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Genomes and Genes | Konstantin SalnikowSummaryAffiliation: National Cancer Institute Country: USA Publications
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Publications
Ascorbate depletion: a critical step in nickel carcinogenesis?Konstantin Salnikow
Laboratory of Comparative Carcinogenesis, Building 538, Room 205 E, National Cancer Institute at Frederick NIH, Frederick, MD 21702, USA
Environ Health Perspect 113:577-84. 2005..Key words: ascorbate, carcinogenesis, collagens, extracellular matrix, hypoxia-inducible transcription factor, metals, nickel, protein hydroxylation...
Depletion of intracellular ascorbate by the carcinogenic metals nickel and cobalt results in the induction of hypoxic stressKonstantin Salnikow
NCI Frederick, National Institutes of Health, Frederick, Maryland 21702, USA
J Biol Chem 279:40337-44. 2004....
Regulation of hypoxia-inducible genes by ETS1 transcription factorKonstantin Salnikow
Laboratory of Comparative Carcinogenesis, National Cancer Institute at Frederick, Frederick, MD 21702, USA
Carcinogenesis 29:1493-9. 2008..Collectively, our data indicate the involvement of ETS1 along with HIF-1 in regulating hypoxia-inducible genes...- Effect of nickel and iron co-exposure on human lung cellsKonstantin Salnikow
Nelson Institute of Environmental Medicine, EPA PM Health Effects Research Center and NIEHS Environmental Health Sciences Center, New York University School of Medicine, New York, NY 10016, USA
Toxicol Appl Pharmacol 196:258-65. 2004..The obtained data indicate that nickel can induce different signaling pathways with or without interference with iron metabolism. Our observations suggest that in some cases the excess of iron in PM can cancel the effects of nickel... - Ascorbate depletion mediates up-regulation of hypoxia-associated proteins by cell density and nickelAldona Karaczyn
Laboratory of Comparative Carcinogenesis, National Cancer Institute at Frederick, Frederick, Maryland 21702, USA
J Cell Biochem 97:1025-35. 2006..We suggest, that, in addition to low oxygenation, insufficient supply of ascorbate or its excessive oxidation in tumors, can contribute to the induction of hypoxia-associated proteins via both HIF-dependent and independent mechanisms... - Metal ions-stimulated iron oxidation in hydroxylases facilitates stabilization of HIF-1 alpha proteinMonika Kaczmarek
Laboratory of Comparative Carcinogenesis, National Cancer Institute at Frederick, Frederick, Maryland 21702, USA
Toxicol Sci 107:394-403. 2009.... - The role of hypoxia-inducible signaling pathway in nickel carcinogenesisKonstantin Salnikow
Nelson Institute of Environmental Medicine, NIEHS Center and Kaplan Comprehensive Cancer Center, New York University School of Medicine, 550 First Avenue, New York, NY 11016, USA
Environ Health Perspect 110:831-4. 2002.... - Enhanced overexpression of an HIF-1/hypoxia-related protein in cancer cellsHakan Cangul
Department of Environmental Medicine, New York University School of Medicine, 550 First Avenue, New York, NY 10016, USA
Environ Health Perspect 110:783-8. 2002..We hypothesize that the mechanism of Cap43 overexpression in cancer cells involves a state of hypoxia characteristic of cancer cells where the Cap43 protein becomes a signature for this hypoxic state... - The involvement of hypoxia-inducible transcription factor-1-dependent pathway in nickel carcinogenesisKonstantin Salnikow
The Nelson Institute of Environmental Medicine, National Institute of Environmental Health Sciences Center, National Institutes of Health and The New York University Cancer Institute, School of Medicine, New York, NY 10016, USA
Cancer Res 63:3524-30. 2003..We hypothesize that the induction of HIF-1 transcription factor by nickel may be important during the nickel-induced carcinogenic process... - Microarray analysis of altered gene expression in murine fibroblasts transformed by nickel(II) to nickel(II)-resistant malignant phenotypeRenata Kowara
Laboratory of Comparative Carcinogenesis, National Cancer Institute at Frederick, MD 21702, USA
Toxicol Appl Pharmacol 205:1-10. 2005.... - Molecular mechanisms of nickel carcinogenesis: gene silencing by nickel delivery to the nucleus and gene activation/inactivation by nickel-induced cell signalingMax Costa
Department of Environmental Medicine, New York University School of Medicine, 550 First Avenue, New York, NY 10016, USA
J Environ Monit 5:222-3. 2003.... - The role of ascorbate in the modulation of HIF-1alpha protein and HIF-dependent transcription by chromium(VI) and nickel(II)Monika Kaczmarek
