Osamu Tetsu

Summary

Affiliation: University of California
Country: USA

Publications

  1. ncbi Mutations in the c-Kit gene disrupt mitogen-activated protein kinase signaling during tumor development in adenoid cystic carcinoma of the salivary glands
    Osamu Tetsu
    Head and Neck Cancer Research Laboratory, Department of Otolaryngology Head and Neck Surgery, School of Medicine, University of California, San Francisco, San Francisco, CA 94143 1330, USA
    Neoplasia 12:708-17. 2010
  2. ncbi A critical role for FBXW8 and MAPK in cyclin D1 degradation and cancer cell proliferation
    Hiroshi Okabe
    Department of Pathology, School of Medicine, University of California San Francisco, San Francisco, California, United States of America UCSF Comprehensive Cancer Center, School of Medicine, University of California San Francisco, San Francisco, California, United States of America
    PLoS ONE 1:e128. 2006
  3. ncbi Genetic profiling reveals cross-contamination and misidentification of 6 adenoid cystic carcinoma cell lines: ACC2, ACC3, ACCM, ACCNS, ACCS and CAC2
    Janyaporn Phuchareon
    Head and Neck Cancer Research Laboratory, Department of Otolaryngology Head and Neck Surgery, School of Medicine, University of California San Francisco, San Francisco, CA, USA
    PLoS ONE 4:e6040. 2009
  4. ncbi Germline mutations of MEK in cardio-facio-cutaneous syndrome are sensitive to MEK and RAF inhibition: implications for therapeutic options
    Thanaset Senawong
    Department of Pathology, School of Medicine, University of California, San Francisco, CA 94143 0128, USA
    Hum Mol Genet 17:419-30. 2008

Collaborators

  • Katherine A Rauen
  • Janyaporn Phuchareon
  • Thanaset Senawong
  • Frank McCormick
  • Hiroshi Okabe
  • Yoshihito Ohta
  • David W Eisele
  • Jonathan M Woo
  • Osamu Ohara
  • Sang Hyun Lee
  • Donna G Albertson

Detail Information

Publications4

  1. ncbi Mutations in the c-Kit gene disrupt mitogen-activated protein kinase signaling during tumor development in adenoid cystic carcinoma of the salivary glands
    Osamu Tetsu
    Head and Neck Cancer Research Laboratory, Department of Otolaryngology Head and Neck Surgery, School of Medicine, University of California, San Francisco, San Francisco, CA 94143 1330, USA
    Neoplasia 12:708-17. 2010
    ..Because ACC seems to proliferate despite inactivation of the c-Kit signaling pathway, we suggest that selective inhibition of c-Kit is probably not a suitable treatment strategy for ACC...
  2. ncbi A critical role for FBXW8 and MAPK in cyclin D1 degradation and cancer cell proliferation
    Hiroshi Okabe
    Department of Pathology, School of Medicine, University of California San Francisco, San Francisco, California, United States of America UCSF Comprehensive Cancer Center, School of Medicine, University of California San Francisco, San Francisco, California, United States of America
    PLoS ONE 1:e128. 2006
    ..Thus, FBXW8 plays an essential role in cancer cell proliferation through proteolysis of cyclin D1. It may present new opportunities to develop therapies targeting destruction of cyclin D1 or its regulator E3 ligase selectively...
  3. ncbi Genetic profiling reveals cross-contamination and misidentification of 6 adenoid cystic carcinoma cell lines: ACC2, ACC3, ACCM, ACCNS, ACCS and CAC2
    Janyaporn Phuchareon
    Head and Neck Cancer Research Laboratory, Department of Otolaryngology Head and Neck Surgery, School of Medicine, University of California San Francisco, San Francisco, CA, USA
    PLoS ONE 4:e6040. 2009
    ..These observations suggest that future studies using ACC cell lines should include cell line authentication to avoid the use of contaminated or non-human cells...
  4. ncbi Germline mutations of MEK in cardio-facio-cutaneous syndrome are sensitive to MEK and RAF inhibition: implications for therapeutic options
    Thanaset Senawong
    Department of Pathology, School of Medicine, University of California, San Francisco, CA 94143 0128, USA
    Hum Mol Genet 17:419-30. 2008
    ..Thus, regardless of mutations identified in an individual with CFC, MEK inhibition is a potential therapeutic approach for this population...