Research Topics
Genomes and Genes | J Martin BrownSummaryAffiliation: Stanford University Country: USA Publications
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Publications
Tumor microenvironment and the response to anticancer therapyJ 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...
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...
Exploiting tumour hypoxia in cancer treatmentJ Martin Brown
Division of Radiation and Cancer Biology, Department of Radiation Oncology, Stanford, California 94305, USA
Nat Rev Cancer 4:437-47. 2004
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...
Integrating phenotypic and expression profiles to map arsenic-response networksAstrid 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...
Global analysis of gene function in yeast by quantitative phenotypic profilingJames 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...
The role of apoptosis in cancer development and treatment responseJ 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...
Stereotactic ablative radiotherapy should be combined with a hypoxic cell radiosensitizerJ Martin Brown
Department of Radiation Oncology, Stanford University School of Medicine, California 94305, USA
Int J Radiat Oncol Biol Phys 78:323-7. 2010....
Henry S. Kaplan Distinguished Scientist Award Lecture 2007. The remarkable yin and yang of tumour hypoxiaMartin Brown
Department of Radiation Oncology, Stanford University, California 94305, USA
Int J Radiat Biol 86:907-17. 2010....
A noninvasive approach for assessing tumor hypoxia in xenografts: developing a urinary marker for hypoxiaDaniel 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...
Inhibition of vasculogenesis, but not angiogenesis, prevents the recurrence of glioblastoma after irradiation in miceMitomu 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....
Homologous recombination is the principal pathway for the repair of DNA damage induced by tirapazamine in mammalian cellsJames 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....
Comparison of the comet assay and the oxygen microelectrode for measuring tumor oxygenation in head-and-neck cancer patientsQuynh 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...
Inhibition of Mac-1 (CD11b/CD18) enhances tumor response to radiation by reducing myeloid cell recruitmentG 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...
Improved potency of the hypoxic cytotoxin tirapazamine by DNA-targetingYvette 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...
Genome-wide identification of genes conferring resistance to the anticancer agents cisplatin, oxaliplatin, and mitomycin CH Irene Wu
Department of Radiation Oncology, Stanford University School of Medicine, Stanford, California 94305-5152, USA
Cancer Res 64:3940-8. 2004....
Evaluation of hypoxia-inducible factor-1alpha (HIF-1alpha) as an intrinsic marker of tumor hypoxia in U87 MG human glioblastoma: in vitro and xenograft studiesDirk 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...
Radiosensitization of yeast cells by inhibition of histone h4 acetylationSuisui 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...
Tumor hypoxia in cancer therapyJ 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...
Optimized clostridium-directed enzyme prodrug therapy improves the antitumor activity of the novel DNA cross-linking agent PR-104Shie 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...
Identification of mitogen-activated protein kinase signaling pathways that confer resistance to endoplasmic reticulum stress in Saccharomyces cerevisiaeYijun 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...
Influence of bone marrow-derived hematopoietic cells on the tumor response to radiotherapy: experimental models and clinical perspectivesG One Ahn
Division of Radiation and Cancer Biology, Department of Radiation Oncology, Stanford, California, USA
Cell Cycle 8:970-6. 2009....
Multiple endonucleases function to repair covalent topoisomerase I complexes in Saccharomyces cerevisiaeChangchun 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...
Deficiency in mammalian histone H2B ubiquitin ligase Bre1 (Rnf20/Rnf40) leads to replication stress and chromosomal instabilitySophia B Chernikova
Department of Radiation Oncology, Stanford University, Stanford, California 94305, USA
Cancer Res 72:2111-9. 2012....
Tirapazamine: a hypoxia-activated topoisomerase II poisonKatherine 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...
Deficiency in Bre1 impairs homologous recombination repair and cell cycle checkpoint response to radiation damage in mammalian cellsSophia 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...
Hypofractionation results in reduced tumor cell kill compared to conventional fractionation for tumors with regions of hypoxiaDavid 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...
Role of endothelial progenitors and other bone marrow-derived cells in the development of the tumor vasculatureG 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...
In vivo 1H magnetic resonance spectroscopy of lactate in patients with stage IV head and neck squamous cell carcinomaQuynh 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...
Inhibiting homologous recombination for cancer therapySophia 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...
Transcriptional response of Saccharomyces cerevisiae to DNA-damaging agents does not identify the genes that protect against these agentsGeoff 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...
Association of reactive oxygen species levels and radioresistance in cancer stem cellsMaximilian Diehn
Department of Radiation Oncology, Stanford University School of Medicine, Stanford, California 94305, USA
Nature 458:780-3. 2009....
A role for Lsmlp in response to ultraviolet-radiation damage in Saccharomyces cerevisiaeTatiana 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....
Similar radiation sensitivities of acutely and chronically hypoxic cells in HT 1080 fibrosarcoma xenograftsDirk 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...
Hypoxia-inducible regulation of a prodrug-activating enzyme for tumor-specific gene therapyToru Shibata
Department of Radiation Oncology, Stanford University School of Medicine, CA 94305-5152, USA
Neoplasia 4:40-8. 2002....
Targeting tumors with hypoxia-activated cytotoxinsG 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....
Estimating DNA repair by sequential evaluation of head and neck tumor radiation sensitivity using the comet assayDavid 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...
Preferential expression of a mutant allele of the amplified MDR1 (ABCB1) gene in drug-resistant variants of a human sarcomaG 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....
Matrix metalloproteinase-9 is required for tumor vasculogenesis but not for angiogenesis: role of bone marrow-derived myelomonocytic cellsG 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...
R-loops and genomic instability in Bre1 (RNF20/40)-deficient cellsSophia B Chernikova
Department of Radiation Oncology, Stanford University, Stanford, CA, USA
Cell Cycle 11:2980-4. 2012....
The 93rd Annual Meeting of the American Association for Cancer Research. 6-10 April 2002, San Francisco, California, USAJ 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 Grants
- EXPERIMENTAL RADIOTHERAPY--BASIS AND MODIFICATIONJohn 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 ..
- Experimental Radiotherapy and Chemotherapy With a Potent New Hypoxic CytotoxinJohn Brown; Fiscal Year: 2007....
- Yeast Gene Ontology by Phenotypic ProfilingJohn Brown; Fiscal Year: 2007..abstract_text> ..
- Effect of Bone Marrow Cells on the Radiosensitivity of Brain and Mouth CancersJOHN 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. ..
- EXPERIMENTAL RADIOTHERAPY BASIS AND MODIFICATIONJohn Brown; Fiscal Year: 1999..In this way the researchers expect to increase the clinical efficacy of this new anticancer agent. ..
- EXPERIMENTAL RADIOTHERAPY: BASIS AND MODIFICATIONJohn 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. ..
- Experimental Radiotherapy and Chemotherapy With a Potent New Hypoxic CytotoxinJOHN MARTIN BROWN; Fiscal Year: 2010....
