Cancer Institute A national cancer institute
designated cancer center
Profile http://med.stanford.edu/profiles/cancer/researcher/Martin_Brown/
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Martin Brown

Academic Appointments

  • Professor of Radiation Oncology, Emeritus

Key Documents

Contact Information

  • Academic Offices
    Personal Information
    Email Tel (650) 723-5881
    Alternate Contact
    Chuck Di Bari Admin Associate, Radiation & Cancer Biology Tel Work 498-4073

Bio

Academic Appointments

Administrative Appointments

  • Director, Division of Radiation and Cancer Biology (1984 - 2004)
  • Director, Graduate Program in Cancer Biology (1990 - 2002)

Honors and Awards

  • Henry S. Kaplan Distinguished Scientist Award, International Association for Radiation Research (2007)
  • Weiss Medal, Association for Radiation Research (2001)
  • Failla Memorial Award, Radiation Research Society (2000)
  • Gold Medal, Americal Society for Therapeutic Radiology and Oncology (1999)
  • Bruce Cain Memorial Award, American Association for Cancer Research (1999)

Professional Education

B.Sc: Birmingham University, Physics (1963)
M.Sc: London University, Radiation biology and physics (1965)
Ph.D: Oxford University, Cancer Biology (1968)

Research & Scholarship

Current Research and Scholarly Interests

We seek to understand the mechanisms responsible for the resistance of solid tumors to cancer therapies and to develop strategies to overcome these resistances. Projects include:

1) We are investigating the role of bone marrow derived cells in restoring the tumor vasculature after radiotherapy (which destroys local angiogenesis). This process is known as vasculogenesis. In particular we seek to improve tumor cure rates by radiotherapy by inhibiting the repair of the tumor vasculature in GBM by circulating cells following radiation to the tumors by selective inhibition of the chemokine pathway(s) responsive for the mobilization and capture in the tumor of the circulating proangiogenic cells.

2) Identification by HTS of small molecule inhibitors of DNA repair by homologous recombination (HR). This DNA repair pathway is crucial to the repair of the cytotoxic lesions caused by many anticancer agents, such as bifunctional alkylating agents and topoisomerase poisons. Many clinical situations exist whereby inhibiting HR will give a therapeutic gain.

Teaching

Courses

2014-15

Postdoctoral Advisees

Gabriel CharestJason Stafford

Graduate and Fellowship Program Affiliations

Publications

Publications

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