T R Devereux

Summary

Affiliation: National Institutes of Health
Country: USA

Publications

  1. ncbi request reprint Map kinase activation correlates with K-ras mutation and loss of heterozygosity on chromosome 6 in alveolar bronchiolar carcinomas from B6C3F1 mice exposed to vanadium pentoxide for 2 years
    Theodora R Devereux
    Laboratory of Molecular Carcinogenesis, National Institute of Environmental Health Sciences, PO Box 12233, National Institutes of Health, Research Triangle Park, NC 27709, USA
    Carcinogenesis 23:1737-43. 2002
  2. ncbi request reprint The putative tumor suppressor Tsc-22 is downregulated early in chemically induced hepatocarcinogenesis and may be a suppressor of Gadd45b
    Mari Iida
    Laboratory of Molecular Carcinogenesis, Toxicology Operations Branch, Environmental Toxicology Program, National Institute of Environmental Health Sciences, National Institute of Health, Research Triangle Park, NC 27709, USA
    Toxicol Sci 99:43-50. 2007
  3. ncbi request reprint DNA methylation analysis of the promoter region of the human telomerase reverse transcriptase (hTERT) gene
    T R Devereux
    Laboratory of Molecular Carcinogenesis, National Institute of Environmental Health Sciences, NIH, Research Triangle Park, North Carolina 27709, USA
    Cancer Res 59:6087-90. 1999
  4. ncbi request reprint Use of quantitative trait loci to map murine lung tumor susceptibility genes
    T R Devereux
    Laboratory of Molecular Carcinogenesis, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina, USA
    Exp Lung Res 24:407-17. 1998
  5. ncbi request reprint High frequency of codon 61 K-ras A-->T transversions in lung and Harderian gland neoplasms of B6C3F1 mice exposed to chloroprene (2-chloro-1,3-butadiene) for 2 years, and comparisons with the structurally related chemicals isoprene and 1,3-butadiene
    R C Sills
    Environmental Toxicology Program, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709, USA
    Carcinogenesis 20:657-62. 1999
  6. ncbi request reprint Hypermethylation of the p16 (Ink4a) promoter in B6C3F1 mouse primary lung adenocarcinomas and mouse lung cell lines
    A C Patel
    Laboratory of Molecular Carcinogenesis, Chemical Exposures and Molecular Biology Branch, National Institute of Environmental Health Sciences, PO Box 12233, Research Triangle Park, NC 27709, USA
    Carcinogenesis 21:1691-700. 2000
  7. ncbi request reprint o-Nitrotoluene-induced large intestinal tumors in B6C3F1 mice model human colon cancer in their molecular pathogenesis
    R C Sills
    Laboratory of Experimental Pathology, National Institute of Environmental Health Sciences PO Box 12233, Research Triangle Park, NC 27709, USA
    Carcinogenesis 25:605-12. 2004
  8. ncbi request reprint High frequency of ras mutations in forestomach and lung tumors of B6C3F1 mice exposed to 1-amino-2,4-dibromoanthraquinone for 2 years
    S Hayashi
    Laboratory of Experimental Pathology, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709, USA
    Toxicol Pathol 29:422-9. 2001
  9. ncbi request reprint Point mutations of K-ras and H-ras genes in forestomach neoplasms from control B6C3F1 mice and following exposure to 1,3-butadiene, isoprene or chloroprene for up to 2-years
    R C Sills
    Laboratory of Experimental Pathology, Environmental Toxicology Program, National Institute of Environmental Health Sciences, PO Box 12233, Research Triangle Park, NC 27709, USA
    Chem Biol Interact 135:373-86. 2001
  10. ncbi request reprint Smad4 (homolog of human DPC4) and Smad2 (homolog of human JV18-1): candidates for murine lung tumor resistance and suppressor genes
    T R Devereux
    Laboratory of Molecular Carcinogenesis, NIEHS, Research Triangle Park, NC 27709, USA
    Carcinogenesis 18:1751-5. 1997

Collaborators

Detail Information

Publications38

  1. ncbi request reprint Map kinase activation correlates with K-ras mutation and loss of heterozygosity on chromosome 6 in alveolar bronchiolar carcinomas from B6C3F1 mice exposed to vanadium pentoxide for 2 years
    Theodora R Devereux
    Laboratory of Molecular Carcinogenesis, National Institute of Environmental Health Sciences, PO Box 12233, National Institutes of Health, Research Triangle Park, NC 27709, USA
    Carcinogenesis 23:1737-43. 2002
    ..These results suggest that MAPK is activated during vanadium pentoxide-induced B6C3F1 mouse lung tumorigenesis following K-ras mutation and loss of the wild-type K-ras allele...
