{"id":274,"date":"2013-05-06T22:25:23","date_gmt":"2013-05-06T20:25:23","guid":{"rendered":"http:\/\/www.naardiagnosenerkraeft.dk\/?page_id=274"},"modified":"2013-08-28T14:15:07","modified_gmt":"2013-08-28T12:15:07","slug":"inflammation-fremmer-kraeftudvikling","status":"publish","type":"page","link":"https:\/\/www.naardiagnosenerkraeft.dk\/?page_id=274","title":{"rendered":"Inflammation fremmer kr\u00e6ftudvikling"},"content":{"rendered":"<p><a href=\"http:\/\/www.naardiagnosenerkraeft.dk\/wp-content\/uploads\/2013\/05\/Gurkemeje.jpg\"><img loading=\"lazy\" decoding=\"async\" class=\"alignright size-full wp-image-387\" alt=\"Gurkemeje\" src=\"http:\/\/www.naardiagnosenerkraeft.dk\/wp-content\/uploads\/2013\/05\/Gurkemeje.jpg\" width=\"150\" height=\"180\" \/><\/a>Inflammation er efter mange forskeres mening en af de vigtigste underliggende faktorer til de fleste former for kr\u00e6ft, fordi den frigiver kraftige iltmolekyler (oxidanter), som b\u00e5de stimulerer celledeling og mutationer. Det er derfor vigtigt at forst\u00e5 mekanismerne og vide, hvad man selv kan g\u00f8re for at modvirke inflammation.<\/p>\n<p>Siden NF-kB (nuclear factor-kappaB) blev opdaget i 1986, har man vidst, at det havde en t\u00e6t sammenh\u00e6ng med udviklingen af kr\u00e6ft.<a title=\"\" href=\"#_ftn1\">[1]<\/a> F.eks. viste et studie i 2010<a title=\"\" href=\"#_ftn2\">[2]<\/a>, at inflammation er n\u00f8dvendig for, at brystkr\u00e6ftceller kan dele sig og lave metastaser.<\/p>\n<p>I dag ved vi, at de fleste &#8211;\u00a0hvis ikke alle &#8211; kr\u00e6fttilf\u00e6lde har unormalt h\u00f8je niveauer af aktivt NF-kB, som holder dem i en tilstand af konstant inflammation.<a title=\"\" href=\"#_ftn3\">[3]<\/a><\/p>\n<p>Omvendt virker visse s\u00e5kaldte onkogener (unormale gener, der kan starte en kr\u00e6ftudvikling) delvis ved at aktivere NF-kB.<a title=\"\" href=\"#_ftn4\">[4]<\/a> Sammen kan disse faktorer producere en stadig str\u00f8m af inflammatoriske og kr\u00e6ftfremkaldende cytokiner inde i den voksende tumor.<a title=\"\" href=\"#_ftn5\">[5]<\/a><\/p>\n<p>Produktionen af disse signalmolekyler g\u00f8r det meget mere sandsynligt, at en given muteret celle vil udvikle sig til kr\u00e6ft. Det kan ogs\u00e5 betyde, at en tumor bliver mere resistent overfor kemo-og str\u00e5lebehandling, fordi NF-kB generelt fremmer kr\u00e6ftcellernes overlevelse.<a title=\"\" href=\"#_ftn6\">[6]<\/a><a href=\"http:\/\/www.naardiagnosenerkraeft.dk\/wp-content\/uploads\/2013\/05\/gr\u00f8n-the3.jpg\"><img loading=\"lazy\" decoding=\"async\" class=\"alignright size-full wp-image-389\" alt=\"gr\u00f8n the3\" src=\"http:\/\/www.naardiagnosenerkraeft.dk\/wp-content\/uploads\/2013\/05\/gr\u00f8n-the3.jpg\" width=\"180\" height=\"150\" \/><\/a><\/p>\n<p>NF-kB stimulerer gener til at producere inflammatoriske cytokiner og andre signalmolekyler, som fremmer kr\u00e6ftv\u00e6kst og udvikling. H\u00e6mning af NF-kB er derfor vigtig b\u00e5de i forebyggelsen af kr\u00e6ft og p\u00e5 ethvert stadie af kr\u00e6ftudviklingen.