Impact of stress and mast cells on brain metastases
Abstract Metastases continue to be the chief cause of morbidity and mortality for many tumors, including brain metastases of lung and mammary adenocarcinoma. Stress appears to increase metastases, but the mechanism is not understood. Recent evidence suggests that local inflammation is conducive for...
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Veröffentlicht in: | Journal of neuroimmunology 2008-12, Vol.205 (1), p.1-7 |
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creator | Theoharides, Theoharis C Rozniecki, Jacek J Sahagian, Gary Jocobson, Stanley Kempuraj, Duraisamy Conti, Pio Kalogeromitros, Dimitris |
description | Abstract Metastases continue to be the chief cause of morbidity and mortality for many tumors, including brain metastases of lung and mammary adenocarcinoma. Stress appears to increase metastases, but the mechanism is not understood. Recent evidence suggests that local inflammation is conducive for cancer growth and a unique immune cell, the mast cell, accumulates in the stroma surrounding tumors and is critically located at the blood-brain-barrier (BBB). Mast cells express receptors for and can be stimulated by corticotropin-releasing hormone (CRH), secreted under stress, to release mediators such as histamine, IL-8, tryptase and vascular endothelial growth factor (VEGF), which disrupt the BBB permitting metastases. Stress and mast cells could serve as new targets for drug development to prevent brain metastases, especially since CRH receptor antagonists and brain mast cell inhibitors have recently been developed. |
doi_str_mv | 10.1016/j.jneuroim.2008.09.014 |
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Stress appears to increase metastases, but the mechanism is not understood. Recent evidence suggests that local inflammation is conducive for cancer growth and a unique immune cell, the mast cell, accumulates in the stroma surrounding tumors and is critically located at the blood-brain-barrier (BBB). Mast cells express receptors for and can be stimulated by corticotropin-releasing hormone (CRH), secreted under stress, to release mediators such as histamine, IL-8, tryptase and vascular endothelial growth factor (VEGF), which disrupt the BBB permitting metastases. Stress and mast cells could serve as new targets for drug development to prevent brain metastases, especially since CRH receptor antagonists and brain mast cell inhibitors have recently been developed.</description><identifier>ISSN: 0165-5728</identifier><identifier>EISSN: 1872-8421</identifier><identifier>DOI: 10.1016/j.jneuroim.2008.09.014</identifier><identifier>PMID: 18977036</identifier><language>eng</language><publisher>Netherlands: Elsevier B.V</publisher><subject>Allergy and Immunology ; Animals ; Blood-Brain Barrier - drug effects ; Blood-Brain Barrier - physiopathology ; Blood-brain-barrier ; Brain Neoplasms - etiology ; Brain Neoplasms - secondary ; Breast cancer ; Humans ; Inflammation ; Inflammation - pathology ; Inflammation - physiopathology ; Inflammation Mediators - metabolism ; Inflammation Mediators - pharmacology ; Mast cells ; Mast Cells - metabolism ; Metastases ; Neurology ; Stress ; Stress, Psychological - pathology ; Stress, Psychological - physiopathology</subject><ispartof>Journal of neuroimmunology, 2008-12, Vol.205 (1), p.1-7</ispartof><rights>Elsevier B.V.</rights><rights>2008 Elsevier B.V.