Inflammation and cancer: An ancient link with novel potentials
Infection and chronic inflammation contribute to about 1 in 4 of all cancer cases. Mediators of the inflammatory response, e.g., cytokines, free radicals, prostaglandins and growth factors, can induce genetic and epigenetic changes including point mutations in tumor suppressor genes, DNA methylation...
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Veröffentlicht in: | International journal of cancer 2007-12, Vol.121 (11), p.2373-2380 |
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description | Infection and chronic inflammation contribute to about 1 in 4 of all cancer cases. Mediators of the inflammatory response, e.g., cytokines, free radicals, prostaglandins and growth factors, can induce genetic and epigenetic changes including point mutations in tumor suppressor genes, DNA methylation and post‐translational modifications, causing alterations in critical pathways responsible for maintaining the normal cellular homeostasis and leading to the development and progression of cancer. Recent discovery of an interaction between microRNAs and innate immunity during inflammation has further strengthened the association between inflammation and cancer. © 2007 Wiley‐Liss, Inc. |
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Mediators of the inflammatory response, e.g., cytokines, free radicals, prostaglandins and growth factors, can induce genetic and epigenetic changes including point mutations in tumor suppressor genes, DNA methylation and post‐translational modifications, causing alterations in critical pathways responsible for maintaining the normal cellular homeostasis and leading to the development and progression of cancer. Recent discovery of an interaction between microRNAs and innate immunity during inflammation has further strengthened the association between inflammation and cancer. © 2007 Wiley‐Liss, Inc.</description><subject>Animals</subject><subject>cancer</subject><subject>Chronic Disease</subject><subject>Cyclooxygenase 2 - metabolism</subject><subject>Cytokines - metabolism</subject><subject>Disease Progression</subject><subject>DNA Methylation</subject><subject>Epigenesis, Genetic</subject><subject>Free Radicals - adverse effects</subject><subject>Genes, p53 - genetics</subject><subject>Humans</subject><subject>Immunity, Innate</subject><subject>inflammation</subject><subject>Inflammation - complications</subject><subject>Inflammation - microbiology</subject><subject>Inflammation - parasitology</subject><subject>Inflammation - virology</subject><subject>Inflammation Mediators - adverse effects</subject><subject>Inflammation Mediators - metabolism</subject><subject>Intercellular Signaling Peptides and Proteins - metabolism</subject><subject>microRNA</subject><subject>MicroRNAs</subject><subject>Neoplasms - etiology</subject><subject>Neoplasms - genetics</subject><subject>Neoplasms - immunology</subject><subject>Neoplasms - metabolism</subject><subject>Neoplasms - microbiology</subject><subject>Neoplasms - virology</subject><subject>NF-kappa B - metabolism</subject><subject>nitric oxide</subject><subject>Nitric Oxide Synthase - metabolism</subject><subject>Point Mutation</subject><subject>Prostaglandins - metabolism</subject><subject>Risk Assessment</subject><subject>Risk Factors</subject><subject>Signal Transduction</subject><issn>0020-7136</issn><issn>1097-0215</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2007</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kE1LAzEQhoMotlYP_gHZk-Bh7STZ7CYehFL8qBS86Dmk2VlM3c3WzdbSf29qC548vczMwzvwEHJJ4ZYCsLFb2lvGacGPyJCCKlJgVByTYbxBWlCeD8hZCEsASgVkp2RAC6m4zPMhuZ_5qjZNY3rX-sT4MrHGW-zukslutA59n9TOfyYb138kvv3GOlm1fVw7U4dzclLFwItDjsj748Pb9Dmdvz7NppN5ann8lOY5qzADqxhKqawqecEyIRTPlZDSMswYCKiULAuVV1iqhQEqC5kJQ0uBlo_I9b531bVfawy9blywWNfGY7sOmoHMmAQawZs9aLs2hA4rvepcY7qtpqB3snSUpX9lRfbqULpeNFj-kQc7ERjvgY2rcft_k569TPeVP38wcZE</recordid><startdate>20071201</startdate><enddate>20071201</enddate><creator>Perwez Hussain, S.</creator><creator>Harris, Curtis C.</creator><general>Wiley Subscription Services, Inc., A Wiley Company</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7T5</scope><scope>7TM</scope><scope>8FD</scope><scope>FR3</scope><scope>H94</scope><scope>P64</scope><scope>RC3</scope></search><sort><creationdate>20071201</creationdate><title>Inflammation and cancer: An ancient link with novel potentials</title><author>Perwez Hussain, S. ; 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subjects | Animals cancer Chronic Disease Cyclooxygenase 2 - metabolism Cytokines - metabolism Disease Progression DNA Methylation Epigenesis, Genetic Free Radicals - adverse effects Genes, p53 - genetics Humans Immunity, Innate inflammation Inflammation - complications Inflammation - microbiology Inflammation - parasitology Inflammation - virology Inflammation Mediators - adverse effects Inflammation Mediators - metabolism Intercellular Signaling Peptides and Proteins - metabolism microRNA MicroRNAs Neoplasms - etiology Neoplasms - genetics Neoplasms - immunology Neoplasms - metabolism Neoplasms - microbiology Neoplasms - virology NF-kappa B - metabolism nitric oxide Nitric Oxide Synthase - metabolism Point Mutation Prostaglandins - metabolism Risk Assessment Risk Factors Signal Transduction |
title | Inflammation and cancer: An ancient link with novel potentials |
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