J M Brown

Summary

Affiliation: Stanford University
Country: USA

Publications

  1. ncbi request reprint Exploiting the hypoxic cancer cell: mechanisms and therapeutic strategies
    J M Brown
    Cancer Biology Research Laboratory, Stanford University Medical School, Stanford, CA 94305, USA
    Mol Med Today 6:157-62. 2000
  2. ncbi request reprint Therapeutic targets in radiotherapy
    J M Brown
    Division of Radiation Biology, Department of Radiation Oncology, Stanford University School of Medicine, Stanford, CA 94305 5152, USA
    Int J Radiat Oncol Biol Phys 49:319-26. 2001
  3. ncbi request reprint The hypoxic cell: a target for selective cancer therapy--eighteenth Bruce F. Cain Memorial Award lecture
    J M Brown
    Department of Radiation Oncology, Stanford University School of Medicine, California 94305 5468, USA
    Cancer Res 59:5863-70. 1999
  4. pmc SR 4233 cytotoxicity and metabolism in DNA repair-competent and repair-deficient cell cultures
    K A Biedermann
    Department of Radiation Oncology, Stanford University School of Medicine, California 94305
    Br J Cancer 63:358-62. 1991
  5. pmc Cisplatin anti-tumour potentiation by tirapazamine results from a hypoxia-dependent cellular sensitization to cisplatin
    M S Kovacs
    Department of Radiation Oncology, Stanford University School of Medicine, CA 94305, USA
    Br J Cancer 80:1245-51. 1999
  6. pmc The DNA damage response in DNA-dependent protein kinase-deficient SCID mouse cells: replication protein A hyperphosphorylation and p53 induction
    L M Fried
    Department of Radiation Oncology, Stanford University School of Medicine, CA 94305, USA
    Proc Natl Acad Sci U S A 93:13825-30. 1996
  7. pmc Tirapazamine-induced DNA damage measured using the comet assay correlates with cytotoxicity towards hypoxic tumour cells in vitro
    B G Siim
    Department of Radiation Oncology, Stanford University School of Medicine, CA 94305 5468, USA
    Br J Cancer 73:952-60. 1996
  8. ncbi request reprint Inhibition of DNA replication by tirapazamine
    K B Peters
    Division of Radiation and Cancer Biology, Department of Radiation Oncology, Stanford University School of Medicine, Stanford, California 94305-5152, USA
    Cancer Res 61:5425-31. 2001
  9. ncbi request reprint Re-evaluating gadolinium(III) texaphyrin as a radiosensitizing agent
    E J Bernhard
    University of Pennsylvania, Department of Radiation Oncology, Philadelphia 19104, USA
    Cancer Res 60:86-91. 2000
  10. ncbi request reprint Metabolism of tirapazamine by multiple reductases in the nucleus
    Y M Delahoussaye
    Division of Radiation and Cancer Biology, Department of Radiation Oncology, Stanford University Medical School, Stanford, CA 94305-5152, USA
    Biochem Pharmacol 62:1201-9. 2001

