Martin Brown
Academic Appointments
- Professor, Radiation Oncology - Radiation and Cancer Biology
- Member, Stanford Cancer Institute
Key Documents
Contact Information
- Academic Offices
Personal Information Email Tel (650) 723-5881Alternate Contact Chuck Di Bari Admin Associate, Radiation & Cancer Biology Email Tel Work 498-4073
Professional Overview
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) |
Graduate & Fellowship Program Affiliations
Internet Links
Scientific Focus
Current Research 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.
Publications
- Dose escalation, not "new biology," can account for the efficacy of stereotactic body radiation therapy with non-small cell lung cancer. Int J Radiat Oncol Biol Phys. 2013; (5): 1159-60
- Deficiency in mammalian histone H2B ubiquitin ligase Bre1 (Rnf20/Rnf40) leads to replication stress and chromosomal instability. Cancer Res. 2012; (8): 2111-9
- Inhibition of Mac-1 (CD11b/CD18) enhances tumor response to radiation by reducing myeloid cell recruitment. Proc Natl Acad Sci U S A. 2010; (18): 8363-8
- Inhibition of vasculogenesis, but not angiogenesis, prevents the recurrence of glioblastoma after irradiation in mice. J Clin Invest. 2010; (3): 694-705
- Association of reactive oxygen species levels and radioresistance in cancer stem cells. Nature. 2009; (7239): 780-3
- Matrix metalloproteinase-9 is required for tumor vasculogenesis but not for angiogenesis: role of bone marrow-derived myelomonocytic cells. Cancer Cell. 2008; (3): 193-205
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