J Martin Brown

Summary

Affiliation: Stanford University
Country: USA

Publications

  1. ncbi request reprint Tumor microenvironment and the response to anticancer therapy
    J Martin Brown
    CCSR 1255, Division of Radiation and Cancer Biology, Dept of Radiation Oncology, Stanford University School of Medicine, 269 Campus Drive, Stanford, CA 94305, USA
    Cancer Biol Ther 1:453-8. 2002
  2. ncbi request reprint Apoptosis genes and resistance to cancer therapy: what does the experimental and clinical data tell us?
    J Martin Brown
    Department of Radiation Oncology, Stanford University School of Medicine Stanford, California, USA
    Cancer Biol Ther 2:477-90. 2003
  3. ncbi request reprint Exploiting tumour hypoxia in cancer treatment
    J Martin Brown
    Division of Radiation and Cancer Biology, Department of Radiation Oncology, Stanford, California 94305, USA
    Nat Rev Cancer 4:437-47. 2004
  4. pmc Global analysis of gene function in yeast by quantitative phenotypic profiling
    James A Brown
    Department of Radiation Oncology, Stanford University School of Medicine, Stanford, CA 94305 5152, USA
    Mol Syst Biol 2:2006.0001. 2006
  5. pmc The tumor radiobiology of SRS and SBRT: are more than the 5 Rs involved?
    J Martin Brown
    Department of Radiation Oncology, Stanford University School of Medicine, Stanford, California Electronic address
    Int J Radiat Oncol Biol Phys 88:254-62. 2014
  6. pmc Blockade of SDF-1 after irradiation inhibits tumor recurrences of autochthonous brain tumors in rats
    Shie Chau Liu
    Corresponding author J Martin Brown, PhD, Division of Radiation and Cancer Biology, Department of Radiation Oncology, Stanford University, A246, 1050A Arastradero Rd, Palo Alto, CA 94304 1334
    Neuro Oncol 16:21-8. 2014
  7. pmc Inhibiting vasculogenesis after radiation: a new paradigm to improve local control by radiotherapy
    Brown J Martin
    Department of Radiation Oncology, Stanford University, Stanford, CA Electronic address
    Semin Radiat Oncol 23:281-7. 2013
  8. doi request reprint Imaging tumor sensitivity to a bioreductive prodrug: two for the price of one!
    J Martin Brown
    Department of Radiation Oncology, Stanford University, Stanford, CA, USA
    Clin Cancer Res 18:1487-9. 2012
  9. pmc Integrating phenotypic and expression profiles to map arsenic-response networks
    Astrid C Haugen
    Laboratory of Molecular Genetics, National Institute of Environmental Health Sciences, NIH, Research Triangle Park, NC 27709, USA
    Genome Biol 5:R95. 2004
  10. doi request reprint Henry S. Kaplan Distinguished Scientist Award Lecture 2007. The remarkable yin and yang of tumour hypoxia
    Martin Brown
    Department of Radiation Oncology, Stanford University, California 94305, USA
    Int J Radiat Biol 86:907-17. 2010

Collaborators

Detail Information

Publications44

  1. ncbi request reprint Tumor microenvironment and the response to anticancer therapy
    J Martin Brown
    CCSR 1255, Division of Radiation and Cancer Biology, Dept of Radiation Oncology, Stanford University School of Medicine, 269 Campus Drive, Stanford, CA 94305, USA
    Cancer Biol Ther 1:453-8. 2002
    ..Finally, tumor hypoxia can be exploited using live obligate anaerobes that have been genetically engineered to express enzymes that can activate non-toxic prodrugs into toxic chemotherapeutic agents...
  2. ncbi request reprint Apoptosis genes and resistance to cancer therapy: what does the experimental and clinical data tell us?
    J Martin Brown
    Department of Radiation Oncology, Stanford University School of Medicine Stanford, California, USA
    Cancer Biol Ther 2:477-90. 2003
    ..Further clinical studies in this area are needed...