Collaborators

Detail Information

Publications23

  1. ncbi request reprint Exploiting the hypoxic cancer cell: mechanisms and therapeutic strategies
    J M Brown
    Cancer Biology Research Laboratory, Stanford University Medical School, Stanford, CA 94305, USA
    Mol Med Today 6:157-62. 2000
    ..The second way to exploit hypoxia is to take advantage of the selective induction of the transcription factor hypoxia-inducible factor 1 (HIF-1) under hypoxic conditions; gene therapy strategies based on this are in development...
  2. ncbi request reprint Therapeutic targets in radiotherapy
    J M Brown
    Division of Radiation Biology, Department of Radiation Oncology, Stanford University School of Medicine, Stanford, CA 94305 5152, USA
    Int J Radiat Oncol Biol Phys 49:319-26. 2001
    ..However, a major barrier to such efforts is the requirement for a preferential effect on tumor vs. normal cells. Such a requirement can only come about by exploiting a known difference between tumor and normal cells...
  3. ncbi request reprint The hypoxic cell: a target for selective cancer therapy--eighteenth Bruce F. Cain Memorial Award lecture
    J M Brown
    Department of Radiation Oncology, Stanford University School of Medicine, California 94305 5468, USA
    Cancer Res 59:5863-70. 1999
    ..The unique presence of hypoxic cells in human tumors provides an important target for selective cancer therapy...
  4. pmc SR 4233 cytotoxicity and metabolism in DNA repair-competent and repair-deficient cell cultures
    K A Biedermann
    Department of Radiation Oncology, Stanford University School of Medicine, California 94305
    Br J Cancer 63:358-62. 1991
    ..Thus, the toxicity by SR 4233 towards hypoxic cells appears to result from two mechanisms; the rate of drug metabolism and the ability to repair DNA double strand breaks...
  5. pmc Cisplatin anti-tumour potentiation by tirapazamine results from a hypoxia-dependent cellular sensitization to cisplatin
    M S Kovacs
    Department of Radiation Oncology, Stanford University School of Medicine, CA 94305, USA
    Br J Cancer 80:1245-51. 1999
    ..The mechanism of the interaction appears to be through a potentiation of cisplatin-induced DNA interstrand cross-links, possibly as a result of a diminished or delayed repair of these lesions..
  6. pmc The DNA damage response in DNA-dependent protein kinase-deficient SCID mouse cells: replication protein A hyperphosphorylation and p53 induction
    L M Fried
    Department of Radiation Oncology, Stanford University School of Medicine, CA 94305, USA
    Proc Natl Acad Sci U S A 93:13825-30. 1996
    ..We conclude that the DNA damage response involving p53 and RPA is not associated with the defect in DNA repair in SCID cells and that the physiological substrate(s) for DNA-PK essential for DNA repair has not yet been identified...
  7. pmc Tirapazamine-induced DNA damage measured using the comet assay correlates with cytotoxicity towards hypoxic tumour cells in vitro
    B G Siim
    Department of Radiation Oncology, Stanford University School of Medicine, CA 94305 5468, USA
    Br J Cancer 73:952-60. 1996
    ..This approach holds promise for predicting the response of individual tumours to tirapazamine in the clinic...
  8. ncbi request reprint Inhibition of DNA replication by tirapazamine
    K B Peters
    Division of Radiation and Cancer Biology, Department of Radiation Oncology, Stanford University School of Medicine, Stanford, California 94305-5152, USA
    Cancer Res 61:5425-31. 2001
    ..These results show that TPZ dramatically inhibits DNA replication and that the mechanism of inhibition, at least in part, involves changes in RPA that alter its cellular localization...
  9. ncbi request reprint Re-evaluating gadolinium(III) texaphyrin as a radiosensitizing agent
    E J Bernhard
    University of Pennsylvania, Department of Radiation Oncology, Philadelphia 19104, USA
    Cancer Res 60:86-91. 2000
    ..Our results raise questions about the efficacy of Gd-tex as a radiosensitizing agent...
  10. ncbi request reprint Metabolism of tirapazamine by multiple reductases in the nucleus
    Y M Delahoussaye
    Division of Radiation and Cancer Biology, Department of Radiation Oncology, Stanford University Medical School, Stanford, CA 94305-5152, USA
    Biochem Pharmacol 62:1201-9. 2001
    ..This study is the first to characterize multiple nuclear reductases capable of activating TPZ...
  11. ncbi request reprint An investigation of the molecular basis for the synergistic interaction of tirapazamine and cisplatin
    Z Goldberg
    Division of Radiation Biology, Department of Radiation Oncology, Stanford University School of Medicine, Stanford CA, 94305 USA
    Int J Radiat Oncol Biol Phys 49:175-82. 2001
    ..Therefore, these studies were undertaken to determine if hypoxia-activated TPZ pretreatment inhibited the cells' normal protective response to cisplatin via inhibiting the upregulation of ERCC1 and/or XPA expression...
  12. pmc Exploiting tumour hypoxia and overcoming mutant p53 with tirapazamine
    J M Brown