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c452t-2f1e67fa97dc67f845a9cc9d6d6e124315f20147810ae0526331f4864a557c713</citedby><cites>FETCH-LOGICAL-c452t-2f1e67fa97dc67f845a9cc9d6d6e124315f20147810ae0526331f4864a557c713</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.jneuroim.2008.09.014$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,777,781,3537,27905,27906,45976</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/18977036$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Theoharides, Theoharis C</creatorcontrib><creatorcontrib>Rozniecki, Jacek J</creatorcontrib><creatorcontrib>Sahagian, Gary</creatorcontrib><creatorcontrib>Jocobson, Stanley</creatorcontrib><creatorcontrib>Kempuraj, Duraisamy</creatorcontrib><creatorcontrib>Conti, Pio</creatorcontrib><creatorcontrib>Kalogeromitros, Dimitris</creatorcontrib><title>Impact of stress and mast cells on brain metastases</title><title>Journal of neuroimmunology</title><addtitle>J Neuroimmunol</addtitle><description>Abstract Metastases continue to be the chief cause of morbidity and mortality for many tumors, including brain metastases of lung and mammary adenocarcinoma. Stress appears to increase metastases, but the mechanism is not understood. Recent evidence suggests that local inflammation is conducive for cancer growth and a unique immune cell, the mast cell, accumulates in the stroma surrounding tumors and is critically located at the blood-brain-barrier (BBB). Mast cells express receptors for and can be stimulated by corticotropin-releasing hormone (CRH), secreted under stress, to release mediators such as histamine, IL-8, tryptase and vascular endothelial growth factor (VEGF), which disrupt the BBB permitting metastases. Stress and mast cells could serve as new targets for drug development to prevent brain metastases, especially since CRH receptor antagonists and brain mast cell inhibitors have recently been developed.</description><subject>Allergy and Immunology</subject><subject>Animals</subject><subject>Blood-Brain Barrier - drug effects</subject><subject>Blood-Brain Barrier - physiopathology</subject><subject>Blood-brain-barrier</subject><subject>Brain Neoplasms - etiology</subject><subject>Brain Neoplasms - secondary</subject><subject>Breast cancer</subject><subject>Humans</subject><subject>Inflammation</subject><subject>Inflammation - pathology</subject><subject>Inflammation - physiopathology</subject><subject>Inflammation Mediators - metabolism</subject><subject>Inflammation Mediators - pharmacology</subject><subject>Mast cells</subject><subject>Mast Cells - metabolism</subject><subject>Metastases</subject><subject>Neurology</subject><subject>Stress</subject><subject>Stress, Psychological - pathology</subject><subject>Stress, Psychological - physiopathology</subject><issn>0165-5728</issn><issn>1872-8421</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2008</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkUtrFUEQRhtRzE30L4RZuZtJVb9nI0rwEQi4UMFd0-mpgR7nce2eEfLv7eFeEdxkVVCcqvo4xdg1QoOA-mZohpm2tMSp4QC2gbYBlM_YAa3htZUcn7NDAVWtDLcX7DLnAQCVkO1LdoG2NQaEPjBxNx19WKulr_KaKOfKz101-bxWgcYxV8tcPSQf52qitXR9pvyKvej9mOn1uV6x7x8_fLv9XN9_-XR3-_6-DlLxteY9kja9b00XSrVS-TaEttOdJuRSoOp5yWwsgidQXAuBvbRaeqVMMCiu2JvT3mNafm2UVzfFvKfyMy1bdrq1nCvVPgly4Bo48gLqExjSknOi3h1TnHx6dAhu9-oG99er2706aF3JWAavzxe2h4m6f2NnkQV4dwKoCPkdKbkcIs2BupgorK5b4tM33v63IoxxjsGPP-mR8rBsaS66HbrMHbiv-3f354IFkCh-iD85eJ-_</recordid><startdate>20081215</startdate><enddate>20081215</enddate><creator>Theoharides, Theoharis C</creator><creator>Rozniecki, Jacek J</creator><creator>Sahagian, Gary</creator><creator>Jocobson, Stanley</creator><creator>Kempuraj, Duraisamy</creator><creator>Conti, Pio</creator><creator>Kalogeromitros, Dimitris</creator><general>Elsevier B.V</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>7TK</scope><scope>H94</scope><scope>7X8</scope></search><sort><creationdate>20081215</creationdate><title>Impact of stress and mast cells on brain metastases</title><author>Theoharides, Theoharis C ; Rozniecki, Jacek J ; Sahagian, Gary ; Jocobson, Stanley ; Kempuraj, Duraisamy ; Conti, Pio ; Kalogeromitros, Dimitris</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c452t-2f1e67fa97dc67f845a9cc9d6d6e124315f20147810ae0526331f4864a557c713</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2008</creationdate><topic>Allergy and Immunology</topic><topic>Animals</topic><topic>Blood-Brain Barrier - drug effects</topic><topic>Blood-Brain Barrier - physiopathology</topic><topic>Blood-brain-barrier</topic><topic>Brain Neoplasms - etiology</topic><topic>Brain Neoplasms - secondary</topic><topic>Breast cancer</topic><topic>Humans</topic><topic>Inflammation</topic><topic>Inflammation - pathology</topic><topic>Inflammation - physiopathology</topic><topic>Inflammation Mediators - metabolism</topic><topic>Inflammation Mediators - pharmacology</topic><topic>Mast cells</topic><topic>Mast Cells - metabolism</topic><topic>Metastases</topic><topic>Neurology</topic><topic>Stress</topic><topic>Stress, Psychological - pathology</topic><topic>Stress, Psychological - physiopathology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Theoharides, Theoharis C</creatorcontrib><creatorcontrib>Rozniecki, Jacek J</creatorcontrib><creatorcontrib>Sahagian, Gary</creatorcontrib><creatorcontrib>Jocobson, Stanley</creatorcontrib><creatorcontrib>Kempuraj, Duraisamy</creatorcontrib><creatorcontrib>Conti, Pio</creatorcontrib><creatorcontrib>Kalogeromitros, Dimitris</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Immunology Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of neuroimmunology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Theoharides, Theoharis C</au><au>Rozniecki, Jacek J</au><au>Sahagian, Gary</au><au>Jocobson, Stanley</au><au>Kempuraj, Duraisamy</au><au>Conti, Pio</au><au>Kalogeromitros, Dimitris</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Impact of stress and mast cells on brain metastases</atitle><jtitle>Journal of neuroimmunology</jtitle><addtitle>J Neuroimmunol</addtitle><date>2008-12-15</date><risdate>2008</risdate><volume>205</volume><issue>1</issue><spage>1</spage><epage>7</epage><pages>1-7</pages><issn>0165-5728</issn><eissn>1872-8421</eissn><abstract>Abstract Metastases continue to be the chief cause of morbidity and mortality for many tumors, including brain metastases of lung and mammary adenocarcinoma. Stress appears to increase metastases, but the mechanism is not understood. Recent evidence suggests that local inflammation is conducive for cancer growth and a unique immune cell, the mast cell, accumulates in the stroma surrounding tumors and is critically located at the blood-brain-barrier (BBB). Mast cells express receptors for and can be stimulated by corticotropin-releasing hormone (CRH), secreted under stress, to release mediators such as histamine, IL-8, tryptase and vascular endothelial growth factor (VEGF), which disrupt the BBB permitting metastases. Stress and mast cells could serve as new targets for drug development to prevent brain metastases, especially since CRH receptor antagonists and brain mast cell inhibitors have recently been developed.</abstract><cop>Netherlands</cop><pub>Elsevier B.V</pub><pmid>18977036</pmid><doi>10.1016/j.jneuroim.2008.09.014</doi><tpages>7</tpages></addata></record> |
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subjects | Allergy and Immunology Animals Blood-Brain Barrier - drug effects Blood-Brain Barrier - physiopathology Blood-brain-barrier Brain Neoplasms - etiology Brain Neoplasms - secondary Breast cancer Humans Inflammation Inflammation - pathology Inflammation - physiopathology Inflammation Mediators - metabolism Inflammation Mediators - pharmacology Mast cells Mast Cells - metabolism Metastases Neurology Stress Stress, Psychological - pathology Stress, Psychological - physiopathology |
title | Impact of stress and mast cells on brain metastases |
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