<\/p>\n<p>Her er nogle af de ting, Dr. Sahdeo Prasad fra Cytokine Research Laboratory ved MD Anderson Cancer Center i Houston\u00a0 i en artikel i Life Extension Magazine fremh\u00e6ver omkring sammenh\u00e6ngen mellem NF-kB og kr\u00e6ft:<a title=\"\" href=\"#_ftn7\">[7]<\/a><\/p>\n<ul>\n<li>NF-kB aktiveres som svar p\u00e5 en r\u00e6kke faktorer, som er impliceret i start og udvikling af 95% af alle kr\u00e6fttilf\u00e6lde. Disse omfatter tobak, stress, visse f\u00f8devarer, fedme, alkohol, infektioner, str\u00e5ling, og milj\u00f8m\u00e6ssige giftstoffer<a title=\"\" href=\"#_ftn8\">[8]<\/a><\/li>\n<li>Aktiveringen af NF-kB er blevet sammenk\u00e6det med omdannelsen af normale celler til kr\u00e6ftceller og ser derfor ud til at fremme kr\u00e6ftudvikling<a title=\"\" href=\"#_ftn9\">[9]<\/a><\/li>\n<li>NF-kB er mere aktiv i kr\u00e6ftceller end i normale celler. En kr\u00e6ft i udvikling for\u00f8ger ogs\u00e5 m\u00e6ngden af aktiv NF-kB<a title=\"\" href=\"#_ftn10\">[10]<\/a><\/li>\n<li>NF-kB er blevet sat i forbindelse med de farlige kr\u00e6ft stamcellers overlevelse. Disse kr\u00e6ft stamceller er de tidlige \u201dfor\u00e6ldre\u201d celler, som vi nu ved findes i ellers normalt v\u00e6v. Kr\u00e6ft stamceller er bedre i stand til at forny sig selv end sunde celler.<\/li>\n<li>NF-kB stimulerer desuden produktionen af genprodukter, som afholder kr\u00e6ftceller fra at d\u00f8 naturligt ved programmeret celled\u00f8d (apoptose)<a title=\"\" href=\"#_ftn11\">[11]<\/a><\/li>\n<li>NF-kB for\u00f8ger ogs\u00e5 produktionen af genprodukter, som vedr\u00f8rer den ukontrollerede celledeling, som er s\u00e5 karakteristisk for kr\u00e6ft<a title=\"\" href=\"#_ftn12\">[12]<\/a><\/li>\n<li>NF-kB kontrollerer ekspressionen af genprodukter, som har betydning for invasion, dannelse af nye blodkar (angiogenese) og spredning via metastaser.<a title=\"\" href=\"#_ftn13\">[13]<\/a><\/li>\n<li>Mange kr\u00e6ftfremkaldende stoffer aktiverer NF-kB,\u00a0 men de fleste effektive kr\u00e6ftbek\u00e6mpende stoffer undertrykker aktiveringen af NF-kB<a title=\"\" href=\"#_ftn14\">[14]<\/a><\/li>\n<\/ul>\n<div>\n<p>Der er heldigvis en bred vifte af naturlige stoffer i vore f\u00f8devarer, som\u00a0h\u00e6mmer NF-kBs sygdomsfremkaldende aktivitet og kan bruges som led i en kr\u00e6ftbek\u00e6mpende strategi. Den lave forekomst af kr\u00e6ft i lande, hvor maden indeholder et h\u00f8jt niveau af naturlige NF-kB-h\u00e6mmende stoffer\u00a0bekr\u00e6fter betydningen af at give disse f\u00f8devarer\u00a0en fremtr\u00e6dende plads i den daglige kost<\/p>\n<p>Det g\u00e6lder f.eks. gurkemeje, hvidl\u00f8g, ingef\u00e6r, gr\u00f8n the og soja. En endnu\u00a0st\u00e6rkere effekt f\u00e5s ved at bruge ekstrakter.