  3. ncbi request reprint Exploiting tumour hypoxia in cancer treatment
    J Martin Brown
    Division of Radiation and Cancer Biology, Department of Radiation Oncology, Stanford, California 94305, USA
    Nat Rev Cancer 4:437-47. 2004
  4. pmc Global analysis of gene function in yeast by quantitative phenotypic profiling
    James A Brown
    Department of Radiation Oncology, Stanford University School of Medicine, Stanford, CA 94305 5152, USA
    Mol Syst Biol 2:2006.0001. 2006
    ..This method will be useful when used alone and in conjunction with other global approaches to identify gene function in yeast...
  5. pmc The tumor radiobiology of SRS and SBRT: are more than the 5 Rs involved?
    J Martin Brown
    Department of Radiation Oncology, Stanford University School of Medicine, Stanford, California Electronic address
    Int J Radiat Oncol Biol Phys 88:254-62. 2014
    ....
  6. pmc Blockade of SDF-1 after irradiation inhibits tumor recurrences of autochthonous brain tumors in rats
    Shie Chau Liu
    Corresponding author J Martin Brown, PhD, Division of Radiation and Cancer Biology, Department of Radiation Oncology, Stanford University, A246, 1050A Arastradero Rd, Palo Alto, CA 94304 1334
    Neuro Oncol 16:21-8. 2014
    ..In the present study we test this strategy by directly neutralizing SDF-1 in a clinically relevant model using autochthonous brain tumors in immune competent hosts...
  7. pmc Inhibiting vasculogenesis after radiation: a new paradigm to improve local control by radiotherapy
    Brown J Martin
    Department of Radiation Oncology, Stanford University, Stanford, CA Electronic address
    Semin Radiat Oncol 23:281-7. 2013
    ..This strategy of inhibiting vasculogenesis following tumor irradiation is a new paradigm in radiotherapy and suggests that higher levels of local control of tumors in several sites would be achievable with this strategy...
  8. doi request reprint Imaging tumor sensitivity to a bioreductive prodrug: two for the price of one!
    J Martin Brown
    Department of Radiation Oncology, Stanford University, Stanford, CA, USA
    Clin Cancer Res 18:1487-9. 2012
    ..A way to combat this effect is with drugs called "bioreductive prodrugs" or "hypoxic cytotoxins," which are metabolized under hypoxia to toxic species. However, the patients with hypoxic tumors need to be identified...
  9. pmc Integrating phenotypic and expression profiles to map arsenic-response networks
    Astrid C Haugen
    Laboratory of Molecular Genetics, National Institute of Environmental Health Sciences, NIH, Research Triangle Park, NC 27709, USA
    Genome Biol 5:R95. 2004
    ..These data were then mapped to a metabolic network composed of all known biochemical reactions in yeast, as well as the yeast network of 20,985 protein-protein/protein-DNA interactions...
  10. doi request reprint Henry S. Kaplan Distinguished Scientist Award Lecture 2007. The remarkable yin and yang of tumour hypoxia
    Martin Brown
    Department of Radiation Oncology, Stanford University, California 94305, USA
    Int J Radiat Biol 86:907-17. 2010
    ..To honour perhaps the most influential man in the radiation sciences, Henry S. Kaplan, by reviewing the field of tumour hypoxia, one of his many interests...
  11. ncbi request reprint The role of apoptosis in cancer development and treatment response
    J Martin Brown
    Division of Radiation and Cancer Biology, Department of Radiation Oncology, Stanford, California 94305, USA
    Nat Rev Cancer 5:231-7. 2005
    ..Importantly, this suggests that other modes of cell death are involved in the response to therapy...
  12. pmc Stereotactic ablative radiotherapy should be combined with a hypoxic cell radiosensitizer
    J Martin Brown
    Department of Radiation Oncology, Stanford University School of Medicine, California 94305, USA
    Int J Radiat Oncol Biol Phys 78:323-7. 2010
    ....
