CHRISTOPHER KEMP

Summary

Affiliation: Fred Hutchinson Cancer Research Center
Country: USA

Publications

  1. pmc CTCF haploinsufficiency destabilizes DNA methylation and predisposes to cancer
    Christopher J Kemp
    Division of Human Biology, Fred Hutchinson Cancer Research Center, Seattle, WA 98109, USA Electronic address
    Cell Rep 7:1020-9. 2014
  2. pmc Plasma proteome profiles associated with inflammation, angiogenesis, and cancer
    Karen S Kelly-Spratt
    Division of Human Biology, Fred Hutchinson Cancer Research Center, Seattle, Washington, United States of America
    PLoS ONE 6:e19721. 2011
  3. pmc p19Arf suppresses growth, progression, and metastasis of Hras-driven carcinomas through p53-dependent and -independent pathways
    Karen S Kelly-Spratt
    Fred Hutchinson Cancer Research Center, Seattle, Washington, USA
    PLoS Biol 2:E242. 2004
  4. ncbi request reprint Resistance to skin tumorigenesis in DNAPK-deficient SCID mice is not due to immunodeficiency but results from hypersensitivity to TPA-induced apoptosis
    C J Kemp
    Fred Hutchinson Cancer Research Center C1 015, 1100 Fairview Avenue North, PO Box 19024, Seattle, WA 98109 1024, USA
    Carcinogenesis 20:2051-6. 1999
  5. ncbi request reprint Multistep skin cancer in mice as a model to study the evolution of cancer cells
    Christopher J Kemp
    Fred Hutchinson Cancer Research Center, 1100 Fairview Ave N, Seattle, WA 98109, USA
    Semin Cancer Biol 15:460-73. 2005
  6. ncbi request reprint The murine gene Cdkn1b (p27(Kip1)) maps to distal chromosome 6 and is excluded as Pas1
    C J Kemp
    Fred Hutchinson Cancer Research Center, 1100 Fairview Ave N, Seattle, Washington 98109, USA
    Mamm Genome 11:402-4. 2000
  7. ncbi request reprint p53 induction and apoptosis in response to radio- and chemotherapy in vivo is tumor-type-dependent
    C J Kemp
    Fred Hutchinson Cancer Research Center, Seattle, Washington 90109 1024, USA
    Cancer Res 61:327-32. 2001
  8. ncbi request reprint Pathway-specific tumor suppression. Reduction of p27 accelerates gastrointestinal tumorigenesis in Apc mutant mice, but not in Smad3 mutant mice
    Jeannette Philipp-Staheli
    Division of Human Biology, Fred Hutchinson Cancer Research Center, Seattle, WA 90109, USA
    Cancer Cell 1:355-68. 2002
  9. doi request reprint Ataxia-telangiectasia mutated is not required for p53 induction and apoptosis in irradiated epithelial tissues
    Kay E Gurley
    Fred Hutchinson Cancer Research Center, 1100 Fairview Avenue North, C1 015, Seattle, WA 90109 1024, USA
    Mol Cancer Res 5:1312-8. 2007
  10. ncbi request reprint Distinct roles for p53, p27Kip1, and p21Cip1 during tumor development
    Jeannette Philipp-Staheli
    Fred Hutchinson Cancer Research Center, C1 015, 1100 Fairview Ave N, Seattle, WA 90109 1024, USA
    Oncogene 23:905-13. 2004