<a href=\"http:\/\/www.naardiagnosenerkraeft.dk\/wp-content\/uploads\/2013\/05\/ingef\u00e6r2.jpg\"><img loading=\"lazy\" decoding=\"async\" class=\"alignright size-full wp-image-390\" alt=\"ingef\u00e6r2\" src=\"http:\/\/www.naardiagnosenerkraeft.dk\/wp-content\/uploads\/2013\/05\/ingef\u00e6r2.jpg\" width=\"150\" height=\"150\" \/><\/a><\/p>\n<p>Herudover studeres mange antioxidanter i disse \u00e5r for specifikke NF-kB-blokerende aktivitet. Det g\u00e6lder f.eks. C-og E-vitamin , karotenoider, glutathione, liponsyre, plantestoffer som flavonoider og polyfenoler (bl.a. i ovenst\u00e5ende), selen, zink og mange andre.<a title=\"\" href=\"#_ftn1\">[15]<\/a><\/p>\n<p>Inge Kellermann<\/p>\n<p><a href=\"http:\/\/www.helsemail.dk\">www.helsemail.dk<\/a><\/p>\n<p><a href=\"http:\/\/www.n\u00e5rdiagnosenerkr\u00e6ft.dk\">www.n\u00e5rdiagnosenerkr\u00e6ft.dk<\/a><\/p>\n<hr align=\"left\" size=\"1\" width=\"33%\" \/>\n<div>\n<div>\n<p><a title=\"\" href=\"#_ftnref1\">[1]<\/a> Aravindaram K, Yang NS. Anti-inflammatory plant natural products for cancer therapy. Planta Med. 2010 Aug;76(11):1103-17.<\/p>\n<p>Valko M, Rhodes CJ, Moncol J, Izakovic M, Mazur M. Free radicals, metals and antioxidants in oxidative stress-induced cancer. Chem Biol Interact. 2006 Mar 10;160(1):1-40.<\/p>\n<p>Guo W, Kong E, Meydani M. Dietary polyphenols, inflammation, and cancer. Nutr Cancer. 2009 Nov;61(6):807-10.<\/p>\n<p>Ho HH, Chang CS, Ho WC, Liao SY, Wu CH, Wang CJ. Anti-metastasis effects of gallic acid on gastric cancer cells involves inhibition of NF-kappaB activity and downregulation of PI3K\/AKT\/small GTPase signals. Food Chem Toxicol. 2010 Aug-Sep;48(8-9):2508-16.<\/p>\n<p><a title=\"\" href=\"#_ftnref1\">[1]<\/a> Aravindaram K, Yang NS. Anti-inflammatory plant natural products for cancer therapy. Planta Med. 2010 Aug;76(11):1103-17.<\/p>\n<\/div>\n<\/div>\n<div>\n<div>\n<p>Valko M, Rhodes CJ, Moncol J, Izakovic M, Mazur M. Free radicals, metals and antioxidants in oxidative stress-induced cancer. Chem Biol Interact. 2006 Mar 10;160(1):1-40.<\/p>\n<p>Guo W, Kong E, Meydani M. Dietary polyphenols, inflammation, and cancer. Nutr Cancer. 2009 Nov;61(6):807-10.<\/p>\n<p>Ho HH, Chang CS, Ho WC, Liao SY, Wu CH, Wang CJ. Anti-metastasis effects of gallic acid on gastric cancer cells involves inhibition of NF-kappaB activity and downregulation of PI3K\/AKT\/small GTPase signals. Food Chem Toxicol. 2010 Aug-Sep;48(8-9):2508-16.<\/p>\n<\/div>\n<\/div>\n<hr align=\"left\" size=\"1\" width=\"33%\" \/>\n<div>\n<p><a title=\"\" href=\"#_ftnref1\">[1]<\/a> Prasad S, Ravindran J, Aggarwal BB. NF-kappaB and cancer: how intimate is this relationship. Mol Cell Biochem. 2010 Mar;336(1-2):25-37.<\/p>\n<\/div>\n<div>\n<p><a title=\"\" href=\"#_ftnref2\">[2]<\/a> Prasad S, Ravindran J, Aggarwal BB. NF-kappaB and cancer: how intimate is this relationship. Mol Cell Biochem. 2010 Mar;336(1-2):25-37.<\/p>\n<\/div>\n<div>\n<p><a title=\"\" href=\"#_ftnref3\">[3]<\/a> Pianetti S, Arsura M, Romieu-Mourez R, Coffey RJ, Sonenshein GE. Her-2\/neu overexpression induces NF-kappaB via a PI3-kinase\/Akt pathway involving calpain-mediated degradation of IkappaB-alpha that can be inhibited by the tumor suppressor PTEN. Oncogene. 2001 Mar 15;20(11):1287-99.