  13. ncbi request reprint A noninvasive approach for assessing tumor hypoxia in xenografts: developing a urinary marker for hypoxia
    Daniel W Nelson
    Department of Radiation Oncology, Stanford University, Stanford, California 94305 5847, USA
    Cancer Res 65:6151-8. 2005
    ..The 5HRE beta-hCG reporter system described here enables serial, noninvasive monitoring of tumor hypoxia in a mouse model by measuring a urinary reporter protein...
  14. pmc Inhibition of vasculogenesis, but not angiogenesis, prevents the recurrence of glioblastoma after irradiation in mice
    Mitomu Kioi
    Division of Radiation and Cancer Biology, Department of Radiation Oncology, Stanford University School of Medicine, California 94305 5152, USA
    J Clin Invest 120:694-705. 2010
    ....
  15. doi request reprint Homologous recombination is the principal pathway for the repair of DNA damage induced by tirapazamine in mammalian cells
    James W Evans
    Department of Radiation Oncology, Division of Radiation and Cancer Biology, Stanford University, Stanford, California 94305 5152, USA
    Cancer Res 68:257-65. 2008
    ....
  16. ncbi request reprint Comparison of the comet assay and the oxygen microelectrode for measuring tumor oxygenation in head-and-neck cancer patients
    Quynh Thu Le
    Department of Radiation Oncology, Stanford University, Stanford, CA 94305, USA
    Int J Radiat Oncol Biol Phys 56:375-83. 2003
    ..To compare the Eppendorf PO2 histograph and the alkaline comet assay as methods of measuring tumor hypoxia in patients with head-and-neck squamous cell carcinomas...
  17. pmc Hypofractionation results in reduced tumor cell kill compared to conventional fractionation for tumors with regions of hypoxia
    David J Carlson
    Stanford University School of Medicine, Department of Radiation Oncology, Stanford, CA, USA
    Int J Radiat Oncol Biol Phys 79:1188-95. 2011
    ..The purpose of this study is to quantify the effect of different radiation fractionation schemes on tumor cell killing, assuming a realistic distribution of tumor oxygenation...
  18. pmc Inhibition of Mac-1 (CD11b/CD18) enhances tumor response to radiation by reducing myeloid cell recruitment
    G One Ahn
    Division of Radiation and Cancer Biology, Department of Radiation Oncology, Stanford University School of Medicine, Stanford, CA 94305, USA
    Proc Natl Acad Sci U S A 107:8363-8. 2010
    ..Our study thus supports the rationale of using clinically available Mac-1 (CD11b/CD18) antibodies as an adjuvant therapy to radiotherapy...
  19. pmc Improved potency of the hypoxic cytotoxin tirapazamine by DNA-targeting
    Yvette M Delahoussaye
    Department of Radiation Oncology, Stanford University School of Medicine, 269 Campus Drive, CCSR 1255, Stanford, CA 94305 5152, USA
    Biochem Pharmacol 65:1807-15. 2003
    ..These results show the promise of DNA-targeting of TPZ to produce a DNA compound with greater clinical efficacy than TPZ itself...
  20. pmc Optimized clostridium-directed enzyme prodrug therapy improves the antitumor activity of the novel DNA cross-linking agent PR-104
    Shie Chau Liu
    Department of Radiation Oncology, Stanford University School of Medicine, Stanford, California, USA
    Cancer Res 68:7995-8003. 2008
    ..sporogenes spores in SiHa tumor-bearing mice showed significantly improved antitumor efficacy when combined with either 5-aziridinyl-2,4-dinitrobenzamide (CB1954) or the novel dinitrobenzamide mustard prodrug, PR-104...
  21. ncbi request reprint Genome-wide identification of genes conferring resistance to the anticancer agents cisplatin, oxaliplatin, and mitomycin C
    H Irene Wu
    Department of Radiation Oncology, Stanford University School of Medicine, Stanford, California 94305 5152, USA
    Cancer Res 64:3940-8. 2004
    ....