  2. ncbi request reprint The putative tumor suppressor Tsc-22 is downregulated early in chemically induced hepatocarcinogenesis and may be a suppressor of Gadd45b
    Mari Iida
    Laboratory of Molecular Carcinogenesis, Toxicology Operations Branch, Environmental Toxicology Program, National Institute of Environmental Health Sciences, National Institute of Health, Research Triangle Park, NC 27709, USA
    Toxicol Sci 99:43-50. 2007
    ..These data provide evidence that Tsc-22 is a suppressor of Gadd45b expression, which may contribute to an early antiapoptotic response...
  3. ncbi request reprint DNA methylation analysis of the promoter region of the human telomerase reverse transcriptase (hTERT) gene
    T R Devereux
    Laboratory of Molecular Carcinogenesis, National Institute of Environmental Health Sciences, NIH, Research Triangle Park, North Carolina 27709, USA
    Cancer Res 59:6087-90. 1999
    ..This study indicates that there are multiple levels of regulation of hTERT expression in CpG island methylation-dependent and -independent manners...
  4. ncbi request reprint Use of quantitative trait loci to map murine lung tumor susceptibility genes
    T R Devereux
    Laboratory of Molecular Carcinogenesis, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina, USA
    Exp Lung Res 24:407-17. 1998
    ..In this overview we discuss the design of QTL mapping studies and some of the findings from studies on the mapping of murine lung tumor susceptibility loci...
  5. ncbi request reprint High frequency of codon 61 K-ras A-->T transversions in lung and Harderian gland neoplasms of B6C3F1 mice exposed to chloroprene (2-chloro-1,3-butadiene) for 2 years, and comparisons with the structurally related chemicals isoprene and 1,3-butadiene
    R C Sills
    Environmental Toxicology Program, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709, USA
    Carcinogenesis 20:657-62. 1999
    ..The major finding of K-ras A-->T transversions in lung and Harderian gland neoplasms suggests that this mutation may be important for tumor induction by this class of carcinogens...
  6. ncbi request reprint Hypermethylation of the p16 (Ink4a) promoter in B6C3F1 mouse primary lung adenocarcinomas and mouse lung cell lines
    A C Patel
    Laboratory of Molecular Carcinogenesis, Chemical Exposures and Molecular Biology Branch, National Institute of Environmental Health Sciences, PO Box 12233, Research Triangle Park, NC 27709, USA
    Carcinogenesis 21:1691-700. 2000
    ..These are the first reported studies to provide strong evidence that DNA methylation is a mechanism for p16 inactivation in mouse lung tumors...
  7. ncbi request reprint o-Nitrotoluene-induced large intestinal tumors in B6C3F1 mice model human colon cancer in their molecular pathogenesis
    R C Sills
    Laboratory of Experimental Pathology, National Institute of Environmental Health Sciences PO Box 12233, Research Triangle Park, NC 27709, USA
    Carcinogenesis 25:605-12. 2004
    ..These alterations, which are hallmarks of human colon cancer, probably contributed to the pathogenesis of the large intestinal carcinomas in mice following o-nitrotoluene exposure...
  8. ncbi request reprint High frequency of ras mutations in forestomach and lung tumors of B6C3F1 mice exposed to 1-amino-2,4-dibromoanthraquinone for 2 years
    S Hayashi
    Laboratory of Experimental Pathology, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709, USA
    Toxicol Pathol 29:422-9. 2001
    ..major finding of A to T transversions or A to G transitions in forestomach and lung tumors suggests that ADBAQ or its metabolites target adenine bases in the ras proto-oncogenes and that these mutations play a dominant role in multi-organ..
