The DOI matches its Crossref record; 10 of the 10 references it cites were found in a registry or an index.
Genetic and Epigenetic Mechanisms in Metal Carcinogenesis and Cocarcinogenesis: Nickel, Arsenic, and Chromium
Open accessAbstract
Chronic exposure to nickel(II), chromium(VI), or inorganic arsenic (iAs) has long been known to increase cancer incidence among affected individuals. Recent epidemiological studies have found that carcinogenic risks associated with chromate and iAs exposures were substantially higher than previously thought, which led to major revisions of the federal standards regulating ambient and drinking water levels. Genotoxic effects of Cr(VI) and iAs are strongly influenced by their intracellular metabolism, which creates several reactive intermediates and byproducts. Toxic metals are capable of potent and surprisingly selective activation of stress-signaling pathways, which are known to contribute to the development of human cancers. Depending on the metal, ascorbate (vitamin C) has been found to act either as a strong enhancer or suppressor of toxic responses in human cells. In addition to genetic damage via both oxidative and nonoxidative (DNA adducts) mechanisms, metals can also cause significant changes in DNA methylation and histone modifications, leading to epigenetic silencing or reactivation of gene expression. In vitro genotoxicity experiments and recent animal carcinogenicity studies provided strong support for the idea that metals can act as cocarcinogens in combination with nonmetal carcinogens. Cocarcinogenic and comutagenic effects of metals are likely to stem from their ability to interfere with DNA repair processes. 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.
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Jaakkola, P., Mole, D. R., Tian, Y.-M., Wilson, M. I., Gielbert, J., Gaskell, S. J., Kriegsheim, A. V., Hebestreit, H. F., Mukherji, M., Schofield, C. J., et al. (2001) · Science · doi:10.1126/science.1059796 · Cited by 5,535
The tumour suppressor protein VHL targets hypoxia-inducible factors for oxygen-dependent proteolysis
Maxwell, P. H., Wiesener, M. S., Chang, G.-W., Clifford, S. C., Vaux, E. C., Cockman, M. E., Wykoff, C. C., Pugh, C. W., Maher, E. R., & Ratcliffe, P. J. (1999) · Nature · doi:10.1038/20459 · Cited by 5,180
HIFα Targeted for VHL-Mediated Destruction by Proline Hydroxylation: Implications for O 2 Sensing
Ivan, M., Kondo, K., Yang, H., Kim, W., Valiando, J., Ohh, M., Salic, A., Asara, J. M., Lane, W. S., & Kaelin Jr., W. G. (2001) · Science · doi:10.1126/science.1059817 · Cited by 4,735
Mitochondrial reactive oxygen species trigger hypoxia-induced transcription
Chandel, N. S., Maltepe, E., Goldwasser, E., Mathieu, C. E., Simon, M. C., & Schumacker, P. T. (1998) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.95.20.11715 · Cited by 1,926
Lando, D., Peet, D. J., Gorman, J. J., Whelan, D. A., Whitelaw, M. L., & Bruick, R. K. (2002) · Genes & Development · doi:10.1101/gad.991402 · Cited by 1,550 · cited 1×
“asparagine 803 hydroxylation, which allows for complex formation between HIF-1α and the CBP and p300 transcriptional co-activators, regulates transactivation of HIF-dependent genes (49,50).”
BackgroundMasson, N., Willam, C., Maxwell, P. H., Pugh, C. W., & Ratcliffe, P. J. (2001) · The EMBO Journal · doi:10.1093/emboj/20.18.5197 · Cited by 1,014
Structural basis for the recognition of hydroxyproline in HIF-1α by pVHL
Hon, W.-C., Wilson, M. I., Harlos, K., Claridge, T. D. W., Schofield, C. J., Pugh, C. W., Maxwell, P. H., Ratcliffe, P. J., Stuart, D. I., & Jones, E. Y. (2002) · Nature · doi:10.1038/nature00767 · Cited by 751
Zhao, C. Q., Young, M. R., Diwan, B. A., Coogan, T. P., & Waalkes, M. P. (1997) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.94.20.10907 · Cited by 559
Cancer in xeroderma pigmentosum and related disorders of DNA repair
Cleaver, J. E. (2005) · Nature Reviews Cancer · doi:10.1038/nrc1652 · Cited by 427
Govindarajan, B., Klafter, R., Miller, M. S., Mansur, C., Mizesko, M., Bai, X., LaMontagne, K., & Arbiser, J. L. (2002) · Molecular Medicine · doi:10.1007/bf03401997 · Cited by 145
Cited by
Nickel: Human Health and Environmental Toxicology
Genchi, G., Carocci, A., Lauria, G., Sinicropi, M. S., & Catalano, A. (2020) · International Journal of Environmental Research and Public Health · doi:10.3390/ijerph17030679 · Cited by 1,602
Carcinogenic metal compounds: recent insight into molecular and cellular mechanisms
Beyersmann, D., & Hartwig, A. (2008) · Archives of Toxicology · doi:10.1007/s00204-008-0313-y · Cited by 1,206
Chromium in Drinking Water: Sources, Metabolism, and Cancer Risks
Zhitkovich, A. (2011) · Chemical Research in Toxicology · doi:10.1021/tx200251t · Cited by 1,132
Self-citationValavanidis, A., Vlachogianni, T., Fiotakis, K., & Loridas, S. (2013) · International Journal of Environmental Research and Public Health · doi:10.3390/ijerph10093886 · Cited by 910
Prasad, S., Yadav, K. K., Kumar, S., Gupta, N., Cabral-Pinto, M. M. S., Rezania, S., Radwan, N., & Alam, J. (2021) · Journal of Environmental Management · doi:10.1016/j.jenvman.2021.112174 · Cited by 744
Metadata
- Authors
- Salnikow, K., & Zhitkovich, A.
- Venue
- Chemical Research in Toxicology
- Publisher
- American Chemical Society (ACS)
- Published
- 2007-10-30
- Volume
- 21
- Issue
- 1
- Pages
- 28-44
- ISSN
- 0893-228X (ISSN-L)
- 1520-5010
- OpenAlex
- W2029367870
- Cited by
- 924
- References
- 10
- FWCI
- 29.12
- Type
- journal article
- Language
- en
- Open access
- hybrid
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- Salnikow, K., & Zhitkovich, A. (2008). Genetic and Epigenetic Mechanisms in Metal Carcinogenesis and Cocarcinogenesis: Nickel, Arsenic, and Chromium. Chemical Research in Toxicology. https://doi.org/10.1021/tx700198a
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