  22. ncbi request reprint Evaluation of hypoxia-inducible factor-1alpha (HIF-1alpha) as an intrinsic marker of tumor hypoxia in U87 MG human glioblastoma: in vitro and xenograft studies
    Dirk Vordermark
    Department of Radiation Oncology, Stanford University School of Medicine, Stanford, CA, USA
    Int J Radiat Oncol Biol Phys 56:1184-93. 2003
    ..High protein levels have been linked to poor prognosis in several tumor types, and HIF-1alpha has been suggested as a potential endogenous marker of tumor hypoxia and associated radioresistance...
  23. pmc Deficiency in Bre1 impairs homologous recombination repair and cell cycle checkpoint response to radiation damage in mammalian cells
    Sophia B Chernikova
    Department of Radiation Oncology, Stanford University School of Medicine, Stanford, California 94305 5152, USA
    Radiat Res 174:558-65. 2010
    ..Thus our data suggest that the observed defects in the radiation response of Bre1a/b-deficient cells are associated with reduced H3K79me2 and not with H4K20me2...
  24. pmc Deficiency in mammalian histone H2B ubiquitin ligase Bre1 (Rnf20/Rnf40) leads to replication stress and chromosomal instability
    Sophia B Chernikova
    Department of Radiation Oncology, Stanford University, Stanford, California 94305, USA
    Cancer Res 72:2111-9. 2012
    ....
  25. pmc R-loops and genomic instability in Bre1 (RNF20/40)-deficient cells
    Sophia B Chernikova
    Department of Radiation Oncology, Stanford University, Stanford, CA, USA
    Cell Cycle 11:2980-4. 2012
    ....
  26. ncbi request reprint Tumor hypoxia in cancer therapy
    J Martin Brown
    Division of Radiation and Cancer Biology, Department of Radiation Oncology, Stanford University School of Medicine, Stanford, California, USA
    Methods Enzymol 435:297-321. 2007
    ..Finally, tumor hypoxia can be exploited using live obligate anaerobes that have been genetically engineered to express enzymes that can activate nontoxic prodrugs into toxic chemotherapeutic agents...
  27. pmc Radiosensitization of yeast cells by inhibition of histone h4 acetylation
    Suisui Song
    Department of Radiation Oncology, Division of Radiation and Cancer Biology, Stanford University of School of Medicine, Stanford, California 94305 5152, USA
    Radiat Res 170:618-27. 2008
    ..We also show that cells treated with HAT inhibitors have intact G1 and G2 checkpoints after exposure to ionizing radiation, suggesting that G1 and G2 checkpoint activation is independent of histone H4 acetylation...
  28. ncbi request reprint Identification of mitogen-activated protein kinase signaling pathways that confer resistance to endoplasmic reticulum stress in Saccharomyces cerevisiae
    Yijun Chen
    Department of Radiation Oncology, Center for Clinical Sciences Research, Stanford University Medical Center, Stanford, CA 94305, USA
    Mol Cancer Res 3:669-77. 2005
    ..We propose that the SLT2 MAPK pathway is an important cell survival signaling pathway during ER stress. This study shows the feasibility of using the yeast deletion pool to identify relevant mammalian orthologues of the UPR...
  29. pmc Multiple endonucleases function to repair covalent topoisomerase I complexes in Saccharomyces cerevisiae
    Changchun Deng
    Department of Radiation Oncology, Stanford University School of Medicine, California 94305 5152, USA
    Genetics 170:591-600. 2005
    ..These results suggest that Mre11 (with Sae2) and Slx4 represent two new structure-specific endonucleases that protect cells from trapped topoisomerase by removing topoisomerase-DNA adducts...
