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Inflammation: Gearing the journey to cancer
DC Field | Value | Language |
---|---|---|
dc.contributor.author | Kundu, Joydeb Kumar | - |
dc.contributor.author | Surh, Young-Joon | - |
dc.date.accessioned | 2021-01-31T10:22:04Z | - |
dc.date.available | 2021-01-31T10:22:04Z | - |
dc.date.created | 2017-11-15 | - |
dc.date.issued | 2008-07 | - |
dc.identifier.citation | Mutation Research - Reviews in Mutation Research, Vol.659 No.1-2, pp.15-30 | - |
dc.identifier.issn | 1383-5742 | - |
dc.identifier.other | 3142 | - |
dc.identifier.uri | https://hdl.handle.net/10371/172867 | - |
dc.description.abstract | Chronic inflammation plays a multifaceted role in carcinogenesis. Mounting evidence from preclinical and clinical studies suggests that persistent inflammation functions as a driving force in the journey to cancer. The possible mechanisms by which inflammation can contribute to carcinogenesis include induction of genomic instability, alterations in epigenetic events and subsequent inappropriate gene expression, enhanced proliferation of initiated cells, resistance to apoptosis, aggressive tumor neovascularization, invasion through tumor-associated basement membrane and metastasis, etc. Inflammation-induced reactive oxygen and nitrogen species cause damage to important cellular components (e.g., DNA, proteins and lipids), which can directly or indirectly contribute to malignant cell transformation. Overexpression, elevated secretion, or abnormal activation of proinflammatory mediators, such as cytokines, chemokines, cyclooxygenase-2, prostaglandins, inducible nitric oxide synthase, and nitric oxide, and a distinct network of intracellular signaling molecules including upstream kinases and transcription factors facilitate tumor promotion and progression. While inflammation promotes development of cancer, components of the tumor microenvironment, such as tumor cells, stromal cells in surrounding tissue and infiltrated inflammatory/immune cells generate an intratumoral inflammatory state by aberrant expression or activation of some proinflammatory molecules. Many of proinflammatory mediators, especially cytokines, chemokines and prostaglandins, turn on the angiogenic switches mainly controlled by vascular endothelial growth factor, thereby inducing inflammatory angiogenesis and tumor cell-stroma communication. This will end up with tumor angiogenesis, metastasis and invasion. Moreover, cellular microRNAs are emerging as a potential link between inflammation and cancer. The present article highlights the role of various proinflammatory mediators in carcinogenesis and their promise as potential targets for chemoprevention of inflammation-associated carcinogenesis. (C) 2008 Elsevier B.V. All rights reserved. | - |
dc.language | 영어 | - |
dc.publisher | Elsevier BV | - |
dc.title | Inflammation: Gearing the journey to cancer | - |
dc.type | Article | - |
dc.contributor.AlternativeAuthor | 서영준 | - |
dc.identifier.doi | 10.1016/j.mrrev.2008.03.002 | - |
dc.citation.journaltitle | Mutation Research - Reviews in Mutation Research | - |
dc.identifier.wosid | 000258811000004 | - |
dc.identifier.scopusid | 2-s2.0-47849098044 | - |
dc.citation.endpage | 30 | - |
dc.citation.number | 1-2 | - |
dc.citation.startpage | 15 | - |
dc.citation.volume | 659 | - |
dc.identifier.sci | 000258811000004 | - |
dc.description.isOpenAccess | N | - |
dc.contributor.affiliatedAuthor | Surh, Young-Joon | - |
dc.type.docType | Article; Proceedings Paper | - |
dc.description.journalClass | 1 | - |
dc.subject.keywordPlus | NITRIC-OXIDE SYNTHASE | - |
dc.subject.keywordPlus | TUMOR-NECROSIS-FACTOR | - |
dc.subject.keywordPlus | NF-KAPPA-B | - |
dc.subject.keywordPlus | ENDOTHELIAL GROWTH-FACTOR | - |
dc.subject.keywordPlus | HELICOBACTER-PYLORI INFECTION | - |
dc.subject.keywordPlus | DEXTRAN SULFATE SODIUM | - |
dc.subject.keywordPlus | NITRATIVE DNA-DAMAGE | - |
dc.subject.keywordPlus | GENE PROMOTER METHYLATION | - |
dc.subject.keywordPlus | MOUSE LUNG TUMORIGENESIS | - |
dc.subject.keywordPlus | SQUAMOUS-CELL CARCINOMAS | - |
dc.subject.keywordAuthor | inflammation | - |
dc.subject.keywordAuthor | carcinogenesis | - |
dc.subject.keywordAuthor | proinflammatory mediators | - |
dc.subject.keywordAuthor | inflammatory angiogenesis | - |
dc.subject.keywordAuthor | cancer epigenetics | - |
dc.subject.keywordAuthor | microRNAs | - |
dc.subject.keywordAuthor | chemoprevention | - |
dc.subject.keywordAuthor | inflammatory signaling | - |
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