<\/p>\n<\/div>\n<div>\n<p><a title=\"\" href=\"#_ftnref4\">[4]<\/a> Bhat-Nakshatri P, Sweeney CJ, Nakshatri H. Identification of signal transduction pathways involved in constitutive NF-kappaB activation in breast cancer cells. Oncogene. 2002 Mar 27;21(13):2066-78.<\/p>\n<\/div>\n<div>\n<p><a title=\"\" href=\"#_ftnref5\">[5]<\/a> Ahmed KM, Cao N, Li JJ. HER-2 and NF-kappaB as the targets for therapy-resistant breast cancer. Anticancer Res. 2006 Nov-Dec;26(6B):4235-43.<\/p>\n<\/div>\n<div>\n<p><a title=\"\" href=\"#_ftnref6\">[6]<\/a> Weldon CB, Burow ME, Rolfe KW, Clayton JL, Jaffe BM, Beckman BS. NF-kappa B-mediated chemoresistance in breast cancer cells. Surgery. 2001 Aug;130(2):143-50.<\/p>\n<\/div>\n<div>\n<p><a title=\"\" href=\"#_ftnref7\">[7]<\/a> David Hoffnung: The Inflammatory Factor Underlying Most Cancers. Life Extension Magazine November 2011. <a href=\"http:\/\/www.lef.org\">www.lef.org<\/a><\/p>\n<\/div>\n<div>\n<p><a title=\"\" href=\"#_ftnref8\">[8]<\/a> Shin SR, Sanchez-Velar N, Sherr DH, Sonenshein GE. 7,12-dimethylbenz(a)anthracene treatment of a c-rel mouse mammary tumor cell line induces epithelial to mesenchymal transition via activation of nuclear factor-kappaB. Cancer Res. 2006 Mar 1;66(5):2570-5.<\/p>\n<p>Renehan AG, Roberts DL, Dive C. Obesity and cancer: pathophysiological and biological mechanisms. Arch Physiol Biochem. 2008 Feb;114(1):71-83.<\/p>\n<p>Enwonwu CO, Meeks VI. Bionutrition and oral cancer in humans. Crit Rev Oral Biol Med. 1995;6(1):5-17.<\/p>\n<\/div>\n<div>\n<p><a title=\"\" href=\"#_ftnref9\">[9]<\/a> Shin SR, Sanchez-Velar N, Sherr DH, Sonenshein GE. 7,12-dimethylbenz(a)anthracene treatment of a c-rel mouse mammary tumor cell line induces epithelial to mesenchymal transition via activation of nuclear factor-kappaB. Cancer Res. 2006 Mar 1;66(5):2570-5.<\/p>\n<p>Pratt MA, Tibbo E, Robertson SJ, et al. The canonical NF-kappaB pathway is required for formation of luminal mammary neoplasias and is activated in the mammary progenitor population. Oncogene. 2009 Jul 30;28(30):2710-22.<\/p>\n<\/div>\n<div>\n<p><a title=\"\" href=\"#_ftnref10\">[10]<\/a> Pianetti S, Arsura M, Romieu-Mourez R, Coffey RJ, Sonenshein GE. Her-2\/neu overexpression induces NF-kappaB via a PI3-kinase\/Akt pathway involving calpain-mediated degradation of IkappaB-alpha that can be inhibited by the tumor suppressor PTEN. Oncogene. 2001 Mar 15;20(11):1287-99.<\/p>\n<p>Li SH, Hawthorne VS, Neal CL, et al. Upregulation of neutrophil gelatinase-associated lipocalin by ErbB2 through nuclear factor-kappaB activation. Cancer Res. 2009 Dec 15;69(24):9163-8.<\/p>\n<\/div>\n<div>\n<p><a title=\"\" href=\"#_ftnref11\">[11]<\/a> deGraffenried LA, Chandrasekar B, Friedrichs WE, et al. NF-kappa B inhibition markedly enhances sensitivity of resistant breast cancer tumor cells to tamoxifen. Ann Oncol. 2004 Jun;15(6):885-90.<\/p>\n<\/div>\n<div>\n<p><a title=\"\" href=\"#_ftnref12\">[12]<\/a> Brantley DM, Chen CL, Muraoka RS, et al. Nuclear factor-kappaB (NF-kappaB) regulates proliferation and branching in mouse mammary epithelium. Mol Biol Cell. 2001 May;12(5):1445-55.