Research Topics
Species | D GiusSummaryAffiliation: National Institutes of Health Country: USA Publications
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Publications
Redox signaling in cancer biologyDavid Gius
Antioxid Redox Signal 8:1249-52. 2006..This Forum is directed at understanding possible redox signaling mechanisms governing cellular radiation response, tumor growth, and response to therapy, as well as the role of nitric oxide in cancer biology...- Redox-sensitive signaling factors and antioxidants: how tumor cells respond to ionizing radiationDavid Gius
Molecular Radiation Oncology Section, National Cancer Institute/NIH, Bethesda, MD 20892, USA
J Nutr 134:3213S-3214S. 2004 
SIRT3 interacts with the daf-16 homolog FOXO3a in the mitochondria, as well as increases FOXO3a dependent gene expressionKristi Muldoon Jacobs
Molecular Radiation Oncology, Center for Cancer Research, Radiation Oncology Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA
Int J Biol Sci 4:291-9. 2008..As such, we propose that SIRT3 and FOXO3a comprise a potential mitochondrial signaling cascade response pathway...- Thermal stress and the disruption of redox-sensitive signalling and transcription factor activation: possible role in radiosensitizationD Gius
Molecular Radiation Oncology Section, Radiation Oncology Branch, Radiation Oncology Sciences Program, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA
Int J Hyperthermia 20:213-23. 2004.... - The epigenome as a molecular marker and targetDavid Gius
Molecular Radiation Oncology Section, Radiation Oncology Branch, Radiation Oncology Sciences Program, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892 1002, USA
Cancer 104:1789-93. 2005..Perhaps more noteworthy is that DNMT genes may be found to be novel molecular targets for new factor-specific anticancer agents. This idea will be addressed... - Profiling microdissected epithelium and stroma to model genomic signatures for cervical carcinogenesis accommodating for covariatesDavid Gius
Radiation Oncology Branch, Center for Cancer Research, National Cancer Institute, NIH, Bethesda, Maryland 20892, USA
Cancer Res 67:7113-23. 2007.... - Heat shock and the activation of AP-1 and inhibition of NF-kappa B DNA-binding activity: possible role of intracellular redox statusD Mattson
Section of Molecular Radiation Oncology, Radiation Oncology Branch, Radiation Oncology Sciences Program, Center for Cancer Research, National Cancer Institute, National Institutes of Health, 9000 Rockville Pike, Bethesda, MD 20892, USA
Int J Hyperthermia 20:224-33. 2004.... - Indomethacin-induced radiosensitization and inhibition of ionizing radiation-induced NF-kappaB activation in HeLa cells occur via a mechanism involving p38 MAP kinaseC M Bradbury
Radiation Oncology Branch, Radiation Oncology Sciences Program, Center for Cancer Research, National Cancer Institute, NIH, Bethesda, Maryland 20892, USA
Cancer Res 61:7689-96. 2001..Taken together, these results suggest that p38 MAPK is a target involved in indomethacin-induced radiosensitization and that NF-kappaB may be one downstream target in this process... - Thioredoxin reductase as a novel molecular target for cancer therapyPhuongmai Nguyen
Molecular Radiation Oncology Section, Radiation Oncology Branch, Radiation Oncology Sciences Program, Center for Cancer Research, National Cancer Institute, National Institutes of Health, 9000 Rockville Pike, Bethesda, MD 20892, USA
Cancer Lett 236:164-74. 2006..Based on these results we believe TR is a potential molecular target and discuss potential clinical possibilities... 