    Mayer Cancer Biology Laboratory, Department of Radiation Oncology, Stanford University School of Medicine, CA 94305 5468, USA
    Br J Cancer 77:12-4. 1998
    ..Thus, the low cellular oxygen levels common in solid tumours can be turned from disadvantage to advantage using the hypoxia-selective cytotoxic drug tirapazamine...
  13. ncbi request reprint Characterization of the DNA double strand break repair defect in scid mice
    C Chang
    Department of Radiation Oncology, Stanford University School of Medicine, California 94305
    Cancer Res 53:1244-8. 1993
    ..Delineating the links between these aberrant recombinational events, abnormal V(D)J recombination, and double strand break repair defects, will aid in the understanding of the basic mechanisms involved in these processes...
  14. ncbi request reprint Immunity to infections following hematopoietic cell transplantation
    J M Brown
    H1353, Bone Marrow Transplantation Program, Department of Medicine, 300 Pasteur Drive, Stanford, CA 94305, USA
    Curr Opin Immunol 13:451-7. 2001
    ..These kinds of transplants can be designed to provide not only hematopoietic rescue but also augmented innate and acquired immunity...
  15. ncbi request reprint Reassessing the organization of the UL42-UL43 region of the human cytomegalovirus strain AD169 genome
    E S Mocarski
    Department of Microbiology and Immunology, Stanford University, California 94305 5124, USA
    Virology 239:169-75. 1997
    ..The additional sequence should be considered a bona fide part of the cytomegalovirus genome and the AD169 genome size should be corrected to 230,283 bp...
  16. ncbi request reprint Anticancer efficacy of systemically delivered anaerobic bacteria as gene therapy vectors targeting tumor hypoxia/necrosis
    S C Liu
    Division of Radiation and Cancer Biology, Department of Radiation Oncology, Stanford University School of Medicine, Stanford, CA 94305 5152, USA
    Gene Ther 9:291-6. 2002
    ..sporogenes produced greater antitumor effect than maximally tolerated doses of 5-FU. Since most human solid tumors have hypoxic and necrotic areas this vector system has considerable promise for tumor-selective gene therapy...
  17. pmc The use of fluorescence in situ hybridisation combined with premature chromosome condensation for the identification of chromosome damage
    J W Evans
    Department of Radiation Oncology, Stanford University Medical Center, CA 94305
    Br J Cancer 63:517-21. 1991
    ..Second, it allows the easy recognition of exchange type aberrations. A number of new applications of this technology, such as predicting the radiosensitivity of human tumours in situ, are feasible...
  18. pmc A genome-wide screen in Saccharomyces cerevisiae for genes affecting UV radiation sensitivity
    G W Birrell
    Department of Radiation Oncology, Stanford University School of Medicine, Stanford, CA 94305, USA
    Proc Natl Acad Sci U S A 98:12608-13. 2001
    ....
  19. ncbi request reprint Pancreatic tumors show high levels of hypoxia
    A C Koong
    Department Radiation Oncology, Stanford University Medical Center, Stanford, CA 94305, USA
    Int J Radiat Oncol Biol Phys 48:919-22. 2000
    ..Because of the dismal outcomes of conventional therapies for pancreatic carcinomas, we postulated that hypoxia may exist within these tumors...
  20. pmc Green fluorescent protein is a suitable reporter of tumor hypoxia despite an oxygen requirement for chromophore formation
    D Vordermark
    Department of Radiation Oncology, Division of Radiation and Cancer Biology, Stanford University School of Medicine, Stanford, CA 94305-5152, USA
    Neoplasia 3:527-34. 2001
    ..The correlation of fluorescence and oxygen concentration is restored by a 4-hour reoxygenation period due to oxidation of pre-synthesized EGFP and a delayed increase in EGFP protein synthesis...
  21. ncbi request reprint DNA-dependent kinase (p350) as a candidate gene for the murine SCID defect
    C U Kirchgessner
    Department of Radiation Oncology, Stanford University School of Medicine, CA 94305
    Science 267:1178-83. 1995
    ..Chromosomal fragments expressing p350 complement the SCID phenotype, and p350 protein levels are greatly reduced in cells derived from SCID mice compared to cells from wild-type mice...
  22. pmc Vasculogenesis: a crucial player in the resistance of solid tumours to radiotherapy
    J M Brown
    Division of Radiation and Cancer Biology, Department of Radiation Oncology, Stanford University, Stanford, CA, USA
    Br J Radiol 87:20130686. 2014
    ..This is a new paradigm with major implications for the treatment of solid tumours by radiotherapy. ..
  23. pmc Targeting SDF-1/CXCR4 to inhibit tumour vasculature for treatment of glioblastomas
    D Tseng
    Department of Radiation Oncology, Division of Radiation and Cancer Biology, Stanford University, 269 Campus Drive West, CCSR Room 1255, Stanford, CA 94305, USA
    Br J Cancer 104:1805-9. 2011
    ..Understanding the processes that mediate tumour revascularisation will guide the improvement of clinical strategies for preventing recurrence of glioblastoma after irradiation...