<\/p>\n<\/div>\n<div>\n<p><a title=\"\" href=\"#_ftnref13\">[13]<\/a>deGraffenried LA, Chandrasekar B, Friedrichs WE, et al. NF-kappa B inhibition markedly enhances sensitivity of resistant breast cancer tumor cells to tamoxifen. Ann Oncol. 2004 Jun;15(6):885-90.<\/p>\n<p>Hagemann T, Wilson J, Kulbe H, et al. Macrophages induce invasiveness of epithelial cancer cells via NF-kappa B and JNK. J Immunol. 2005 Jul 15;175(2):1197-205.<\/p>\n<p>Liu M, Ju X, Willmarth NE, et al. Nuclear factor-kappaB enhances ErbB2-induced mammary tumorigenesis and neoangiogenesis in vivo. Am J Pathol. 2009 May;174(5):1910-20.<\/p>\n<p>Beshir AB, Ren G, Magpusao AN, Barone LM, Yeung KC, Fenteany G. Raf kinase inhibitor protein suppresses nuclear factor-kappaB-dependent cancer cell invasion through negative regulation of matrix metalloproteinase expression. Cancer Lett. 2010 Dec 28;299(2):137-49.<\/p>\n<\/div>\n<div>\n<p><a title=\"\" href=\"#_ftnref14\">[14]<\/a> Shin SR, Sanchez-Velar N, Sherr DH, Sonenshein GE. 7,12-dimethylbenz(a)anthracene treatment of a c-rel mouse mammary tumor cell line induces epithelial to mesenchymal transition via activation of nuclear factor-kappaB. Cancer Res. 2006 Mar 1;66(5):2570-5. Reuter S, Prasad S, Phromnoi K, et al. Thiocolchicoside exhibits anticancer effects through downregulation of NF-{kappa}B pathway and its regulated gene products linked to inflammation and cancer. Cancer Prev Res (Phila). 2010 Nov;3(11):1462-72.<\/p>\n<p>Tapia MA, Gonzalez-Navarrete I, Dalmases A, et al. Inhibition of the canonical IKK\/NF kappa B pathway sensitizes human cancer cells to doxorubicin. Cell Cycle. 2007 Sep 15;6(18):2284-92.<\/p>\n<p><a title=\"\" href=\"#_ftnref14\">[15]<\/a>\u00a0Aravindaram K, Yang NS. Anti-inflammatory plant natural products for cancer therapy. Planta Med. 2010 Aug;76(11):1103-17.<\/p>\n<p>Valko M, Rhodes CJ, Moncol J, Izakovic M, Mazur M. Free radicals, metals and antioxidants in oxidative stress-induced cancer. Chem Biol Interact. 2006 Mar 10;160(1):1-40.<\/p>\n<p>Guo W, Kong E, Meydani M. Dietary polyphenols, inflammation, and cancer. Nutr Cancer. 2009 Nov;61(6):807-10.<\/p>\n<p>Ho HH, Chang CS, Ho WC, Liao SY, Wu CH, Wang CJ. Anti-metastasis effects of gallic acid on gastric cancer cells involves inhibition of NF-kappaB activity and downregulation of PI3K\/AKT\/small GTPase signals. Food Chem Toxicol. 2010 Aug-Sep;48(8-9):2508-16.<\/p>\n<\/div>\n<\/div>\n<div style=\"padding-bottom:20px; padding-top:10px;\" class=\"hupso-share-buttons\"><!-- Hupso Share Buttons - https:\/\/www.hupso.com\/share\/ --><a class=\"hupso_toolbar\" href=\"https:\/\/www.hupso.com\/share\/\"><img decoding=\"async\" src=\"https:\/\/static.hupso.com\/share\/buttons\/lang\/da\/share-small.png\" style=\"border:0px; padding-top: 5px; float:left;\" alt=\"Share Button\"\/><\/a><script type=\"text\/javascript\">var hupso_services_t=new Array(\"Twitter\",\"Facebook\",\"Google Plus\",\"Pinterest\",\"Linkedin\");var hupso_background_t=\"#EAF4FF\";var hupso_border_t=\"#66CCFF\";var hupso_toolbar_size_t=\"small\";var hupso_image_folder_url = \"\";var hupso_url_t=\"\";var hupso_title_t=\"Inflammation%20fremmer%20kr%C3%A6ftudvikling\";<\/script><script type=\"text\/javascript\" src=\"https:\/\/static.hupso.com\/share\/js\/share_toolbar.js\"><\/script><!