DNMT1 as a molecular target in a multimodality-resistant phenotype in tumor cellsMark V Mishra
Radiation Oncology Branch, National Cancer Institute, NIH, Bethesda, MD 20892, USA
Mol Cancer Res 6:243-9. 2008....- Distinct effects on gene expression of chemical and genetic manipulation of the cancer epigenome revealed by a multimodality approachDavid Gius
Radiation Oncology Branch, Radiation Oncology Sciences Program, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA
Cancer Cell 6:361-71. 2004..In addition, a 75 kb cluster of metallothionein genes was coordinately regulated... - BAT3 and SET1A form a complex with CTCFL/BORIS to modulate H3K4 histone dimethylation and gene expressionPhuongmai Nguyen
Radiation Oncology Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA
Mol Cell Biol 28:6720-9. 2008..Thus, we propose that BORIS acts as a platform upon which BAT3 and SET1A assemble and exert effects upon chromatin structure and gene expression... - Inhibition of cyclooxygenase-2 with NS-398 and the prevention of radiation-induced transformation, micronuclei formation and clonogenic cell death in C3H 10T1/2 cellsK S Bisht
Molecular Radiation Oncology Section, Radiation Oncology Branch, Radiation Oncology Sciences Program, Center for Cancer Research, National Cancer Institute National Institutes of Health, 9000 Rockville Pike, Bethesda, MD 20892, USA
Int J Radiat Biol 79:879-88. 2003.... - Inhibition of nuclear factor-kappaB and target genes during combined therapy with proteasome inhibitor bortezomib and reirradiation in patients with recurrent head-and-neck squamous cell carcinomaCarter Van Waes
Head and Neck Surgery Branch, National Institute on Deafness and Other Communication Disorders, Bethesda, MD 20892, USA
Int J Radiat Oncol Biol Phys 63:1400-12. 2005.... - BAG-4/SODD and associated antiapoptotic proteins are linked to aggressiveness of epithelial ovarian cancerChristina M Annunziata
Medical Oncology Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, 10 Center Drive, Bethesda, MD 20892, USA
Clin Cancer Res 13:6585-92. 2007..We hypothesized that elevated expression in ovarian cancer of the BAG family of prosurvival proteins and associated partners would be associated with clinical features of aggressiveness in ovarian cancer... - Thioredoxin reductase as a potential molecular target for anticancer agents that induce oxidative stressDeedee K Smart
Molecular Radiation Oncology Section, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892, USA
Cancer Res 64:6716-24. 2004..Finally, IV-2-treated cells showed increased tumor cell death when treated with H2O2 and IR. These results identify TR as a potential target to enhance the cytotoxic effects of agents that induce oxidative stress, including IR... - Oxidative stress, redox, and the tumor microenvironmentJohn A Cook
Radiation Biology Branch, Center for Cancer Research, National Cancer Institute, Bethesda, MD 20892, USA
Semin Radiat Oncol 14:259-66. 2004..With respect to the radiation treatment of cancer, components of the cellular redox armamentarium may be targeted to enhance cell killing in the case of tumors and/or protection in the case of normal tissues... - Patterns of care for women with cervical cancer in the United StatesEdward L Trimble
National Cancer Institute, Surgery Section, Bethesda, Maryland 20892 7436, USA
Cancer 113:743-9. 2008..This analysis was initiated to determine any systemic changes in management of cervical cancers... - SIRT3 is a mitochondria-localized tumor suppressor required for maintenance of mitochondrial integrity and metabolism during stressHyun Seok Kim
Genetics of Development and Disease Branch, NIDDK, NIH, Bethesda, MD 20892, USA
Cancer Cell 17:41-52. 2010..Finally, human breast and other human cancer specimens exhibit reduced SIRT3 levels. These results identify SIRT3 as a genomically expressed, mitochondria-localized tumor suppressor... - Molecular and clinical responses in a pilot study of gefitinib with paclitaxel and radiation in locally advanced head-and-neck cancerCarter Van Waes
Head and Neck Surgery Branch, National Institute of Deafness and Communication Disorders, National Institutes of Health, Bethesda, MD, USA
Int J Radiat Oncol Biol Phys 77:447-54. 2010.... - Ionizing radiation-induced oxidative stress alters miRNA expressionNicole L Simone
Radiation Oncology Branch, Center for Cancer Research, National Cancer Institute, NIH, Bethesda, MD, USA
PLoS ONE 4:e6377. 2009..Alterations in miRNA expression may occur following exposure to several stress-inducing anticancer agents including ionizing radiation, etoposide, and hydrogen peroxide (H(2)O(2))... - Genomic and phenotypic analysis reveals a key role for CCN1 (CYR61) in BAG3-modulated adhesion and invasionJareer N Kassis
Medical Oncology Branch, Center for Cancer Research, National Cancer Institute, Bethesda, MD 20892, USA
