About

Dr. Pauline A. Thomas is a Professor and Director of Preventive Medicine Residency in the Department of Medicine at Rutgers New Jersey Medical School. She has over 40 years of experience practicing public health, pediatrics, and preventive medicine in New York City and New Jersey. Her career began as an EIS officer with the CDC, after which she researched the epidemiology of pediatric HIV, supervised HIV surveillance, and contributed to the establishment of the World Trade Center Health Registry with the New York City Department of Health and Mental Hygiene. She oversees preventive medicine training at NJMS and maintained a part-time pediatric practice until mid-2023. Dr. Thomas received her medical degree from Yale Medical School and is board certified in Pediatrics and Preventive Medicine. Her areas of interest include Public Health, Public Health Practice, Preventive Medicine, Lifestyle Medicine, Pediatrics, Climate and Health, and HIV.

Research topics

• Chemistry
• Biochemistry
• Biology
• Internal medicine
• Endocrinology

Selected publications

• A Next generation PLD2 inhibitor with improved physiochemical properties and DMPK profile for translational in vivo

  2015-01-16 · 1 citations

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  Publisher

• Tocopherols inhibit oxidative and nitrosative stress in estrogen‐induced early mammary hyperplasia in ACI rats

  Molecular Carcinogenesis · 2014-04-30 · 47 citations

  articleOpen access

  Oxidative stress is known to play a key role in estrogen-induced breast cancer. This study assessed the chemopreventive activity of the naturally occurring γ-tocopherol-rich mixture of tocopherols (γ-TmT) in early stages of estrogen-induced mammary hyperplasia in ACI rats. ACI rats provide an established model of rodent mammary carcinogenesis due to their high sensitivity to estrogen. Female rats were implanted with 9 mg of 17β-estradiol (E2) in silastic tubings and fed with control or 0.3% γ-TmT diet for 1, 3, 7, and 14 d. γ-TmT increased the levels of tocopherols and their metabolites in the serum and mammary glands of the rats. Histological analysis revealed mammary hyperplasia in the E2 treated rats fed with control or γ-TmT diet. γ-TmT decreased the levels of E2-induced nitrosative and oxidative stress markers, nitrotyrosine, and 8-oxo-dG, respectively, in the hyperplastic mammary tissues. 8-Isoprostane, a marker of oxidative stress in the serum, was also reduced by γ-TmT. Noticeably, γ-TmT stimulated Nrf2-dependent antioxidant response in the mammary glands of E2 treated rats, evident from the induced mRNA levels of Nrf2 and its downstream antioxidant enzymes, superoxide dismutase, catalase, and glutathione peroxidase. Therefore, inhibition of nitrosative/oxidative stress through induction of antioxidant response is the primary effect of γ-TmT in early stages of E2-induced mammary hyperplasia. Due to its cytoprotective activity, γ-TmT could be a potential natural agent for the chemoprevention of estrogen-induced breast cancer.

  PublisherOA PDFDOI

• Development of a Selective, Allosteric PLD1/2 Inhibitor in a Novel Scaffold

  2013-03-14

  article

  A diversity-oriented synthesis approach of the neuroleptic drug halopemide, reported to be a phospholipase D2 (PLD2) inhibitor (but later shown to be a dual PLD1/2 inhibitor) afforded ML299 (CID 56593087), a potent, dual PLD1/2 selective allosteric inhibitor (cellular PLD1, IC50 = 5.6 nM, cellular PLD2, IC50 = 20 nM) developed within the traditionally PLD2-preferring triazasprione core. ML299 displays balanced, low nanomolar inhibition of both PLD1 and PLD2, is CNS penetrant and has improved physiochemical and dystrophia myotonica protein kinase (DMPK) properties relative to our earlier dual PLD1/2 inhibitors, making it a useful tool to probe selective PLD1 and PLD2 function in vitro and in vivo. Data here shows therapeutic relevance in virology and oncology.