-- Hupso Share Buttons --><\/div>","protected":false},"excerpt":{"rendered":"<p>Inflammation er efter mange forskeres mening en af de vigtigste underliggende faktorer til de fleste former for kr\u00e6ft, fordi den frigiver kraftige iltmolekyler (oxidanter), som b\u00e5de stimulerer celledeling og mutationer. Det er derfor vigtigt at forst\u00e5 mekanismerne og vide, hvad &hellip; <a href=\"https:\/\/www.naardiagnosenerkraeft.dk\/?page_id=274\">L\u00e6s resten <span class=\"meta-nav\">&rarr;<\/span><\/a><\/p>\n<div style=\"padding-bottom:20px; padding-top:10px;\" class=\"hupso-share-buttons\"><!-- Hupso Share Buttons - https:\/\/www.hupso.com\/share\/ --><a class=\"hupso_toolbar\" href=\"https:\/\/www.hupso.com\/share\/\"><img src=\"https:\/\/static.hupso.com\/share\/buttons\/lang\/da\/share-small.png\" style=\"border:0px; padding-top: 5px; float:left;\" alt=\"Share Button\"\/><\/a><script type=\"text\/javascript\">var hupso_services_t=new Array(\"Twitter\",\"Facebook\",\"Google Plus\",\"Pinterest\",\"Linkedin\");var hupso_background_t=\"#EAF4FF\";var hupso_border_t=\"#66CCFF\";var hupso_toolbar_size_t=\"small\";var hupso_image_folder_url = \"\";var hupso_url_t=\"\";var hupso_title_t=\"Inflammation%20fremmer%20kr%C3%A6ftudvikling\";<\/script><script type=\"text\/javascript\" src=\"https:\/\/static.hupso.com\/share\/js\/share_toolbar.js\"><\/script><!-- Hupso Share Buttons --><\/div>","protected":false},"author":2,"featured_media":0,"parent":0,"menu_order":0,"comment_status":"closed","ping_status":"closed","template":"","meta":{"footnotes":""},"class_list":["post-274","page","type-page","status-publish","hentry"],"_links":{"self":[{"href":"https:\/\/www.naardiagnosenerkraeft.dk\/index.php?rest_route=\/wp\/v2\/pages\/274","targetHints":{"allow":["GET"]}}],"collection":[{"href":"https:\/\/www.naardiagnosenerkraeft.dk\/index.php?rest_route=\/wp\/v2\/pages"}],"about":[{"href":"https:\/\/www.naardiagnosenerkraeft.dk\/index.php?rest_route=\/wp\/v2\/types\/page"}],"author":[{"embeddable":true,"href":"https:\/\/www.naardiagnosenerkraeft.dk\/index.php?rest_route=\/wp\/v2\/users\/2"}],"replies":[{"embeddable":true,"href":"https:\/\/www.naardiagnosenerkraeft.dk\/index.php?rest_route=%2Fwp%2Fv2%2Fcomments&post=274"}],"version-history":[{"count":5,"href":"https:\/\/www.naardiagnosenerkraeft.dk\/index.php?rest_route=\/wp\/v2\/pages\/274\/revisions"}],"predecessor-version":[{"id":277,"href":"https:\/\/www.naardiagnosenerkraeft.dk\/index.php?rest_route=\/wp\/v2\/pages\/274\/revisions\/277"}],"wp:attachment":[{"href":"https:\/\/www.naardiagnosenerkraeft.dk\/index.php?rest_route=%2Fwp%2Fv2%2Fmedia&parent=274"}],"curies":[{"name":"wp","href":"https:\/\/api.w.org\/{rel}","templated":true}]}}