J Pathol 218:495-504. 2009..We propose that BAG3 regulates CCN1 expression to regulate tumour cell adhesion and migration... - Redox-sensitive signaling factors as a novel molecular targets for cancer therapyJ Daniel Pennington
Molecular Radiation Oncology Section, Radiation Oncology Branch, Radiation Oncology Sciences Program, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bldg. 10, Room B3B69 9000 Rockville Pike, Bethesda, MD 20892, USA
Drug Resist Updat 8:322-30. 2005..It further suggests that redox-sensitive, signaling factors may be potential novel targets for drug discovery... - Simultaneous inhibition of hsp 90 and the proteasome promotes protein ubiquitination, causes endoplasmic reticulum-derived cytosolic vacuolization, and enhances antitumor activityEdward G Mimnaugh
Urologic Oncology Branch, Center for Cancer Research, National Cancer Institute, NIH, Rockville, Maryland 20850, USA
Mol Cancer Ther 3:551-66. 2004.... - Geldanamycin and 17-allylamino-17-demethoxygeldanamycin potentiate the in vitro and in vivo radiation response of cervical tumor cells via the heat shock protein 90-mediated intracellular signaling and cytotoxicityKheem S Bisht
Radiation Oncology Branch and. Radiation Biology Branch, Center for Cancer Research, National Cancer Institute, NIH, Bethesda, Maryland 20892-1002, USA
Cancer Res 63:8984-95. 2003..This work shows that altered HSP90 function induces significant tumor cytotoxicity and radiosensitization, suggesting a potential therapeutic utility... - DNA methyltransferase 1 and 3B activate BAG-1 expression via recruitment of CTCFL/BORIS and modulation of promoter histone methylationLunching Sun
Radiation Oncology Branch, Center for Cancer Research, National Cancer Institute, NIH, Bethesda, Maryland, USA
Cancer Res 68:2726-35. 2008..These results suggest that DNMT1 and DNMT3B regulate BAG-1 expression via insulator protein DNA-binding and chromatin dynamics by regulating histone dimethylation... - Thioredoxin and thioredoxin reductase as redox-sensitive molecular targets for cancer therapyJ Daniel Pennington
Molecular Radiation Oncology Section, Radiation Oncology Branch, Radiation Oncology Sciences Program, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892, USA
Curr Pharm Des 13:3368-77. 2007..These observations suggest that redox-sensitive signaling factors may be potential novel molecular targets for drug discovery... - DNA (cytosine-5)-methyltransferase 1 as a mediator of mutant p53-determined p16(ink4A) down-regulationZhanjun Guo
Radiation Biology and Oncology Branches, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD, 20892, USA
J Biomed Sci 15:163-8. 2008..Our results indicate that mutant p53 loses its ability to suppress DNMT1 expression, and thus enhances methylation levels of the p16 ( ink4A ) promoter and subsequently down-regulates p16(ink4A )protein... - CTCFL/BORIS is a methylation-independent DNA-binding protein that preferentially binds to the paternal H19 differentially methylated regionPhuongmai Nguyen
Radiation Oncology Branch, Center for Cancer Research, National Cancer Institute, NIH, Bethesda, Maryland 20892, USA
Cancer Res 68:5546-51. 2008.... - Histone deacetylase inhibitor and demethylating agent chromatin compaction and the radiation response by cancer cellsGil Bar Sela
Radiation Oncology Branch, Radiation Oncology Sciences Program, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA
Cancer J 13:65-9. 2007..In this review, we discuss the potential for histone deacetylases inhibitors as radiosensitizing agents... - High incidence of oral dysesthesias on a trial of gefitinib, Paclitaxel, and concurrent external beam radiation for locally advanced head and neck cancersHadley Sharp
Radiation Oncology Branch, Center for Cancer Research, National Cancer Institute, NIH, Bethesda, MD, USA
Am J Clin Oncol 31:557-60. 2008.... - Characterization of the murine SIRT3 mitochondrial localization sequence and comparison of mitochondrial enrichment and deacetylase activity of long and short SIRT3 isoformsJianjun Bao
Translational Medicine Branch, NHLBI, NIH, Bethesda, Maryland, USA
J Cell Biochem 110:238-47. 2010..This overexpression effect, may partially account for previously observed divergent phenotypes attributed to SIRT3... - In vitro and in vivo radiosensitization induced by the ribonucleotide reductase inhibitor Triapine (3-aminopyridine-2-carboxaldehyde-thiosemicarbazone)Christopher A Barker
Radiation Oncology Branch, National Cancer Institute, Bethesda, Maryland, USA
Clin Cancer Res 12:2912-8. 2006..CONCLUSIONS: These results indicate that Triapine can enhance tumor cell radiosensitivity in vitro and in vivo and suggest that this effect involves an inhibition of DNA repair... - Thioredoxin reductase regulates AP-1 activity as well as thioredoxin nuclear localization via active cysteines in response to ionizing radiationShervin Karimpour
Radiation Oncology Branch, Radiation Oncology Sciences Program, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892, USA
