Christopher D Houle

Summary

Affiliation: National Institutes of Health
Country: USA

Publications

  1. ncbi Frequent p53 and H-ras mutations in benzene- and ethylene oxide-induced mammary gland carcinomas from B6C3F1 mice
    Christopher D Houle
    Laboratory of Experimental Pathology, Research Triangle Park, North Carolina 27709, USA
    Toxicol Pathol 34:752-62. 2006
  2. ncbi K-ras mutations in lung tumors and tumors from other organs are consistent with a common mechanism of ethylene oxide tumorigenesis in the B6C3F1 mouse
    Hue Hua L Hong
    Laboratory of Experimental Pathology, National Institute of Environmental Health Sciences, NIH, Research Triangle Park, NC 27709, USA
    Toxicol Pathol 35:81-5. 2007
  3. ncbi 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
  4. ncbi Spontaneous and irradiation-induced tumor susceptibility in BRCA2 germline mutant mice and cooperative effects with a p53 germline mutation
    Kimberly A McAllister
    National Institute of Environmental Health Sciences, NIH, Research Triangle Park, North Carolina 27711, USA
    Toxicol Pathol 34:187-98. 2006
  5. ncbi Mutant Brca2/p53 mice exhibit altered radiation responses in the developing mammary gland
    Christopher D Houle
    Laboratory of Women s Health, National Institute of Environmental Health Sciences, NIH, P O Box 12233, Research Triangle Park, NC 27709, USA
    Exp Toxicol Pathol 57:105-15. 2005

Collaborators

Detail Information

Publications5

  1. ncbi Frequent p53 and H-ras mutations in benzene- and ethylene oxide-induced mammary gland carcinomas from B6C3F1 mice
    Christopher D Houle
    Laboratory of Experimental Pathology, Research Triangle Park, North Carolina 27709, USA
    Toxicol Pathol 34:752-62. 2006
    ..Our results demonstrate that p53 and H-ras mutations are relatively common in control and chemically induced mouse mammary carcinomas although both chemicals can alter the mutational spectra and more commonly induce concurrent mutations...
  2. ncbi K-ras mutations in lung tumors and tumors from other organs are consistent with a common mechanism of ethylene oxide tumorigenesis in the B6C3F1 mouse
    Hue Hua L Hong
    Laboratory of Experimental Pathology, National Institute of Environmental Health Sciences, NIH, Research Triangle Park, NC 27709, USA
    Toxicol Pathol 35:81-5. 2007
    ..This suggests that EO specifically targets the K-ras gene in multiple tissue types and that this event is a critical component of EO-induced tumorigenesis...
  3. ncbi 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
    ....
  4. ncbi Spontaneous and irradiation-induced tumor susceptibility in BRCA2 germline mutant mice and cooperative effects with a p53 germline mutation
    Kimberly A McAllister
    National Institute of Environmental Health Sciences, NIH, Research Triangle Park, North Carolina 27711, USA
    Toxicol Pathol 34:187-98. 2006
    ..In addition, these findings include extensive in vivo data demonstrating that germline Brca2 and p53 mutations cooperatively affect animal survivals, tumor susceptibilities, and tumor onsets...
  5. ncbi Mutant Brca2/p53 mice exhibit altered radiation responses in the developing mammary gland
    Christopher D Houle
    Laboratory of Women s Health, National Institute of Environmental Health Sciences, NIH, P O Box 12233, Research Triangle Park, NC 27709, USA
    Exp Toxicol Pathol 57:105-15. 2005
    ..We also demonstrate distinct spatial differences in the cellular functions of Brca2 and p53 and show that combined mutation of both genes is more detrimental than loss of either gene alone...