  9. ncbi request reprint Point mutations of K-ras and H-ras genes in forestomach neoplasms from control B6C3F1 mice and following exposure to 1,3-butadiene, isoprene or chloroprene for up to 2-years
    R C Sills
    Laboratory of Experimental Pathology, Environmental Toxicology Program, National Institute of Environmental Health Sciences, PO Box 12233, Research Triangle Park, NC 27709, USA
    Chem Biol Interact 135:373-86. 2001
    ....
  10. ncbi request reprint Smad4 (homolog of human DPC4) and Smad2 (homolog of human JV18-1): candidates for murine lung tumor resistance and suppressor genes
    T R Devereux
    Laboratory of Molecular Carcinogenesis, NIEHS, Research Triangle Park, NC 27709, USA
    Carcinogenesis 18:1751-5. 1997
    ..Thus, in this study we found no evidence that either Smad4 or Smad2 represents the Par2 lung tumor resistance locus or is a lung tumor suppressor gene in the B6CF1 mice...
  11. ncbi request reprint Sequence and chromosomal mapping of the mouse homolog (Madh4) of the human DPC4/MADH4 gene
    C H Anna
    Laboratory of Molecular Carcinogenesis, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709, USA
    Mamm Genome 8:443-4. 1997
  12. ncbi request reprint Frequency of ras mutations in liver neoplasms from B6C3F1 mice exposed to tetrafluoroethylene for two years
    H H Hong
    Environmental Toxicology Program, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709, USA
    Toxicol Pathol 26:646-50. 1998
    ..The ras mutation frequency and spectrum were similar to those of the structurally related chemical tetrachloroethylene...
  13. ncbi request reprint Comparison of pulmonary O6-methylguanine DNA adduct levels and Ki-ras activation in lung tumors from resistant and susceptible mouse strains
    T R Devereux
    Laboratory of Molecular Toxicology, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709
    Mol Carcinog 8:177-85. 1993
    ..Thus, although Ki-ras activation was detected in some tumors, pathways independent of ras activation and p53 inactivation also appear to be involved in lung tumorigenesis in this resistant mouse strain...
  14. ncbi request reprint Allelotype analysis of mouse lung carcinomas reveals frequent allelic losses on chromosome 4 and an association between allelic imbalances on chromosome 6 and K-ras activation
    M E Hegi
    Laboratory of Molecular Carcinogenesis, National Institute of Environmental Health Sciences, NIH, Research Triangle Park, North Carolina 27709
    Cancer Res 54:6257-64. 1994
    ..Finally, an association between K-ras gene activation and allelic imbalances on chromosome 6 was observed for B6C3F1 lung tumors...
  15. ncbi request reprint Loss of E-cadherin expression in gastric intestinal metaplasia and later stage p53 altered expression in gastric carcinogenesis
    T R Devereux
    Laboratory of Experimental Pathology and NIEHS, NIH, Research Triangle Park, NC 27709, USA
    Exp Toxicol Pathol 53:237-46. 2001
    ..These results suggest that the Wnt signaling pathway is not upregulated in this type of cancer...
  16. ncbi request reprint Chemical-specific alterations in ras, p53, and beta-catenin genes in hemangiosarcomas from B6C3F1 mice exposed to o-nitrotoluene or riddelliine for 2 years
    H L Hong
    Laboratory of Experimental Pathology, National Institute of Environmental Health Sciences, P O Box 12233, Research Triangle Park, NC 27709, USA
    Toxicol Appl Pharmacol 191:227-34. 2003
    ..It also suggests that these mutations play a role in the pathogenesis of the respective hemangiosarcomas in B6C3F1(1) mice...
  17. ncbi request reprint Assignment of a locus for mouse lung tumor susceptibility to proximal chromosome 19
    T R Devereux
    Environmental Carcinogenesis Program, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709
    Mamm Genome 5:749-55. 1994
    ..Linkage analysis on Chr 19 with 270 AB6N2 mice localized the region flanked by D19Mit42 and D19Mit19 that is most closely associated with lung tumor susceptibility. The Pas3 locus may be an enhancer of the susceptibility locus on Chr 6...
  18. ncbi request reprint CTNNB1 mutations and beta-catenin protein accumulation in human hepatocellular carcinomas associated with high exposure to aflatoxin B1
    T R Devereux
    Laboratory of Molecular Carcinogenesis, National Institute of Environmental Health Sciences, NIH, Research Triangle Park, North Carolina 27709, USA
    Mol Carcinog 31:68-73. 2001
    ..Published 2001 Wiley-Liss, Inc...
