The DOI matches its Crossref record; 19 of the 19 references it cites were found in a registry or an index.
Molecular mechanisms underlying chronic inflammation-associated cancers
Open accessAbstract
Although it is now accepted that chronic inflammation plays an essential role in tumorigenesis, the underlying molecular mechanisms linking inflammation and cancer remain to be fully explored. Inflammatory mediators present in the tumor microenvironment, including cytokines and growth factors, as well as reactive oxygen species (ROS) and reactive nitrogen species (RNS), have been implicated in the etiology of inflammation-associated cancers. Epithelial NADPH oxidase (Nox) family proteins, which generate ROS regulated by cytokines, are upregulated during chronic inflammation and cancer. ROS serve as effector molecules participating in host defense or as chemo-attractants recruiting leukocytes to wounds, thereby influencing the inflammatory reaction in damaged tissues. ROS can alter chromosomal DNA, leading to genomic instability, and may serve as signaling molecules that affect tumor cell proliferation, survival, metabolism, angiogenesis, and metastasis. Targeting Noxs and their downstream signaling components may be a promising approach to pre-empting inflammation-related malignancies.
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Mantovani, A., Allavena, P., Sica, A., & Balkwill, F. (2008) · Nature · doi:10.1038/nature07205 · Cited by 11,399
The NOX Family of ROS-Generating NADPH Oxidases: Physiology and Pathophysiology
Bedard, K., & Krause, K.-H. (2007) · Physiological Reviews · doi:10.1152/physrev.00044.2005 · Cited by 6,989
Darnell, J. E., Kerr, L. M., & Stark, G. R. (1994) · Science · doi:10.1126/science.8197455 · Cited by 6,080
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
STATs in cancer inflammation and immunity: a leading role for STAT3
Yu, H., Pardoll, D., & Jove, R. (2009) · Nature reviews. Cancer · doi:10.1038/nrc2734 · Cited by 4,383
Crosstalk of reactive oxygen species and NF-κB signaling
Morgan, M. J., & Liu, Z.-G. (2011) · Cell Research · doi:10.1038/cr.2010.178 · Cited by 3,505
IKKβ Links Inflammation and Tumorigenesis in a Mouse Model of Colitis-Associated Cancer
Greten, F. R., Eckmann, L., Greten, T. F., Park, J. M., Li, Z.-W., Egan, L. J., Kagnoff, M. F., & Karin, M. (2004) · Cell · doi:10.1016/j.cell.2004.07.013 · Cited by 2,433
Role of transcription factor NF-kappa B/Rel in induction of nitric oxide synthase.
Xie, Q. W., Kashiwabara, Y., & Nathan, C. (1994) · Journal of Biological Chemistry · doi:10.1016/s0021-9258(17)37600-7 · Cited by 2,212 · cited 1×
“located in the proximal promoter region of genes encoding proinflammatory mediators, such as cytokines [9], INOS [10], and”
BackgroundZhong, Z., Wen, Z., & Darnell, J. E. (1994) · Science · doi:10.1126/science.8140422 · Cited by 2,070
Park, E. J., Lee, J. H., Yu, G.-Y., He, G., Ali, S. R., Holzer, R. G., Österreicher, C. H., Takahashi, H., & Karin, M. (2010) · Cell · doi:10.1016/j.cell.2009.12.052 · Cited by 1,764
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Molecular pharmacology of inflammation: Medicinal plants as anti-inflammatory agents
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Environmental immune disruptors, inflammation and cancer risk
Thompson, P. A., Khatami, M., Baglole, C. J., Sun, J., Harris, S. A., Moon, E.-Y., Al-Mulla, F., Al-Temaimi, R., Brown, D. G., Colacci, A. M., et al. (2015) · Carcinogenesis · doi:10.1093/carcin/bgv038 · Cited by 227
Review of yoga therapy during cancer treatment
Danhauer, S. C., Addington, E. L., Sohl, S. J., Chaoul, A., & Cohen, L. (2017) · Supportive Care in Cancer · doi:10.1007/s00520-016-3556-9 · Cited by 114
Disruptive chemicals, senescence and immortality
Carnero, A., Blanco-Aparicio, C., Kondoh, H., Lleonart, M. E., Martinez-Leal, J. F., Mondello, C., Scovassi, A. I., Bisson, W. H., Amedei, A., Roy, R., et al. (2015) · Carcinogenesis · doi:10.1093/carcin/bgv029 · Cited by 29
Metadata
- Authors
- Wu, Y., Antony, S., Meitzler, J. L., & Doroshow, J. H.
- Venue
- Cancer Letters
- Publisher
- Elsevier BV
- Published
- 2014-04
- Volume
- 345
- Issue
- 2
- Pages
- 164-173
- ISSN
- 0304-3835 (ISSN-L)
- OpenAlex
- W2024328614
- Cited by
- 308
- References
- 19
- FWCI
- 9.44
- Type
- journal article
- Language
- en
- Open access
- green
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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