  30. pmc Influence of bone marrow-derived hematopoietic cells on the tumor response to radiotherapy: experimental models and clinical perspectives
    G One Ahn
    Division of Radiation and Cancer Biology, Department of Radiation Oncology, Stanford, California, USA
    Cell Cycle 8:970-6. 2009
    ....
  31. ncbi request reprint Tirapazamine: a hypoxia-activated topoisomerase II poison
    Katherine B Peters
    Division of Radiation and Cancer Biology, Department of Radiation Oncology, Stanford University School of Medicine, 269 Campus Drive, Stanford, CA 94305 5152, USA
    Cancer Res 62:5248-53. 2002
    ..Because TPZ is activated only under hypoxic conditions, which are characteristic of solid tumors, these data implicate TPZ as a tumor-specific topo II poison...
  32. pmc Role of endothelial progenitors and other bone marrow-derived cells in the development of the tumor vasculature
    G One Ahn
    Division of Cancer and Radiation Biology, Department of Radiation Oncology, Stanford University School of Medicine, 269 Campus Drive, CCSR South, Rm1255, Stanford, CA 94305 5152, USA
    Angiogenesis 12:159-64. 2009
    ..In this review, we highlight some of the recent findings on each of these cell types by outlining some of the essential proangiogenic cytokines that these cells secrete to promote tumor angiogenesis and vasculogenesis...
  33. pmc In vivo 1H magnetic resonance spectroscopy of lactate in patients with stage IV head and neck squamous cell carcinoma
    Quynh Thu Le
    Department of Radiation Oncology, Stanford University Medical Center, Stanford, CA 94305 5847, USA
    Int J Radiat Oncol Biol Phys 71:1151-7. 2008
    ..To investigate in vivo(1)H magnetic resonance spectroscopy imaging of lactate for assessing tumor hypoxia in head and neck cancers and to determine its utility in predicting the response and outcomes...
  34. pmc Inhibiting homologous recombination for cancer therapy
    Sophia B Chernikova
    Department of Radiation Oncology, Stanford University, Stanford, CA USA
    Cancer Biol Ther 13:61-8. 2012
    ..We review strategies for identifying HR inhibitors and discuss current progress...
  35. pmc Transcriptional response of Saccharomyces cerevisiae to DNA-damaging agents does not identify the genes that protect against these agents
    Geoff W Birrell
    Department of Radiation Oncology, Stanford University School of Medicine, Stanford, CA 94305, USA
    Proc Natl Acad Sci U S A 99:8778-83. 2002
    ..The data also suggest that the nature of the lesions produced by DNA-damaging agents cannot easily be deduced from gene expression profiling...
  36. ncbi request reprint Estimating DNA repair by sequential evaluation of head and neck tumor radiation sensitivity using the comet assay
    David J Terris
    Division of Otolaryngology Head and Neck Surgery, Stanford University Medical Center, R135, Edwards Bldg, Stanford, CA 94305 5328, USA
    Arch Otolaryngol Head Neck Surg 128:698-702. 2002
    ..The alkaline comet assay is a microelectrophoretic technique for detecting single-strand DNA breaks, and may be used as an indirect measure of hypoxia by determining the radiation sensitivity of individual cells...
  37. pmc A role for Lsmlp in response to ultraviolet-radiation damage in Saccharomyces cerevisiae
    Tatiana Spicakova
    Division of Radiation and Cancer Biology, Department of Radiation Oncology, Stanford University School of Medicine, Stanford, California 94305, USA
    Radiat Res 170:411-21. 2008
    ....
  38. pmc Association of reactive oxygen species levels and radioresistance in cancer stem cells
    Maximilian Diehn
    Department of Radiation Oncology, Stanford University School of Medicine, Stanford, California 94305, USA
    Nature 458:780-3. 2009
    ....
  39. pmc Hypoxia-inducible regulation of a prodrug-activating enzyme for tumor-specific gene therapy
    Toru Shibata
    Department of Radiation Oncology, Stanford University School of Medicine, CA 94305 5152, USA
    Neoplasia 4:40-8. 2002
    ....