National Cancer Institute at Frederick, Building 538, Room 205 E, Frederick, MD 21701, USA
Free Radic Biol Med 42:1246-57. 2007..Thus, the obtained data emphasize the important role of ascorbate in regulation of HIF-1 transcriptional activity in metal-exposed human lung cells... - GeneChip analysis of signaling pathways effected by nickelKonstantin Salnikow
Nelson Institute of Environmental Medicine, NYU NIEHS Center of Excellence, The NYU Cancer Institute, New York University School of Medicine, 550 First Avenue, New York, NY 10016, USA
J Environ Monit 5:206-9. 2003..The activation of the same signaling pathways by soluble and insoluble nickel compounds suggested that both nickel compounds have similar carcinogenic potential in vitro... - The role of oxidative stress in nickel and chromate genotoxicityMax Costa
Department of Environmental Medicine, New York University School of Medicine, Tuxedo 10987, USA
Mol Cell Biochem 234:265-75. 2002..In addition to nickel, the role of oxidative stress in chromate-induced genotoxicity will also be discussed with particular attention directed to the effects of vitamin E on mutations and chromosomal aberrations inducedby chromate... - Genetic and epigenetic mechanisms in metal carcinogenesis and cocarcinogenesis: nickel, arsenic, and chromiumKonstantin Salnikow
National Cancer Institute, Frederick, MD 21702, USA
Chem Res Toxicol 21:28-44. 2008..Overall, metal carcinogenesis appears to require the formation of specific metal complexes, chromosomal damage, and activation of signal transduction pathways promoting survival and expansion of genetically/epigenetically altered cells... - Nickel-induced down-regulation of serpin by hypoxic signalingJianhua Zhao
Department of Environmental Medicine, New York University School of Medicine, Tuxedo, NY 10987, USA
Toxicol Appl Pharmacol 194:60-8. 2004..Serpina3g gene expression returned to basal levels following Ni removal, suggesting that the observed silencing was a dynamic and reversible process... - Nickel carcinogenesisKazimierz S Kasprzak
Laboratory of Comparative Carcinogenesis, National Cancer Institute at Frederick, Frederick, MD 21702 1201, USA
Mutat Res 533:67-97. 2003.... - Hypoxia inducible factor-1 alpha-independent suppression of aryl hydrocarbon receptor-regulated genes by nickelTodd Davidson
Nelson Institute of Environmental Medicine, New York University School of Medicine, NewYork, USA
Mol Pharmacol 64:1485-93. 2003..Our data suggest that an Fe(II)-, oxoglutarate-, and oxygen-dependent enzyme may directly or indirectly be involved in the regulation of AhR-dependent transcriptional activity by nickel and other hypoxia-mimicking agents... - Two novel VHL targets, TGFBI (BIGH3) and its transactivator KLF10, are up-regulated in renal clear cell carcinoma and other tumorsSergey V Ivanov
Basic Research Program, SAIC Frederick, Inc, 462 First Avenue, Bellevue Hospital, Room 15N20, NY 10016, USA
Biochem Biophys Res Commun 370:536-40. 2008..These data provide the molecular basis for the observed VHL effect on TGFBI and stimulate further research into the KLF10 and TGFBI roles in cancer... - Quantum chemical modeling of reaction mechanism for 2-oxoglutarate dependent enzymes: effect of substitution of iron by nickel and cobaltIgor A Topol
Advanced Biomedical Computing Center, SAIC Frederick, National Cancer Institute at Frederick, Frederick, Maryland 21702, USA
J Phys Chem A 110:4223-8. 2006..Thus, we would postulate that if the iron ion in the active site were substitutable by nickel and/or cobalt ions enzyme activity would be considerably altered due to high activation barriers... - Downregulation of major histocompatibility complex antigens in invading glioma cells: stealth invasion of the brainDavid Zagzag
Microvascular and Molecular Neuro Oncology Laboratory, New York University School of Medicine, New York, NY, USA
Lab Invest 85:328-41. 2005..These results suggest that the very process of tumor invasion is associated with decreased expression of MHC antigens allowing glioma cells to invade the surrounding brain in a 'stealth'-like manner... - Effects of ascorbic acid on carcinogenicity and acute toxicity of nickel subsulfide, and on tumor transplants growth in gulonolactone oxidase knock-out mice and wild-type C57BL miceKazimierz S Kasprzak
Laboratory of Comparative Carcinogenesis, National Cancer Institute at Frederick, Frederick, MD 21702, USA
Toxicol Appl Pharmacol 257:32-7. 2011..Dietary ascorbate tends to attenuate acute toxicity of Ni₃S₂ and to extend the latency of transplanted tumors. The latter effects may be of practical importance to humans and thus deserve further studies... - Extracellular matrix and HIF-1 signaling: the role of prolidaseArkadiusz Surazynski
