The DOI matches its Crossref record; 8 of the 8 references it cites were found in a registry or an index.
Increased colonic inflammatory injury and formation of aberrant crypt foci in Nrf2‐deficient mice upon dextran sulfate treatment
Abstract
Chronic inflammation has been associated with increased risk of developing cancer. The transcription factor NF‐E2‐related factor 2 (Nrf2) controls the expression of numerous antioxidative enzymes that have been shown to attenuate acute inflammation. The present study investigated the role of Nrf2 genotype in modulating inflammation‐promoted colorectal tumorigenesis. Nrf2 wild‐type (WT) and Nrf2‐deficient (N0) mice were administered a single dose of azoxymethane followed by a 1‐week dose of drinking water with or without 1% dextran sulfate sodium (DSS). Aberrant crypt foci were counted 3 weeks after the cessation of DSS treatment. DSS treatment significantly increased numbers of aberrant crypt foci in N0 mice, but not WT mice. The extent of inflammation over the course of DSS treatment was analyzed in both genotypes. Histological analysis of colon sections revealed that N0 mice had markedly increased inflammation and mucosal damage when compared to WT mice beginning on Day 6 of DSS treatment. Although similar levels of inflammatory and oxidative damage biomarkers were evident in colons from WT and N0 mice at the start of DSS treatment, increased colonic proinflammatory cytokine mRNA transcript levels, myeloperoxidase activity and 3‐nitrotyrosine immunoreactivity were observed on Day 6 of DSS treatment in N0 mice, but not WT mice. Additionally, DSS treatment resulted in increased lipid peroxidation and loss of aconitase activity in N0 mice, but not WT mice, reflecting increased oxidative damage in colons from N0 mice. Taken together, these results clearly illustrate the role of Nrf2 in regulating an adaptive response that protects against early‐phase inflammation‐mediated tumorigenesis. © 2007 Wiley‐Liss, Inc.
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IKKβ Links Inflammation and Tumorigenesis in a Mouse Model of Colitis-Associated Cancer
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Nrf2 is a critical regulator of the innate immune response and survival during experimental sepsis
Thimmulappa, R. K. (2006) · Journal of Clinical Investigation · doi:10.1172/jci25790 · Cited by 1,028 · cited 5×
“Thimmulappa et al.23 demonstrated that an active Nrf2 adaptive response can decrease lipopolysaccharide (LPS)-induced expression of TNF-a in lung tissue resulting in decreased lethality of WT mice, compared to N0 mice, in a murine model of sepsis.”
BackgroundInfluentialDisruption of Nrf2 enhances susceptibility to severe airway inflammation and asthma in mice
Rangasamy, T., Guo, J., Mitzner, W. A., Roman, J., Singh, A., Fryer, A. D., Yamamoto, M., Kensler, T. W., Tuder, R. M., Georas, S. N., et al. (2005) · The Journal of Experimental Medicine · doi:10.1084/jem.20050538 · Cited by 580
Self-citationSeril, D. N. (2003) · Carcinogenesis · doi:10.1093/carcin/24.3.353 · Cited by 467
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Self-citationChromosomal instability in ulcerative colitis is related to telomere shortening
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Cited by
Nrf2 signaling pathway: pivotal roles in inflammation
Ahmed, S. M. U., Luo, L., Namani, A., Wang, X. J., & Tang, X. (2017) · Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease · doi:10.1016/j.bbadis.2016.11.005 · Cited by 1,794
Stress-activated cap’n’collar transcription factors in aging and human disease
Sykiotis, G. P., & Bohmann, D. (2010) · Science Signaling · doi:10.1126/scisignal.3112re3 · Cited by 776
The Nrf2–Keap1 defence pathway: Role in protection against drug-induced toxicity
Copple, I. M., Goldring, C. E., Kitteringham, N. R., & Park, B. K. (2008) · Toxicology · doi:10.1016/j.tox.2007.10.029 · Cited by 329
Nrf1 and Nrf2 Play Distinct Roles in Activation of Antioxidant Response Element-dependent Genes
Ohtsuji, M., Katsuoka, F., Kobayashi, A., Aburatani, H., Hayes, J. D., & Yamamoto, M. (2008) · Journal of Biological Chemistry · doi:10.1074/jbc.m804597200 · Cited by 317
Self-citationIncreased susceptibility of Nrf2 knockout mice to colitis-associated colorectal cancer
Khor, T. O., Huang, M.-T., Prawan, A., Liu, Y., Hao, X., Yu, S., Cheung, W. K. L., Chan, J. Y., Reddy, B. S., Yang, C. S., et al. (2008) · Cancer Prevention Research · doi:10.1158/1940-6207.capr-08-0028 · Cited by 306
Metadata
- Authors
- Osburn, W. O., Karim, B., Dolan, P. M., Liu, G., Yamamoto, M., Huso, D. L., & Kensler, T. W.
- Venue
- International Journal of Cancer
- Publisher
- Wiley
- Published
- 2007-07-13
- Volume
- 121
- Issue
- 9
- Pages
- 1883-1891
- ISSN
- 0020-7136 (ISSN-L)
- 1097-0215
- OpenAlex
- W2058520274
- Cited by
- 197
- References
- 8
- FWCI
- 3.95
- Type
- journal article
- Language
- en
- Open access
- closed
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- Osburn, W. O., Karim, B., Dolan, P. M., Liu, G., Yamamoto, M., Huso, D. L., & Kensler, T. W. (2007). Increased colonic inflammatory injury and formation of aberrant crypt foci in Nrf2‐deficient mice upon dextran sulfate treatment. International Journal of Cancer. https://doi.org/10.1002/ijc.22943
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