Oncogene 21:6317-27. 2002..These results identify a novel function of the TR enzyme as a signaling factor in the regulation of AP-1 activity via a cysteine motif located in the protein... - 2-Deoxy-D-glucose-induced cytotoxicity and radiosensitization in tumor cells is mediated via disruptions in thiol metabolismXiao Lin
Section of Cancer Biology, Mallinckrodt Institute of Radiology, Washington University School of Medicine, St. Louis, Missouri, USA
Cancer Res 63:3413-7. 2003.... - Metabolic oxidation/reduction reactions and cellular responses to ionizing radiation: a unifying concept in stress response biologyDouglas R Spitz
B180 Medical Laboratories, Free Radical and Radiation Biology Program, Department of Radiation Oncology, Holden Comprehensive Cancer Center, University of Iowa, Iowa City, Iowa 52242, USA
Cancer Metastasis Rev 23:311-22. 2004.... - Co-activation of ERK, NF-kappaB, and GADD45beta in response to ionizing radiationTieli Wang
Division of Radiation Oncology, Beckman Research Institute and City of Hope National Medical Center, Duarte, California 91010, USA
J Biol Chem 280:12593-601. 2005..Overall, these results demonstrate a possibility that NF-kappaB, ERK, and GADD45beta are able to coordinate in a loop-like signaling network to defend cells against the cytotoxicity induced by ionizing radiation... - Epigenetic silencing of tumour suppressor gene p15 by its antisense RNAWenqiang Yu
Center for Epigenetics and Department of Medicine, Johns Hopkins University School of Medicine, 720 Rutland Avenue, Baltimore, Maryland 21205, USA
Nature 451:202-6. 2008..Thus, natural antisense RNA may be a trigger for heterochromatin formation and DNA methylation in TSG silencing in tumorigenesis... - Identification of chromosomal alterations important in the development of cervical intraepithelial neoplasia and invasive carcinoma using alignment of DNA microarray dataMargaret A Fitzpatrick
Department of Obstetrics and Gynecology, Division of Gynecologic Oncology, Washington University School of Medicine, St Louis, MO 63110, USA
Gynecol Oncol 103:458-62. 2006..CONCLUSIONS: Alignment of microarray expression data by chromosomes can be used to estimate regions of potential chromosomal aberration and identify differentially expressed genes important in the development of CIN and invasive cancer... - Radiosensitizing and anti-proliferative effects of resveratrol in two human cervical tumor cell linesImran Zoberi
Section of Cancer Biology, Mallinckrodt Institute of Radiology, Washington University School of Medicine, St. Louis, MO, USA
Cancer Lett 175:165-73. 2002..These results suggest that resveratrol alters both cell cycle progression and the cytotoxic response to IR in two cervical tumor cell lines... - Redox-sensitive interaction between KIAA0132 and Nrf2 mediates indomethacin-induced expression of gamma-glutamylcysteine synthetaseKonjeti R Sekhar
Dept of Radiation Oncology, Vanderbilt University School of Medicine, Nashville, TN 37232, USA
Free Radic Biol Med 32:650-62. 2002..These results also support the hypothesis that indomethacin-induced transcriptional activation of GCLC involves the redox-dependent release of KIAA0132 from Nrf2 followed by the nuclear translocation of Nrf2... - A novel p53-inducible apoptogenic gene, PRG3, encodes a homologue of the apoptosis-inducing factor (AIF)Yoichi Ohiro
Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02215, USA
FEBS Lett 524:163-71. 2002..The PRG3 gene is thus a novel p53 target gene in a p53-dependent apoptosis pathway... - Distinct effects of ionizing radiation on in vivo murine kidney and brain normal tissue gene expressionWeiling Zhao
Department of Radiation Oncology, Brain Tumor Center of Wake Forest University, Wake Forest University School of Medicine, Winston-Salem, North Carolina, USA
Clin Cancer Res 12:3823-30. 2006.... - Inhibition of stress-inducible kinase pathways by tumorigenic mutant p53Yoichi Ohiro
Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts 02215, USA
Mol Cell Biol 23:322-34. 2003..Thus, the accumulation of mutant p53 in tumor cells may contribute to tumorigenesis by inhibiting stress-inducible kinase pathways... - The holy grail of radiation oncology: lessons learned from hyperthermiaShervin Karimpour
Int J Radiat Oncol Biol Phys 55:3-4. 2003 - Thioredoxin and lipoic acid catalyze the denitrosation of low molecular weight and protein S-nitrosothiolsDetcho A Stoyanovsky
Department of Surgery, University of Pittsburgh, Pittsburgh, Pennsylvania 15213, USA
J Am Chem Soc 127:15815-23. 2005..We conclude that both thioredoxin and dihydrolipoic acid may be involved in the regulation of cellular S-nitrosothiols... - Indomethacin and ibuprofen induce Hsc70 nuclear localization and activation of the heat shock response in HeLa cellsLucio Lagunas
Division of Radiation and Cancer Biology, Department of Radiation Oncology, Mallinckrodt Institute of Radiology, Washington University School of Medicine, St. Louis, MO, USA
Biochem Biophys Res Commun 313:863-70. 2004....