  19. ncbi request reprint Mutations of ras protooncogenes and p53 tumor suppressor gene in cardiac hemangiosarcomas from B6C3F1 mice exposed to 1,3-butadiene for 2 years
    H H Hong
    Environmental Toxicology Program, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709, USA
    Toxicol Pathol 28:529-34. 2000
    ....
  20. ncbi request reprint High frequency of K-ras mutations in spontaneous and vinyl carbamate-induced lung tumors of relatively resistant B6CF1 (C57BL/6J x BALB/cJ) mice
    T E Massey
    Environmental Carcinogenesis Program, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709, USA
    Carcinogenesis 16:1065-9. 1995
    ..These results are consistent with previous findings in other mouse hybrids showing parental bias for K-ras mutations and suggest that mutation of the allele of the susceptible parent may provide a growth advantage to the tumor...
  21. ncbi request reprint Evaluation of genetic alterations in cancer-related genes in lung and brain tumors from B6C3F1 mice exposed to 1,3-butadiene or chloroprene
    Thai Vu Ton
    Environmental Toxicology Program and Environmental Carcinogenesis Program, National Institute of Environmental Health Sciences, MD B3 08, 111 Alexander Drive, Research Triangle Park, NC 27709, USA
    Chem Biol Interact 166:112-20. 2007
    ....
  22. ncbi request reprint Genetic alterations in K-ras and p53 cancer genes in lung neoplasms from Swiss (CD-1) male mice exposed transplacentally to AZT
    Hue Hua L Hong
    Laboratory of Experimental Pathology, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina, USA
    Environ Mol Mutagen 48:299-306. 2007
    ....
  23. ncbi request reprint Genetic alterations in brain tumors following 1,3-butadiene exposure in B6C3F1 mice
    Yongbaek Kim
    Laboratory of Experimental Pathology National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709, USA
    Toxicol Pathol 33:307-12. 2005
    ..The observed findings are similar in part to the genetic alterations reported in human brain tumors...
  24. ncbi request reprint Aberrant promoter hypermethylation of the death-associated protein kinase gene is early and frequent in murine lung tumors induced by cigarette smoke and tobacco carcinogens
    Leah C Pulling
    Lung Cancer Program, Lovelace Respiratory Research Institute, Albuquerque, New Mexico 87108, USA
    Cancer Res 64:3844-8. 2004
    ..This study is the first to use a murine model of cigarette smoke-induced lung cancer and demonstrate commonality for inactivation by promoter hypermethylation of a gene implicated in the development of this disease in humans...
  25. ncbi request reprint Carcinogen-specific targeting of chromosome 12 for loss of heterozygosity in mouse lung adenocarcinomas: implications for chromosome instability and tumor progression
    Christopher R Herzog
    Institute for Cancer Prevention, Valhalla, NY 10595, USA
    Oncogene 23:3033-9. 2004
    ....
  26. ncbi request reprint Predominant K-ras codon 12 G --> A transition in chemically induced lung neoplasms in B6C3F1 mice
    Thai Vu T Ton
    National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709, USA
    Toxicol Pathol 32:16-21. 2004
    ....
  27. ncbi request reprint Carcinogenic induction directs the selection of allelic losses in mouse lung tumorigenesis
    Christopher R Herzog
    American Health Foundation, Valhalla, New York 10595, USA
    Cancer Res 62:6424-9. 2002
    ....
  28. doi request reprint Gene expression studies demonstrate that the K-ras/Erk MAP kinase signal transduction pathway and other novel pathways contribute to the pathogenesis of cumene-induced lung tumors
    Nobuko Wakamatsu
    Cellular and Molecular Pathology Branch, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709, USA
    Toxicol Pathol 36:743-52. 2008
    ..The gene expression analysis suggested the formation of alveolar/bronchiolar carcinomas in cumene-exposed mice typically involves mutation of K-ras, which results in increased Erk MAP kinase signaling and modification of histones...
