S J James

Summary

Affiliation: Food and Drug Administration
Country: USA

Publications

  1. ncbi Elevation in S-adenosylhomocysteine and DNA hypomethylation: potential epigenetic mechanism for homocysteine-related pathology
    S Jill James
    Division of Biochemical Toxicology, National Center for Toxicological Research, Jefferson, AR 72079, USA
    J Nutr 132:2361S-2366S. 2002
  2. pmc Upregulation of apoptosis with dietary restriction: implications for carcinogenesis and aging
    S J James
    Division of Biochemical Toxicology, U S Food and Drug Administration, National Center for Toxicological Research, Jefferson, AR 72079, USA
    Environ Health Perspect 106:307-12. 1998
  3. ncbi Abnormal folate metabolism and mutation in the methylenetetrahydrofolate reductase gene may be maternal risk factors for Down syndrome
    S J James
    Food and Drug Administration National Center for Toxicological Research, the Division of Biochemical Toxicology, Jefferson, AR 72079, USA
    Am J Clin Nutr 70:495-501. 1999
  4. pmc Homocysteine metabolism in children with Down syndrome: in vitro modulation
    M Pogribna
    Division of Biochemical Toxicology, Food and Drug Administration, National Center for Toxicological Research, Jefferson, AR 72079, USA
    Am J Hum Genet 69:88-95. 2001
  5. doi Role of DNA damage and alterations in cytosine DNA methylation in rat liver carcinogenesis induced by a methyl-deficient diet
    Igor P Pogribny
    Division of Biochemical Toxicology, National Center for Toxicological Research, Jefferson, AR 72079, USA
    Mutat Res 669:56-62. 2009
  6. ncbi P53 synthesis and phosphorylation in the aging diet-restricted rat following retinoic acid administration
    J L Pipkin
    Division of Genetic Toxicology, National Center for Toxicological Research, Jefferson, AR 72079 9502, USA
    Mech Ageing Dev 97:15-34. 1997
  7. ncbi De novo methylation of the p16INK4A gene in early preneoplastic liver and tumors induced by folate/methyl deficiency in rats
    Igor P Pogribny
    Division of Biochemical Toxicology, Federal Drug Administration, National Center for Toxicological Research, 3900 NCTR Road, Jefferson, AR 72079, USA
    Cancer Lett 187:69-75. 2002
  8. ncbi Genomic hypomethylation is specific for preneoplastic liver in folate/methyl deficient rats and does not occur in non-target tissues
    Igor P Pogribny
    Division of Biochemical Toxicology, FDA National Center for Toxicological Research, NCTR, 3900 NCTR Road, Jefferson, AR 72079, USA
    Mutat Res 548:53-9. 2004
  9. ncbi Irreversible global DNA hypomethylation as a key step in hepatocarcinogenesis induced by dietary methyl deficiency
    Igor P Pogribny
    Division of Biochemical Toxicology, National Center for Toxicological Research, 3900 NCTR Dr, Jefferson, AR 72079, USA
    Mutat Res 593:80-7. 2006
  10. ncbi Reduction of p53 gene expression in human primary hepatocellular carcinoma is associated with promoter region methylation without coding region mutation
    I P Pogribny
    Division of Biochemical Toxicology, National Center for Toxicological Research, Food and Drug Administration, 3900 NCTR Road, Jefferson, AR 72079, USA
    Cancer Lett 176:169-74. 2002

Collaborators

Detail Information

Publications49

  1. ncbi Elevation in S-adenosylhomocysteine and DNA hypomethylation: potential epigenetic mechanism for homocysteine-related pathology
    S Jill James
    Division of Biochemical Toxicology, National Center for Toxicological Research, Jefferson, AR 72079, USA
    J Nutr 132:2361S-2366S. 2002
    ..SAH-mediated DNA hypomethylation and associated alterations in gene expression and chromatin structure may provide new hypotheses for pathogenesis of diseases related to homocysteinemia...
  2. pmc Upregulation of apoptosis with dietary restriction: implications for carcinogenesis and aging
    S J James
    Division of Biochemical Toxicology, U S Food and Drug Administration, National Center for Toxicological Research, Jefferson, AR 72079, USA
    Environ Health Perspect 106:307-12. 1998
    ..If during tumor promotion an adaptive increase in apoptosis effectively balances the dysregulated increase proliferation, the risk of permanent genetic error and carcinogenesis would be minimized...