Research Grants

  1. The Role of Double Strand Breaks in Carcinogenesis
    CHRISTOPHER KEMP; Fiscal Year: 2006
  2. Mouse Models of Tumor Progression and Therapy Response
    CHRISTOPHER KEMP; Fiscal Year: 2006
  3. The Role of Double Strand Breaks in Carcinogenesis
    CHRISTOPHER KEMP; Fiscal Year: 2005
  4. Mouse Models of Tumor Progression and Therapy Response
    CHRISTOPHER KEMP; Fiscal Year: 2005
  5. The Role of Double Strand Breaks in Carcinogenesis
    CHRISTOPHER KEMP; Fiscal Year: 2004
  6. Mouse Models of Tumor Progression and Therapy Response
    CHRISTOPHER KEMP; Fiscal Year: 2004
  7. The Role of Double Strand Breaks in Carcinogenesis
    CHRISTOPHER KEMP; Fiscal Year: 2003
  8. Mouse Models of Tumor Progression and Therapy Response
    CHRISTOPHER KEMP; Fiscal Year: 2003
  9. The Role of Double Strand Breaks in Carcinogenesis
    CHRISTOPHER KEMP; Fiscal Year: 2002
  10. DOUBLE STRAND BREAKS AND CARCINOGENESIS
    CHRISTOPHER KEMP; Fiscal Year: 2000

