable cellular behavior. Outcomes include the prediction of new nutraceutical / drug targets based on intracellular signaling pathways. Cutting edge applications include: (i) the influences of diet and the gut microbiome on host (using exfoliated cells) epigenetic modulation in neonates, and (ii) simultaneous analysis of the multivariate structure between the gut metatranscriptome and host transcriptome using noninvasive methodologies.

    1. M. Wang, M. Li, C.B. Lebrilla, R.S. Chapkin, I. Ivanov and S.M. Donovan. Fecal microbiota composition of breast-fed infants differs from formula-fed and is correlated with human milk oligosaccharides consumed. Journal of Pediatric Gastroentrology & Nutrition 60:825-833, 2015. PMID:25651488 PMCID: PMC4441539
    2. J.M. Knight, L.A. Davidson, D. Herman, C.R. Martin, J.S. Goldsby, I.V. Ivanov, S.M. Donovan and R.S. Chapkin. Non-invasive analysis of intestinal development in premature and full term infants using RNA-Sequencing. Scientific Reports Nature 4:5453; DOI:10.1038/srep05453, 2014. PMCID:PMC4071321
    3. S. Schwartz, I. Friedberg, I.V. Ivanov, L.A. Davidson, J.S. Goldsby, D.B. Dahl, D. Herman, M. Wang, S.M. Donovan and R.S. Chapkin. A Metagenomic study of diet-dependent interaction between gut microflora and host in infants reveals differences in developmental and immune responses. Genome Biology 13:R32 doi:10.1186/gb-2012-13-4-r32, 2012. PMCID:PMC3446306
    4. R.S. Chapkin, C. Zhao, I. Ivanov, L.A. Davidson, J.S. Goldsby, J.R. Lupton, R.A. Mathai, M. Siegel, D. Rai, M. Russell, S.M. Donovan and E.R. Dougherty. Non-invasive stool-based detection of infant gastrointestinal development using gene expression profiles from exfoliated epithelial cells. American Journal of Physiology 298:G582-G589, 2010. PMID: 20203060 PMCID: PMC2867429
  4. Effects of dietary lipidS on membrane structure and function. 
    Select long chain polyunsaturated fatty acids, e.g., arachidonic acid (AA), regulate inflammation and promote cancer development. Previous studies have targeted prostaglandin enzymes in an attempt to modulate AA metabolism. We determined the utility of antagonizing tissue AA levels as a novel approach to suppressing AA-derived eicosanoids. Specifically, we globally disrupted the Fads1 (∆5 desaturase) gene in mouse tissues. This resulted in a profound increase in one- and a concurrent decrease in two-series-derived prostaglandins. The lack of AA-derived eicosanoids, e.g., PGE2, was associated with perturbed intestinal crypt proliferation, immune cell homeostasis, and a heightened sensitivity to acute inflammatory challenge. In addition, Null mice failed to thrive, dying off by 12 weeks of age. Dietary supplementation with AA extended the longevity of Null mice to levels comparable to Wild type mice. We propose that this new mouse model will expand our understanding of how long chain PUFA and their metabolites mediate inflammation and modulate diseases such as NAFLD.

    1. H.F. Turk, J.M. Monk, Y.Y. Fan, E.S. Callaway, B. Weeks and R.S. Chapkin. Inhibitory effects of omega-3 fatty acids on injury induced epidermal growth factor transactivation contribute to delayed wound healing. American Journal of Physiology 304:C905-C917, 2013. PMID:23426968.
    2. Y.Y. Fan, J. Monk, T. Hou, E. Callaway, L. Vincent, B. Weeks, P. Yang and R.S. Chapkin. Characterization of an arachidonic acid-deficient (FADS1 knock-out) mouse model. Journal of Lipid Research 53:1287-1295, 2012. PMCID: PMC3371240
    3. H.F. Turk, R. Barhoumi, R.S. Chapkin. Alteration of EGFR spatiotemporal dynamics suppresses signal transduction. PLoS One 7(6):e39682, June, 2012. doi:10.1371/journal.pone.0039682 PMCID: PMC3384615
    4. R.S. Chapkin, N. Wang, Y.Y. Fan, J.R. Lupton and I.A. Prior. Docosahexaenoic acid alters the size and distribution of cell surface microdomains. Biochimica et Biophysica Acta – Biomembranes 1778:466-471, 2008. PMCID:PMC2244794


Research Area

Biochemical Mechanisms of Marine and Plant Species-Derived Bioactive Agents:  Role in Immune Modulation and Chemoprevention.


  1. Jin, UH, Cheng, Y, Park, H, Davidson, LA, Callaway, ES, Chapkin, RS et al.. Short Chain Fatty Acids Enhance Aryl Hydrocarbon (Ah) Responsiveness in Mouse Colonocytes and Caco-2 Human Colon Cancer Cells. Sci Rep. 2017;7 (1):10163. doi: 10.1038/s41598-017-10824-x. PubMed PMID:28860561 PubMed Central PMC5579248.
  2. Kumar, R, Herold, JL, Schady, D, Davis, J, Kopetz, S, Martinez-Moczygemba, M et al.. Streptococcus gallolyticus subsp. gallolyticus promotes colorectal tumor development. PLoS Pathog. 2017;13 (7):e1006440. doi: 10.1371/journal.ppat.1006440. PubMed PMID:28704539 PubMed Central PMC5509344.
  3. Seidel, DV, Azcárate-Peril, MA, Chapkin, RS, Turner, ND. Shaping functional gut microbiota using dietary bioactives to reduce colon cancer risk. Semin. Cancer Biol. 2017; :. doi: 10.1016/j.semcancer.2017.06.009. PubMed PMID:28676459 .
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