  3. ncbi Abnormal folate metabolism and mutation in the methylenetetrahydrofolate reductase gene may be maternal risk factors for Down syndrome
    S J James
    Food and Drug Administration National Center for Toxicological Research, the Division of Biochemical Toxicology, Jefferson, AR 72079, USA
    Am J Clin Nutr 70:495-501. 1999
    ..Although advanced maternal age is a major risk factor for trisomy 21, most children with Down syndrome are born to mothers <30 y of age...
  4. pmc Homocysteine metabolism in children with Down syndrome: in vitro modulation
    M Pogribna
    Division of Biochemical Toxicology, Food and Drug Administration, National Center for Toxicological Research, Jefferson, AR 72079, USA
    Am J Hum Genet 69:88-95. 2001
    ..The decreased availability of homocysteine promotes the well-established "folate trap," creating a functional folate deficiency that may contribute to the metabolic pathology of this complex genetic disorder...
  5. doi Role of DNA damage and alterations in cytosine DNA methylation in rat liver carcinogenesis induced by a methyl-deficient diet
    Igor P Pogribny
    Division of Biochemical Toxicology, National Center for Toxicological Research, Jefferson, AR 72079, USA
    Mutat Res 669:56-62. 2009
    ..Additionally, the results indicate that epigenetic changes may be more reliable markers than DNA lesions of the carcinogenic process and carcinogen exposure...
  6. ncbi P53 synthesis and phosphorylation in the aging diet-restricted rat following retinoic acid administration
    J L Pipkin
    Division of Genetic Toxicology, National Center for Toxicological Research, Jefferson, AR 72079 9502, USA
    Mech Ageing Dev 97:15-34. 1997
    ..Further, these results confirm and extend our previous observations that chronic diet-restriction attenuates the age related decline in the metabolic activity of nuclear protein products...
  7. ncbi De novo methylation of the p16INK4A gene in early preneoplastic liver and tumors induced by folate/methyl deficiency in rats
    Igor P Pogribny
    Division of Biochemical Toxicology, Federal Drug Administration, National Center for Toxicological Research, 3900 NCTR Road, Jefferson, AR 72079, USA
    Cancer Lett 187:69-75. 2002
    ..Our data show that site-specific de novo methylation of 5' CpG island of p16 gene precedes tumor development and undergoes dynamic expansion during tumor progression...
  8. ncbi Genomic hypomethylation is specific for preneoplastic liver in folate/methyl deficient rats and does not occur in non-target tissues
    Igor P Pogribny
    Division of Biochemical Toxicology, FDA National Center for Toxicological Research, NCTR, 3900 NCTR Road, Jefferson, AR 72079, USA
    Mutat Res 548:53-9. 2004
    ..They also demonstrate that DNA hypomethylation is localized to tissue that undergoes carcinogenesis, and is not altered in non-target tissues...
  9. ncbi Irreversible global DNA hypomethylation as a key step in hepatocarcinogenesis induced by dietary methyl deficiency
    Igor P Pogribny
    Division of Biochemical Toxicology, National Center for Toxicological Research, 3900 NCTR Dr, Jefferson, AR 72079, USA
    Mutat Res 593:80-7. 2006
    ..These results provide an experimental evidence and a mechanistic basis by which epigenetic alterations may contribute to the initiation and promotion steps of carcinogenesis...
  10. ncbi Reduction of p53 gene expression in human primary hepatocellular carcinoma is associated with promoter region methylation without coding region mutation
    I P Pogribny
    Division of Biochemical Toxicology, National Center for Toxicological Research, Food and Drug Administration, 3900 NCTR Road, Jefferson, AR 72079, USA
    Cancer Lett 176:169-74. 2002
    ..None of the samples exhibited coding region mutations. Given that p53 mutations are rare in primary human liver tumors, these data suggest that transcriptional repression by p53 promoter methylation may contribute to tumor progression...