  Publisher

• Dietary tocopherols inhibit cell proliferation, regulate expression of ERα, PPARγ, and Nrf2, and decrease serum inflammatory markers during the development of mammary hyperplasia

  Molecular Carcinogenesis · 2012-03-02 · 61 citations

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  Previous clinical and epidemiological studies of vitamin E have used primarily α-tocopherol for the prevention of cancer. However, γ-tocopherol has demonstrated greater anti-inflammatory and anti-tumor activity than α-tocopherol in several animal models of cancer. This study assessed the potential chemopreventive activities of a tocopherol mixture containing 58% γ-tocopherol (γ-TmT) in an established rodent model of mammary carcinogenesis. Female ACI rats were utilized due to their sensitivity to 17β-estradiol (E2 ) to induce mammary hyperplasia and neoplasia. The rats were implanted subcutaneously with sustained release E2 pellets and given dietary 0.3% or 0.5% γ-TmT for 2 or 10 wk. Serum E2 levels were significantly reduced by the treatment with 0.5% γ-TmT. Serum levels of inflammatory markers, prostaglandin E2 and 8-isoprostane, were suppressed by γ-TmT treatment. Histology of mammary glands showed evidence of epithelial hyperplasia in E2 -treated rats. Immunohistochemical analysis of the mammary glands revealed a decrease in proliferating cell nuclear antigen (PCNA), cyclooxygenase-2 (COX-2), and estrogen receptor α (ERα), while there was an increase in cleaved-caspase 3, peroxisome proliferator-activated receptor γ (PPARγ), and nuclear factor (erythroid-derived 2)-like 2 (Nrf2) in γ-TmT-treated rats. In addition, treatment with γ-TmT resulted in a decrease in the expression of ERα mRNA, whereas mRNA levels of ERβ and PPARγ were increased. In conclusion, γ-TmT was shown to suppress inflammatory markers, inhibit E2 -induced cell proliferation, and upregulate PPARγ and Nrf2 expression in mammary hyperplasia, suggesting that γ-TmT may be a promising agent for human breast cancer prevention.

  PublisherDOI

• Severe diabetes and leptin resistance cause differential hepatic and renal transporter expression in mice

  Comparative Hepatology · 2012-04-23 · 36 citations

  articleOpen access

  BACKGROUND: Type-2 Diabetes is a major health concern in the United States and other Westernized countries, with prevalence increasing yearly. There is a need to better model and predict adverse drug reactions, drug-induced liver injury, and drug efficacy in this population. Because transporters significantly contribute to drug clearance and disposition, it is highly significant to determine whether a severe diabetes phenotype alters drug transporter expression, and whether diabetic mouse models have altered disposition of acetaminophen (APAP) metabolites. RESULTS: Transporter mRNA and protein expression were quantified in livers and kidneys of adult C57BKS and db/db mice, which have a severe diabetes phenotype due to a lack of a functional leptin receptor. The urinary excretion of acetaminophen-glucuronide, a substrate for multidrug resistance-associated proteins transporters was also determined. The mRNA expression of major uptake transporters, such as organic anion transporting polypeptide Slco1a1 in liver and kidney, 1a4 in liver, and Slc22a7 in kidney was decreased in db/db mice. In contrast, Abcc3 and 4 mRNA and protein expression was more than 2 fold higher in db/db male mouse livers as compared to C57BKS controls. Urine levels of APAP-glucuronide, -sulfate, and N-acetyl cysteine metabolites were higher in db/db mice. CONCLUSION: A severe diabetes phenotype/presentation significantly altered drug transporter expression in liver and kidney, which corresponded with urinary APAP metabolite levels.

  PublisherOA PDFDOI

• Regulation of Hepatic Phase II Metabolism in Pregnant Mice

  Journal of Pharmacology and Experimental Therapeutics · 2012-10-11 · 27 citations

  articleOpen access
  PublisherOA PDFDOI

• Inhibition of Genistein Glucuronidation by Bisphenol A in Human and Rat Liver Microsomes

  Drug Metabolism and Disposition · 2011-12-07 · 23 citations

  articleOpen access
  PublisherOA PDFDOI

• Abstract 1851: Dietary mixed tocopherols inhibit cell proliferation in mammary hyperplasia, suppress the expression of inflammatory markers, and upregulate PPARγ