Collaborators

Detail Information

Publications26

  1. pmc CTCF haploinsufficiency destabilizes DNA methylation and predisposes to cancer
    Christopher J Kemp
    Division of Human Biology, Fred Hutchinson Cancer Research Center, Seattle, WA 98109, USA Electronic address
    Cell Rep 7:1020-9. 2014
    ..These findings establish CTCF as a prominent tumor-suppressor gene and point to CTCF-mediated epigenetic stability as a major barrier to neoplastic progression...
  2. pmc Plasma proteome profiles associated with inflammation, angiogenesis, and cancer
    Karen S Kelly-Spratt
    Division of Human Biology, Fred Hutchinson Cancer Research Center, Seattle, Washington, United States of America
    PLoS ONE 6:e19721. 2011
    ..This approach provides a basis for distinguishing between protein changes in plasma that are cancer-related and those that are part of a non-specific host response...
  3. pmc p19Arf suppresses growth, progression, and metastasis of Hras-driven carcinomas through p53-dependent and -independent pathways
    Karen S Kelly-Spratt
    Fred Hutchinson Cancer Research Center, Seattle, Washington, USA
    PLoS Biol 2:E242. 2004
    ..This indicates that selection for p53 mutations is a direct result of signaling from the initiating oncogenic lesion, Hras, acting through p19(Arf)...
  4. ncbi request reprint Resistance to skin tumorigenesis in DNAPK-deficient SCID mice is not due to immunodeficiency but results from hypersensitivity to TPA-induced apoptosis
    C J Kemp
    Fred Hutchinson Cancer Research Center C1 015, 1100 Fairview Avenue North, PO Box 19024, Seattle, WA 98109 1024, USA
    Carcinogenesis 20:2051-6. 1999
    ..This hypersensitivity of SCID (severe combined immunodeficient) cells to TPA indicates that the resistance to skin tumor formation in scid/scid mice is due to loss of initiated cells through TPA-induced cell killing...
  5. ncbi request reprint Multistep skin cancer in mice as a model to study the evolution of cancer cells
    Christopher J Kemp
    Fred Hutchinson Cancer Research Center, 1100 Fairview Ave N, Seattle, WA 98109, USA
    Semin Cancer Biol 15:460-73. 2005
    ..This indicates that tumor cells have an inherent reduced capacity to buffer against perturbations. Reduced buffering may play an important role in both tumor evolution and therapy response and may be a hallmark of cancer cells...
  6. ncbi request reprint The murine gene Cdkn1b (p27(Kip1)) maps to distal chromosome 6 and is excluded as Pas1
    C J Kemp
    Fred Hutchinson Cancer Research Center, 1100 Fairview Ave N, Seattle, Washington 98109, USA
    Mamm Genome 11:402-4. 2000
  7. ncbi request reprint p53 induction and apoptosis in response to radio- and chemotherapy in vivo is tumor-type-dependent
    C J Kemp
    Fred Hutchinson Cancer Research Center, Seattle, Washington 90109 1024, USA
    Cancer Res 61:327-32. 2001
    ..This variation provides one explanation for the tissue specificity of tumor suppression by p53. It also indicates that the role of apoptosis in the response of tumors to therapy varies significantly among tumor types...
  8. ncbi request reprint Pathway-specific tumor suppression. Reduction of p27 accelerates gastrointestinal tumorigenesis in Apc mutant mice, but not in Smad3 mutant mice
    Jeannette Philipp-Staheli
    Division of Human Biology, Fred Hutchinson Cancer Research Center, Seattle, WA 90109, USA
    Cancer Cell 1:355-68. 2002
    ..These results indicate that reduction of p27 cooperates with mutations in Apc but not in Smad3 during GI tumorigenesis. Thus, tumor suppression by p27 is contingent on the specific oncogenic pathway that drives tumor development...
  9. doi request reprint Ataxia-telangiectasia mutated is not required for p53 induction and apoptosis in irradiated epithelial tissues
    Kay E Gurley
    Fred Hutchinson Cancer Research Center, 1100 Fairview Avenue North, C1 015, Seattle, WA 90109 1024, USA
    Mol Cancer Res 5:1312-8. 2007
    ..This indicates that marked differences in DNA damage signaling pathways exist between tissues, which could explain some of the tissue-specific phenotypes, especially tumor suppression, associated with Atm deficiency...
  10. ncbi request reprint Distinct roles for p53, p27Kip1, and p21Cip1 during tumor development
    Jeannette Philipp-Staheli
    Fred Hutchinson Cancer Research Center, C1 015, 1100 Fairview Ave N, Seattle, WA 90109 1024, USA
    Oncogene 23:905-13. 2004
    ..Although p21 is functionally similar to both p53 and p27, it plays a lesser role in tumor suppression. These results further highlight the highly cooperative nature of p27 and its central role in tumor suppression...
  11. ncbi request reprint Deficiency in the gap junction protein connexin32 alters p27Kip1 tumor suppression and MAPK activation in a tissue-specific manner
    Timothy J King
    Cancer Prevention Research Program, Public Health Sciences Division, Fred Hutchinson Cancer Research Center, Seattle, WA 98109, USA
    Oncogene 24:1718-26. 2005
    ..This study demonstrates that tissues dependent on Cx32 tumor suppression, such as the liver and lung, exhibit altered tumorigenesis and tumor biology (MAPK pathway activation) related to p27 status...
  12. doi request reprint Plasma proteome profiling of a mouse model of breast cancer identifies a set of up-regulated proteins in common with human breast cancer cells