  11. pmc Pi-class glutathione-S-transferase-positive hepatocytes in aging B6C3F1 mice undergo apoptosis induced by dietary restriction
    L Muskhelishvili
    Division of Nutritional Toxicology, FDA National Center for Toxicological Research, Jefferson, Arkansas, USA
    Am J Pathol 149:1585-91. 1996
    ..These results suggest that spontaneous, potentially preneoplastic hepatocytes in tumor-prone B6C3F1 mice are eliminated by apoptosis with dietary restriction...
  12. ncbi Lack of embryotoxicity of homocysteine thiolactone in mouse embryos in vitro
    D K Hansen
    Division of Genetic and Reproductive Toxicology, National Center for Toxicological Research, Food and Drug Administration, Jefferson, Arkansas 72079 9502, USA
    Reprod Toxicol 15:239-44. 2001
    ..These data suggest that homocysteine does not produce NTDs in mouse embryos cultured in vitro and that early organogenesis-stage embryos are able to metabolize homocysteine...
  13. pmc Interactions of ethanol and folate deficiency in development of alcoholic liver disease in the micropig
    Charles H Halsted
    University of California, Davis, California and National Toxicological Research Center, Jefferson, Arkansas, USA
    Trans Am Clin Climatol Assoc 113:151-62; discussion 162-3. 2002
    ..Thus, the development of ALD is linked to abnormal methionine metabolism and is accelerated in the presence of folate deficiency...
  14. ncbi Maternal metabolic phenotype and risk of Down syndrome: beyond genetics
    S Jill James
    Department of Pediatrics, University of Arkansas for Medical Sciences, Little Rock, AR 72202, USA
    Am J Med Genet A 127:1-4. 2004
  15. pmc Betaine rescue of an animal model with methylenetetrahydrofolate reductase deficiency
    Bernd C Schwahn
    Department of Pediatrics, Human Genetics and Biology, McGill University Montreal Children s Hospital, Montreal, Canada
    Biochem J 382:831-40. 2004
    ....
  16. ncbi Uteroplacental insufficiency alters DNA methylation, one-carbon metabolism, and histone acetylation in IUGR rats
    Nicole K Maclennan
    David Geffen School of Medicine, UCLA, Department of Pediatrics, Division of Neonatology and Developmental Biology, Mattel Children s Hospital, UCLA, Los Angeles, California, 90095 1752, USA
    Physiol Genomics 18:43-50. 2004
    ....
  17. ncbi Metabolic biomarkers of increased oxidative stress and impaired methylation capacity in children with autism
    S Jill James
    Department of Pediatrics, University of Arkansas for Medical Sciences, and the Arkansas Children s Hospital Research Institute, Little Rock, AR 72202, USA
    Am J Clin Nutr 80:1611-7. 2004
    ..Although abnormal metabolism of methionine and homocysteine has been associated with other neurologic diseases, these pathways have not been evaluated in persons with autism...
  18. ncbi Congenital heart defects and abnormal maternal biomarkers of methionine and homocysteine metabolism
    Charlotte A Hobbs
    Department of Pediatrics, College of Medicine, University of Arkansas for Medical Sciences and Arkansas Children s Hospital Research Institute, Little Rock, AR 72211, USA
    Am J Clin Nutr 81:147-53. 2005
    ..It is well established that folic acid prevents neural tube defects. Although the mechanisms remain unclear, multivitamins containing folic acid may also protect against other birth defects, including congenital heart defects...
  19. ncbi Phosphatidylcholine and lysophosphatidylcholine excretion is increased in children with cystic fibrosis and is associated with plasma homocysteine, S-adenosylhomocysteine, and S-adenosylmethionine
    Alice H Chen
    Department of Paediatrics and the Nutrition Research Program, University of British Columbia, Vancouver, Canada
    Am J Clin Nutr 81:686-91. 2005
    ..The intestinal absorption of phosphatidylcholine in CF is unknown...
  20. ncbi No association between common polymorphisms in genes of folate and homocysteine metabolism and the risk of Down's syndrome among French mothers
    Abalo Chango
    INSERM U 724, Laboratory of Nutritional Genomics, ISAB Agrohealth, 60026 Beauvais, France
    Br J Nutr 94:166-9. 2005
    ..The risk of having a child with trisomy 21 did not appear to be linked to polymorphisms in genes associated with folate and homocysteine metabolism...