  40. ncbi request reprint Similar radiation sensitivities of acutely and chronically hypoxic cells in HT 1080 fibrosarcoma xenografts
    Dirk Vordermark
    Department of Radiation Oncology, Division of Radiation and Cancer Biology, Stanford University School of Medicine, CCSR South, Room 1255, 269 Campus Drive, Stanford, California 94305 5152, USA
    Radiat Res 159:94-101. 2003
    ..We therefore conclude that, at least in this tumor model, the radiation sensitivity of chronically hypoxic cells is similar to that of the acutely hypoxic cells...
  41. ncbi request reprint Targeting tumors with hypoxia-activated cytotoxins
    G One Ahn
    Division of Radiation and Cancer Biology, Department of Radiation Oncology, Stanford University School of Medicine, Stanford, CA 94305 5152, USA
    Front Biosci 12:3483-501. 2007
    ....
  42. pmc Matrix metalloproteinase-9 is required for tumor vasculogenesis but not for angiogenesis: role of bone marrow-derived myelomonocytic cells
    G One Ahn
    Division of Radiation and Cancer Biology, Department of Radiation Oncology, Stanford University School of Medicine, 269 Campus Drive, CCSR South, Room 1255, Stanford, CA 94305, USA
    Cancer Cell 13:193-205. 2008
    ..Our results suggest that MMP-9 could be an important target for adjunct therapy to enhance the response of tumors to radiotherapy...
  43. ncbi request reprint Preferential expression of a mutant allele of the amplified MDR1 (ABCB1) gene in drug-resistant variants of a human sarcoma
    G Kevin Chen
    Oncology Division, Department of Medicine, Stanford University School of Medicine, 269 Campus Drive, Stanford, CA 94305 5151, USA
    Genes Chromosomes Cancer 34:372-83. 2002
    ....
  44. ncbi request reprint The 93rd Annual Meeting of the American Association for Cancer Research. 6-10 April 2002, San Francisco, California, USA
    J Martin Brown
    Stanford University, Stanford, California, USA
    Expert Opin Pharmacother 3:629-32. 2002
    ..There was a mind-boggling array of choices for those interested in cancer research. This meeting was the largest ever convened on a single disease. We will endeavour to provide some of the highlights of this exciting meeting...

Research Grants36

  1. Experimental Radiotherapy and Chemotherapy With a Potent New Hypoxic Cytotoxin
    JOHN MARTIN BROWN; Fiscal Year: 2010
    ....
  2. EXPERIMENTAL RADIOTHERAPY--BASIS AND MODIFICATION
    John Brown; Fiscal Year: 2002
    ..To test this hypothesis we will employ inhibitors of the topo II catalytic cycle as well as cells induced to express high levels of topo II following TPZ treatment ..
  3. Experimental Radiotherapy and Chemotherapy With a Potent New Hypoxic Cytotoxin
    John Brown; Fiscal Year: 2007
    ....
  4. Yeast Gene Ontology by Phenotypic Profiling
    John Brown; Fiscal Year: 2007
    ..abstract_text> ..
  5. Effect of Bone Marrow Cells on the Radiosensitivity of Brain and Mouth Cancers
    JOHN MARTIN BROWN; Fiscal Year: 2010
    ..Targeting both the local tumor and the bone marrow derived cells is a novel paradigm and could lead to a major increase in the curability of GBM and head and neck tumors by radiotherapy. ..
  6. EXPERIMENTAL RADIOTHERAPY BASIS AND MODIFICATION
    John Brown; Fiscal Year: 1999
    ..In this way the researchers expect to increase the clinical efficacy of this new anticancer agent. ..
  7. EXPERIMENTAL RADIOTHERAPY: BASIS AND MODIFICATION
    John Brown; Fiscal Year: 1980
    ..g., lung irradiation, systemic chemotherapy) will be performed to determine their influence on metastatic spread via both the bloodstream and the lymphatics. ..