    Sharon J Pitteri
    Fred Hutchinson Cancer Research Center, Seattle, Washington 98109 1024, USA
    J Proteome Res 7:1481-9. 2008
    ....
  13. pmc Endocrine dysfunction in p27Kip1 deficient mice and susceptibility to Wnt-1 driven breast cancer
    Cynthia E Glover
    Fred Hutchinson Cancer Research Center, Seattle, WA 98109, USA
    Carcinogenesis 30:1058-63. 2009
    ..This study shows that while not a significant inhibitor of Wnt-1-driven breast cancer, p27 inhibits gastric tumors, whose latency is modulated by sex steroids...
  14. pmc Tumor suppression by p53 in the absence of Atm
    S Lawrence Bailey
    Fred Hutchinson Cancer Research Center, Seattle, WA 90109 1024, USA
    Mol Cancer Res 6:1185-92. 2008
    ..In conclusion, in these models of oncogene- or DNA damage-induced tumors, p53 retains tumor suppressor activity in the absence of Atm...
  15. ncbi request reprint p27(Kip1) (Cdkn1b)-deficient mice are susceptible to chemical carcinogenesis and may be a useful model for carcinogen screening
    Shannon R Payne
    Fred Hutchinson Cancer Research Center C1 015, PO Box 19024, 1100 Fairview Ave N, Seattle, Washington 90109 1024, USA
    Toxicol Pathol 31:355-63. 2003
    ....
  16. ncbi request reprint High throughput quantitative analysis of serum proteins using glycopeptide capture and liquid chromatography mass spectrometry
    Hui Zhang
    Institute for Systems Biology, Seattle, WA 98103, USA
    Mol Cell Proteomics 4:144-55. 2005
    ..We further identify, by tandem mass spectrometry, some of the peptides that were consistently elevated in cancer mice compared with their control littermates...
  17. pmc p27kip1 deficiency impairs G2/M arrest in response to DNA damage, leading to an increase in genetic instability
    Shannon R Payne
    Fred Hutchinson Cancer Research Center C1 015, 1100 Fairview Ave N, Seattle, WA 90109 1024, USA
    Mol Cell Biol 28:258-68. 2008
    ..The second is by transient inhibition of cell cycle progression following genotoxic insult, thereby minimizing chromosome damage and fixation of mutations...
  18. ncbi request reprint Integrated pipeline for mass spectrometry-based discovery and confirmation of biomarkers demonstrated in a mouse model of breast cancer
    Jeffrey R Whiteaker
    Fred Hutchinson Cancer Research Center, Seattle, Washington 98109, USA
    J Proteome Res 6:3962-75. 2007
    ..Furthermore, the approach can be extended to find biomarkers relevant to human disease...
  19. pmc A pathway in quiescent cells that controls p27Kip1 stability, subcellular localization, and tumor suppression
    Arnaud Besson
    Howard Hughes Medical Institute, Division of Basic Sciences, Seattle, Washington 98109, USA
    Genes Dev 20:47-64. 2006
    ..Thus, phosphorylation of p27 on Ser10 is an important event in the regulation of the tumor suppressor function of p27...
  20. ncbi request reprint Tumor suppressor genetics
    Shannon R Payne
    Fred Hutchinson Cancer Research Center, Seattle, WA 90109, USA
    Carcinogenesis 26:2031-45. 2005
    ..Incorporating these new findings into existing models of the clonal evolution will be a challenge for the future...
  21. pmc TRAIL-R deficiency in mice enhances lymph node metastasis without affecting primary tumor development
    Anne Grosse-Wilde
    Human Biology Division, Fred Hutchinson Cancer Research Center, Seattle, Washington 98109, USA
    J Clin Invest 118:100-10. 2008
    ..Hence, treatment of cancer patients with agonists of the apoptosis-inducing receptors for TRAIL may prove useful in reducing the incidence of metastasis...
  22. pmc DNA-PK suppresses a p53-independent apoptotic response to DNA damage
    Kay E Gurley
    Division of Human Biology, Fred Hutchinson Cancer Research Center, Seattle, Washington 98109, USA
    EMBO Rep 10:87-93. 2009
    ..This shows that there are two separate, but equally effective, apoptotic responses to DNA damage: one is p53 dependent and the other, engaged in the absence of DNA-PK, does not require p53...
  23. ncbi request reprint Non-invasive imaging of carcinogen-induced early neoplasia using ultrahigh-resolution optical coherence tomography
    Michael J Cobb
    Department of Bioengineering, University of Washington, Seattle, WA 98195, USA
    Cancer Biomark 2:163-73. 2006
    ....
  24. ncbi request reprint Estradiol-dependent decrease in the orexigenic potency of ghrelin in female rats
    Deborah J Clegg
    Department of Psychiatry, University of Cincinnati, P O Box 670559, Cincinnati, OH 45267 0559, USA
    Diabetes 56:1051-8. 2007
    ....
  25. pmc A mouse model repository for cancer biomarker discovery
    Karen S Kelly-Spratt
    Fred Hutchinson Cancer Research Center, Seattle, WA 98109, USA
    J Proteome Res 7:3613-8. 2008
    ..We present the overall design of this resource and its potential use by the research community for biomarker discovery...
  26. ncbi request reprint Role of epidermal growth factor and its receptor in chemotherapy-induced intestinal injury
    Frederick S Huang
    Division of Hematology Oncology, Children s Hospital Medical Center, Cincinnati, Ohio 45229, USA
    Am J Physiol Gastrointest Liver Physiol 282:G432-42. 2002
    ..These findings do not support a critical role for EGF or its receptor in chemotherapy-induced intestinal injury...