  21. ncbi Congenital heart defects and maternal biomarkers of oxidative stress
    Charlotte A Hobbs
    Department of Pediatrics, College of Medicine, University of Arkansas for Medical Sciences, Little Rock, AR 72211, USA
    Am J Clin Nutr 82:598-604. 2005
    ....
  22. ncbi Congenital heart defects, maternal homocysteine, smoking, and the 677 C>T polymorphism in the methylenetetrahydrofolate reductase gene: evaluating gene-environment interactions
    Charlotte A Hobbs
    Department of Pediatrics, Arkansas Children s Hospital Research Institute, University of Arkansas for Medical Sciences, College of Medicine, Little Rock, AR, USA
    Am J Obstet Gynecol 194:218-24. 2006
    ..This study was undertaken to investigate the association between congenital heart defects (CHD), and maternal homocysteine, smoking, and the MTHFR 677 C>T polymorphism...
  23. pmc Neural tube defects and maternal biomarkers of folate, homocysteine, and glutathione metabolism
    Weizhi Zhao
    Section of Birth Defects Research, Department of Pediatrics, Arkansas Children s Hospital Research Institute, College of Medicine, University of Arkansas for Medical Sciences, Little Rock, 72211, USA
    Birth Defects Res A Clin Mol Teratol 76:230-6. 2006
    ..Alterations in maternal folate and homocysteine metabolism are associated with neural tube defects (NTDs). The role played by specific micronutrients and metabolites in the causal pathway leading to NTDs is not fully understood...
  24. ncbi A mathematical model gives insights into nutritional and genetic aspects of folate-mediated one-carbon metabolism
    Michael C Reed
    Department of Mathematics, Duke University, Durham, NC 27708, USA
    J Nutr 136:2653-61. 2006
    ..These mathematical simulations of folate-mediated 1-carbon metabolism provide a cost-efficient approach to in silico experimentation that can complement and help guide laboratory studies...
  25. ncbi Choline-related supplements improve abnormal plasma methionine-homocysteine metabolites and glutathione status in children with cystic fibrosis
    Sheila M Innis
    Department of Paediatrics, University of British Columbia, Vancouver, BC, Canada
    Am J Clin Nutr 85:702-8. 2007
    ....
  26. ncbi Long-range allosteric interactions between the folate and methionine cycles stabilize DNA methylation reaction rate
    H Frederik Nijhout
    Department of Biology, Duke University, Durham, North Carolina 27708, USA
    Epigenetics 1:81-7. 2006
    ..In silico experimentation allows us to evaluate the independent effects of various combinations of the long-range interactions, and thereby propose a plausible evolutionary scenario...
  27. pmc Metabolic endophenotype and related genotypes are associated with oxidative stress in children with autism
    S Jill James
    Department of Pediatrics, University of Arkansas for Medical Sciences, Arkansas Children s Hospital Research Institute, Little Rock, Arkansas 72202, USA
    Am J Med Genet B Neuropsychiatr Genet 141:947-56. 2006
    ..We propose that an increased vulnerability to oxidative stress (endogenous or environmental) may contribute to the development and clinical manifestations of autism...
  28. ncbi S-adenosylhomocysteine, but not homocysteine, is toxic to yeast lacking cystathionine beta-synthase
    Scott A Christopher
    Division of Population Science, Fox Chase Cancer Center, 7701 Burholme Avenue, Philadelphia, PA 19111, USA
    Mol Genet Metab 75:335-43. 2002
    ..We hypothesize that elevated extracellular homocysteine present in humans may reflect an altered intracellular SAM/SAH ratio and that this may be related to disease pathogenesis...
  29. pmc Folate deficiency disturbs hepatic methionine metabolism and promotes liver injury in the ethanol-fed micropig
    Charles H Halsted
    Department of Internal Medicine, School of Medicine, University of California, Davis, CA 95616, USA
    Proc Natl Acad Sci U S A 99:10072-7. 2002
    ..Steatohepatitis occurred in five of six pigs in FDE but not in the other groups. In summary, folate deficiency enhances perturbations in hepatic methionine metabolism and DNA damage while promoting alcoholic liver injury...