Metabolism and Cancer Susceptibility Section, Laboratory of Comparative Carcinogenesis, National Cancer Institute at Frederick, Frederick, MD 21702, USA
Int J Cancer 122:1435-40. 2008..These findings show that metabolism of imidodipeptides by prolidase plays a previously unrecognized role in angiogenic signaling... - Altered N-myc downstream-regulated gene 1 protein expression in African-American compared with caucasian prostate cancer patientsRobert P Caruso
Department of Urology, New York University Cancer Institute, Kaplan Comprehensive Cancer Center, New York, USA
Clin Cancer Res 10:222-7. 2004..Further studies are needed to determine the contribution of NDRG1 to the disparity in clinical outcome observed between the two groups... - The regulation of hypoxic genes by calcium involves c-Jun/AP-1, which cooperates with hypoxia-inducible factor 1 in response to hypoxiaKonstantin Salnikow
Department of Environmental Medicine, NIEHS and Kaplan Comprehensive Cancer Center, New York University School of Medicine, 550 First Avenue, New York, NY 10016, USA
Mol Cell Biol 22:1734-41. 2002..Cooperation between the HIF-1 and AP-1 pathways allows fine regulation of gene expression during hypoxia... - Effects of select PM-associated metals on alveolar macrophage phosphorylated ERK1 and -2 and iNOS expression during ongoing alteration in iron homeostasisColette Prophete
NYU-EPA Particulate Matter Health Research Center, Nelson Institute of Environmental Medicine, New York University School of Medicine, Tuxedo, New York 10987, USA
J Toxicol Environ Health A 69:935-51. 2006..These results confirmed our hypothesis that certain metals associated with PM(2.5) might alter the pulmonary immunocompetence of exposed hosts by affecting the Fe status of AM, a major class of deep lung defense cells... - Reduced Fhit protein expression in nickel-transformed mouse cells and in nickel-induced murine sarcomasRenata Kowara
Laboratory of Comparative Carcinogenesis, National Cancer Institute at Frederick, Frederick, MD 21702-1201, USA
Mol Cell Biochem 255:195-202. 2004..Overall, the decline of Fhit in cells or tissues malignantly transformed by nickel may indicate possible involvement of this effect in the mechanisms of nickel carcinogenesis... - Comparison of the cytotoxicity, cellular uptake, and DNA-protein crosslinks induced by potassium chromate in lymphoblast cell lines derived from three different individualsQunwei Zhang
Department of Environmental Medicine, New York University School of Medicine, Tuxedo 10987, USA
Biol Trace Elem Res 86:11-22. 2002..This lower uptake of chromate combined with interindividual differences in extracellular Cr(VI) reducing capacity are probably the two most important determinants of genetic susceptibility to chromate toxicity... - A new intrinsic hypoxia marker in esophageal cancerIvan Ding
University of Rochester School of Medicine and Dentistry, Rochester, New York 14642, USA
Adv Exp Med Biol 540:227-33. 2003 - HIF-1: an oxygen and metal responsive transcription factorPatrick Maxwell
Imperial College, London, UK
Cancer Biol Ther 3:29-35. 2004..Here we review the implications of the metal sensitivity of the HIF-1 system, and examine the hypothesis that HIF-1 activation may play an important role in metal induced carcinogenesis... - Inhibition and reversal of nickel-induced transformation by the histone deacetylase inhibitor trichostatin AQunwei Zhang
Department of Environmental Medicine, NYU School of Medicine, 57 Old Forge Road, Tuxedo, NY 10987, USA
Toxicol Appl Pharmacol 192:201-11. 2003..In contrast, treatment with TSA was not able to revert established cancer cell lines as readily as the nickel-transformed cells. These data indicated that modulation of gene expression is important for nickel-induced transformation... - Molecular mechanisms in nickel carcinogenesis: modeling Ni(II) binding site in histone H4Maria Antonietta Zoroddu
Department of Chemistry, University of Sassari, Via Vienna 2, 07100 Sassari, Italy
Environ Health Perspect 110:719-23. 2002..The results allowed us to propose that the binding of Ni(II) is able to promote a secondary structure with organized side-chain orientation on the N-terminal tail of histone H4... - Backing into cancer: effects of arsenic on cell differentiationKonstantin Salnikow
Department of Environmental Medicine, New York University Medical Center, 57 Old Forge Road, Tuxedo, New York 10987, USA
Toxicol Sci 65:161-3. 2002