  29. ncbi request reprint Molecular profiling of mouse lung tumors: association with tumor progression, lung development, and human lung adenocarcinomas
    Allison E Bonner
    Division of Human Cancer Genetics, The Ohio State University Comprehensive Cancer Center, 420 West 12th Avenue, Columbus, OH 43210, USA
    Oncogene 23:1166-76. 2004
    ..We have also attempted to compare the expression profiles found in mouse lung cancers and those in human lung ACs...
  30. pmc Overview of the molecular carcinogenesis of mouse lung tumor models of human lung cancer
    Nobuko Wakamatsu
    Laboratory of Experimental Pathology, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709, USA
    Toxicol Pathol 35:75-80. 2007
    ..In this report, the major known molecular alterations in lung tumorigenesis of mice are reviewed and compared to those in humans...
  31. ncbi request reprint Perturbations of the Ink4a/Arf gene locus in aflatoxin B1-induced mouse lung tumors
    Andrew S Tam
    Queen s University, Department of Pharmacology and Toxicology, Kingston, Ontario K7L 3N6, Canada
    Carcinogenesis 24:121-32. 2003
    ....
  32. ncbi request reprint Analysis of p53 tumor suppressor gene, H-ras protooncogene and proliferating cell nuclear antigen (PCNA) in squamous cell carcinomas of HRA/Skh mice following exposure to 8-methoxypsoralen (8-MOP) and UVA radiation (PUVA therapy)
    Luca Lambertini
    Laboratory of Experimental Pathology, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709, USA
    Toxicol Pathol 33:292-9. 2005
    ..The p53 mutational frequency and patterns from our study were different from those reported in human PUVA-type tumors...
  33. ncbi request reprint Analysis of the Par2 modifier of pulmonary adenoma formation in mice
    Min Wang
    Department of Surgery, Washington University School of Medicine, St Louis, MO, USA
    Exp Lung Res 31:193-204. 2005
    ..The authors recently conducted studies to positionally clone the Par2 gene. This review summarizes the effort and progress towards the identification of Par2 candidates...
  34. ncbi request reprint Unique patterns of gene expression changes in liver after treatment of mice for 2 weeks with different known carcinogens and non-carcinogens
    Mari Iida
    Laboratory of Molecular Carcinogenesis, National Institute of Environmental Health Sciences, National Institute of Health, Research Triangle Park, NC 27709, USA
    Carcinogenesis 26:689-99. 2005
    ....
  35. ncbi request reprint Expression of potential beta-catenin targets, cyclin D1, c-Jun, c-Myc, E-cadherin, and EGFR in chemically induced hepatocellular neoplasms from B6C3F1 mice
    Colleen H Anna
    Laboratory of Molecular Carcinogenesis NIEHS, NIH, Research Triangle Park, NC 27709, USA
    Toxicol Appl Pharmacol 190:135-45. 2003
    ..Moreover, it is likely increased cyclin D1 expression results at least in part from Catnb mutation, beta-catenin accumulation, and increased Wnt signaling...
  36. ncbi request reprint Pol iota is a candidate for the mouse pulmonary adenoma resistance 2 locus, a major modifier of chemically induced lung neoplasia
    Min Wang
    Department of Surgery and The Alvin J Siteman Cancer Center, Washington University School of Medicine, 660 South Euclid Avenue, St Louis, MO 63110, USA
    Cancer Res 64:1924-31. 2004
    ..Thus, our data support the Pol iota gene as a modifier of lung tumorigenesis by altering DNA polymerase activity...
  37. ncbi request reprint Genetic alterations in the Catnb gene but not the H-ras gene in hepatocellular neoplasms and hepatoblastomas of B6C3F(1) mice following exposure to diethanolamine for 2 years
    Shim Mo Hayashi
    Laboratory of Experimental Pathology, National Institute of Environmental Health Sciences, PO Box 12233, Research Triangle Park, NC 27709, USA
    Chem Biol Interact 146:251-61. 2003
    ....
  38. ncbi request reprint Changes in global gene and protein expression during early mouse liver carcinogenesis induced by non-genotoxic model carcinogens oxazepam and Wyeth-14,643
    Mari Iida
    Laboratory of Molecular Carcinogenesis, National Institute of Environmental Health Sciences, National Institute of Health, Research Triangle Park, NC 27709, USA
    Carcinogenesis 24:757-70. 2003
    ....