  30. ncbi Cobalamin deficiency with and without neurologic abnormalities: differences in homocysteine and methionine metabolism
    Ralph Carmel
    Department of Medicine, New York Methodist Hospital, Brooklyn, NY, USA
    Blood 101:3302-8. 2003
    ..The origin of the folate differences is unclear and possibly varied. Low AdoMet and GSH levels were independent predictors of anemia...
  31. ncbi Impact of Dnmt1 deficiency, with and without low folate diets, on tumor numbers and DNA methylation in Min mice
    Jacquetta Trasler
    Department of Pediatrics, McGill University Montreal Children s Hospital, 4060 Ste Catherine St West, Montreal, Quebec H3Z 2Z3, Canada
    Carcinogenesis 24:39-45. 2003
    ....
  32. ncbi Mechanisms of DNA damage, DNA hypomethylation, and tumor progression in the folate/methyl-deficient rat model of hepatocarcinogenesis
    S Jill James
    Department of Pediatrics, University of Arkansas for Medical Sciences, Little Rock, AR 72202, USA
    J Nutr 133:3740S-3747S. 2003
    ..These insights in an experimental model are consistent with the possibility that DNA lesions may be a necessary prerequisite for the disruption of normal DNA methylation patterns in preneoplastic and neoplastic cells...
  33. ncbi Methyl deficiency causes reduction of the methyl-CpG-binding protein, MeCP2, in rat liver
    Farah Esfandiari
    University of California Davis, School of Medicine, Department of Medical Pathology, Research 3, Room 3200A, 4645 Second Avenue, Sacramento, CA 95817, USA
    Carcinogenesis 24:1935-40. 2003
    ..Reduction of MeCP2 protein expression may influence the initiation and/or progression of hepatic cancer induced by methyl deficiency and may provide a useful marker of pre-neoplastic change...
  34. pmc Suppression of the protein tyrosine phosphatase receptor type O gene (PTPRO) by methylation in hepatocellular carcinomas
    Tasneem Motiwala
    Department of Molecular and Cellular Biochemistry, The Ohio State University, Columbus, OH 43210, USA
    Oncogene 22:6319-31. 2003
    ....
  35. ncbi Increased plasma homocysteine and S-adenosylhomocysteine and decreased methionine is associated with altered phosphatidylcholine and phosphatidylethanolamine in cystic fibrosis
    Sheila M Innis
    Department of Pediatrics, University of British Columbia, Vancouver, BC, Canada
    J Pediatr 143:351-6. 2003
    ..Methyl groups from methionine via SAM are used for sequential methylation of PE to form phosphatidylcholine (PC) with the generation of S-adenosylhomocysteine (SAH) and homocysteine...
  36. ncbi Effects of dietary folate intake and folate binding protein-1 (Folbp1) on urinary speciation of sodium arsenate in mice
    Ofer Spiegelstein
    Center for Environmental and Genetic Medicine, Institute of Biosciences and Technology, Texas A and M University System Health Science Center, 77030, Houston, TX, USA
    Toxicol Lett 145:167-74. 2003
    ..The present data suggest that inadequate folate intake may result in decreased biotransformation and excretion of arsenic, which is likely to increase arsenic exposure and related toxicities...
  37. ncbi Studies of methionine cycle intermediates (SAM, SAH), DNA methylation and the impact of folate deficiency on tumor numbers in Min mice
    Sahar Sibani
    Department of Pediatrics, McGill University Montreal Children s Hospital Research Institute, 4060 Ste Catherine Street West, Montreal, Quebec H3Z 2Z3, Canada
    Carcinogenesis 23:61-5. 2002
    ..As an increase in tumor numbers was observed only in folate- and choline-deficient mice with low levels of SAM and DNA hypomethylation, the modulatory role of folate may be dependent on the transformation state of the cell...
  38. ncbi NKX2.5 and congenital heart defects: A population-based study
    Charlotte A Hobbs
    Am J Med Genet A 134:223-5. 2005
  39. ncbi Altered expression of methylenetetrahydrofolate reductase modifies response to methotrexate in mice
    Basak Celtikci
    Departments of Human Genetics and Pediatrics, McGill University Health Centre, Montreal Children s Hospital Research Institute, Montreal, Quebec, Canada
    Pharmacogenet Genomics 18:577-89. 2008
    ..To study potential interactions between MTHFR activity and MTX, we examined the impact of decreased and increased MTHFR expression on MTX response in mice...