Research Grants15

  1. The Role of Double Strand Breaks in Carcinogenesis
    CHRISTOPHER KEMP; Fiscal Year: 2006
    ..Understanding the functional interaction of the P13 Ks, in regulating p53, apoptosis, development and carcinogenesis at the level of the whole animal is a necessary link to apply knowledge gained from cell culture models to the clinic. ..
  2. Mouse Models of Tumor Progression and Therapy Response
    CHRISTOPHER KEMP; Fiscal Year: 2006
    ..These experiments will reveal the molecular and cellular basis for the poor clinical outcome associated with p27 deficient tumors. This knowledge can then be applied to improve treatment design and regimen in the clinical setting. ..
  3. The Role of Double Strand Breaks in Carcinogenesis
    CHRISTOPHER KEMP; Fiscal Year: 2005
    ..Understanding the functional interaction of the P13 Ks, in regulating p53, apoptosis, development and carcinogenesis at the level of the whole animal is a necessary link to apply knowledge gained from cell culture models to the clinic. ..
  4. Mouse Models of Tumor Progression and Therapy Response
    CHRISTOPHER KEMP; Fiscal Year: 2005
    ..These experiments will reveal the molecular and cellular basis for the poor clinical outcome associated with p27 deficient tumors. This knowledge can then be applied to improve treatment design and regimen in the clinical setting. ..
  5. The Role of Double Strand Breaks in Carcinogenesis
    CHRISTOPHER KEMP; Fiscal Year: 2004
    ..Understanding the functional interaction of the P13 Ks, in regulating p53, apoptosis, development and carcinogenesis at the level of the whole animal is a necessary link to apply knowledge gained from cell culture models to the clinic. ..
  6. Mouse Models of Tumor Progression and Therapy Response
    CHRISTOPHER KEMP; Fiscal Year: 2004
    ..These experiments will reveal the molecular and cellular basis for the poor clinical outcome associated with p27 deficient tumors. This knowledge can then be applied to improve treatment design and regimen in the clinical setting. ..
  7. The Role of Double Strand Breaks in Carcinogenesis
    CHRISTOPHER KEMP; Fiscal Year: 2003
    ..Understanding the functional interaction of the P13 Ks, in regulating p53, apoptosis, development and carcinogenesis at the level of the whole animal is a necessary link to apply knowledge gained from cell culture models to the clinic. ..
  8. Mouse Models of Tumor Progression and Therapy Response
    CHRISTOPHER KEMP; Fiscal Year: 2003
    ..These experiments will reveal the molecular and cellular basis for the poor clinical outcome associated with p27 deficient tumors. This knowledge can then be applied to improve treatment design and regimen in the clinical setting. ..
  9. The Role of Double Strand Breaks in Carcinogenesis
    CHRISTOPHER KEMP; Fiscal Year: 2002
    ..Understanding the functional interaction of the P13 Ks, in regulating p53, apoptosis, development and carcinogenesis at the level of the whole animal is a necessary link to apply knowledge gained from cell culture models to the clinic. ..
  10. DOUBLE STRAND BREAKS AND CARCINOGENESIS
    CHRISTOPHER KEMP; Fiscal Year: 2000
    ....
  11. DOUBLE STRAND BREAKS AND CARCINOGENESIS
    CHRISTOPHER KEMP; Fiscal Year: 1999
    ....
  12. Mouse Models of Tumor Progression and Therapy Response
    CHRISTOPHER KEMP; Fiscal Year: 2007
    ..These experiments will reveal the molecular and cellular basis for the poor clinical outcome associated with p27 deficient tumors. This knowledge can then be applied to improve treatment design and regimen in the clinical setting. ..