  Cancer Research · 2011-04-01

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  Abstract Dietary intake of vitamin E, a fat-soluble vitamin, has been suggested to reduce cancer risk because of antioxidant properties. There are eight different forms of vitamin E which include four tocopherols (with a saturated phytyl tail) and four tocotrienols (with an unsaturated isoprenoid side chain) designated as α, β, γ, and Δ variants. Previous clinical and epidemiological studies on vitamin E and cancer have focused on α-tocopherol. However, γ-tocopherol has demonstrated greater anti-inflammatory and anti-tumor activity than α-tocopherol. This study assessed the potential chemopreventive activities of a tocopherol mixture containing 58% γ-tocopherol (γ-TmT) in an established rodent model of mammary carcinogenesis. Female ACI rats were utilized due to their sensitivity to 17β-estradiol to induce mammary hyperplasia and eventually mammary tumors. The rats were implanted subcutaneously with estradiol (E2) pellets containing 2.5 mg of E2 and given 0.3% or 0.5% γ-TmT in the diet for 2 or 10 weeks. Serum E2 levels were significantly reduced by the treatment with 0.5% γ-TmT. Serum levels of anti-inflammatory markers, prostaglandin E2 and 8-isoprostane, were suppressed by γ-TmT treatment. Histology of mammary glands showed evidence of epithelial hyperplasia in E2 treated rats. Immunohistochemical analysis revealed a decrease in estrogen receptor α (ERα) and proliferating cell nuclear antigen (PCNA), and an increase in cleaved-caspase3 and peroxisome proliferator-activated receptor γ (PPARγ) in the γ-TmT treated rats, indicating that tocopherol treatment inhibits cell proliferation and induces apoptosis. Treatment with γ-TmT resulted in a decrease in the expression of ERα mRNA, while ERβ and PPARγ mRNA levels were increased. These data suggest that γ-TmT inhibits the cell proliferation in mammary hyperplasia, suppresses the expression of inflammatory markers, and upregulates PPARγ. In conclusion, γ-TmT may be a promising agent for human breast cancer prevention. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 1851. doi:10.1158/1538-7445.AM2011-1851

  PublisherDOI

• Ethanolamine is a novel STAT-3 dependent cardioprotective agent

  Basic Research in Cardiology · 2010-10-12 · 61 citations

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  PublisherDOI

• Factors affecting the enzymatic hydrolysis of primary clarifier sludges

  cIRcle (University of British Columbia) · 2009-01-01

  articleOpen access1st authorCorresponding

  Bioconversion of cellulose to ethanol, by means of enzymatic hydrolysis, has been, and still is, the focus of much research interest since the early 1980s. The enzymatic hydrolysis process is well developed and offers an environmentally attractive option. However, many obstacles prevent the process from becoming commercially attractive. These obstacles include kinetic inhibitions (competitive reactions with lignin, intermediate and end-product inhibitions), difficulties in enzyme recycling, and economics. These hurdles have resulted in intense research over the last several decades. Despite the economic disadvantages of the enzymatic hydrolysis process, niche opportunities, such as the operations at the Tembec mill in Temiscaming, Quebec, still exist. The ethanol produced from its spent sulphite liquor is distilled to food-grade ethanol, which demands higher prices than fuel ethanol. Additional ethanol produced from Tembec's waste primary clarifier sludge (PCS), using enzymatic hydrolysis, could also be sold for similar use. This work explored several aspects of enzymatic hydrolysis to optimise the production of ethanol from Tembec's sulphite PCS. Batch hydrolysis results indicated that up to 50% of the PCS was hydrolysable by Trichoderma reesei enzymes. Adsorption experiments revealed that a significant fraction of enzyme activity was recoverable in the liquid hydrolysate. Oxygen delignification, as a pretreatment option for the PCS, was also examined. It was found that on a mass basis, a 68% increase in sugar yield from delignified PCS was possible over untreated PCS. A semi-continuous laboratory-scale hydrolysis reactor (22 L working volume) was run on both untreated and oxygen delignified PCS. In both cases, the yields represented 90% of the levels attained by batch hydrolysis.

  PublisherDOI

Recent grants

• NIH Grant R01GM044982

  NIH · $1.7M · 2001

Frequent coauthors

• Wayne Levin

  Icahn School of Medicine at Mount Sinai

  59 shared

• Dene E. Ryan

  California Institute of Technology

  49 shared

• Lauren M. Aleksunes

  Environmental and Occupational Health Sciences Institute

  20 shared

• Wen Xia

  Rutgers, The State University of New Jersey

  20 shared

• Angela L. Slitt

  University of Rhode Island

  18 shared

• Robert J. King

  University of Rhode Island

  16 shared

• Ajay C. Donepudi

  16 shared

• Donald M. Jerina

  National Institute of Diabetes and Digestive and Kidney Diseases

  14 shared

Education

• M.D.

  Yale University, School of Medicine

  1977

• B.S.

  Yale University

  1973