  40. pmc A mathematical model of glutathione metabolism
    Michael C Reed
    Department of Mathematics, Duke University, Durham, NC 27708, USA
    Theor Biol Med Model 5:8. 2008
    ..Deficits in glutathione have been implicated in aging and a host of diseases including Alzheimer's disease, Parkinson's disease, cardiovascular disease, cancer, Down syndrome and autism...
  41. ncbi Dextromethorphan is effective in the treatment of subacute methotrexate neurotoxicity
    Richard A Drachtman
    Cancer Institute of New Jersey Robert Wood Johnson Medical School, New Brunswick 08816, USA
    Pediatr Hematol Oncol 19:319-27. 2002
    ..These data provide support for a placebo-controlled clinical trial to examine the ability of DM to prevent or alleviate MTX-Ntox...
  42. ncbi Alcohol abuse: an important cause of severe hyperhomocysteinemia
    Ralph Carmel
    Department of Medicine, New York Methodist Hospital, Brooklyn, NY 11215, USA
    Nutr Rev 60:215-21. 2002
    ..Both patients had severe neurologic symptoms as well as macrocytic red blood cells, which, along with the high homocysteine levels, were misattributed to cobalamin deficiency, in one case despite serum cobalamin levels that were normal...
  43. pmc Targeting Ras signaling through inhibition of carboxyl methylation: an unexpected property of methotrexate
    Ann M Winter-Vann
    Department of Pharmacology and Cancer Biology, Duke University Medical Center, Durham, NC 27710, USA
    Proc Natl Acad Sci U S A 100:6529-34. 2003
    ..These results suggest that inhibition of Icmt is a critical component of the antiproliferative effect of methotrexate, expanding our understanding of this widely used drug and identifying Icmt as a target for drug discovery...
  44. ncbi Abnormal transsulfuration and glutathione metabolism in the micropig model of alcoholic liver disease
    Jesus A Villanueva
    Department of Internal Medicine, University of California, Davis, California 95616, USA
    Alcohol Clin Exp Res 30:1262-70. 2006
    ....
  45. ncbi Preferential transmission of the MTHFR 677 T allele to infants with Down syndrome: implications for a survival advantage
    Charlotte A Hobbs
    Arkansas Center for Birth Defects Research and Prevention, Arkansas Children s Hospital, University of Arkansas for Medical Sciences, Little Rock, Arkansas, USA
    Am J Med Genet 113:9-14. 2002
    ..Published 2002 Wiley-Liss, Inc...
  46. ncbi Maternal homocysteine and congenital heart defects
    Charlotte A Hobbs
    J Am Coll Cardiol 47:683-5. 2006
  47. ncbi Prenatal origin of GATA1 mutations may be an initiating step in the development of megakaryocytic leukemia in Down syndrome
    Jeffrey W Taub
    Blood 104:1588-9. 2004
  48. ncbi Genome hypermethylation in Pinus silvestris of Chernobyl--a mechanism for radiation adaptation?
    Olga Kovalchuk
    Department of Biological Sciences, University of Lethbridge, 4401 University Drive, Lethbridge, Alta, Canada T1K 3M4
    Mutat Res 529:13-20. 2003
    ..Further studies are clearly needed to analyze in detail the involvement of DNA methylation and other epigenetic mechanisms in the complex process of radiation stress and adaptive response...
  49. pmc S-adenosylhomocysteine hydrolase deficiency in a human: a genetic disorder of methionine metabolism
    Ivo Baric
    Department of Pediatrics, University Hospital Center, Kispaticeva 12, 10000 Zagreb, Croatia
    Proc Natl Acad Sci U S A 101:4234-9. 2004
    ..Gene analysis revealed two mutations in exon 4: a maternally derived stop codon, and a paternally derived missense mutation. We discuss reasons for biochemical abnormalities and pathophysiological aspects of AdoHcy hydrolase deficiency...