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<!DOCTYPE html> <html lang="en" dir="ltr" xmlns="http://www.w3.org/1999/xhtml" xmlns:mml="http://www.w3.org/1998/Math/MathML"> <head prefix="og: http://ogp.me/ns# article: http://ogp.me/ns/article# book: http://ogp.me/ns/book#" >  <link rel="dns-prefetch" href="//cdn.jsdelivr.net" /> <link rel="dns-prefetch" href="//cdn.foxycart.com" /> <link rel="dns-prefetch" href="//scholar.google.com" /> <meta http-equiv="Content-Type" content="text/html; charset=utf-8" /> <meta name="Generator" content="Drupal 7 (http://drupal.org)" /> <link rel="canonical" href="https://ar.iiarjournals.org/content/24/5A/2783" /> <link rel="alternate" type="application/pdf" title="Full Text (PDF)" href="/content/24/5A/2783.full.pdf" /> <meta name="issue_cover_image" content="https://ar.iiarjournals.org/sites/default/files/highwire/default/covers/acr_default_cover_0.gif" /> <meta name="type" content="article" /> <meta name="category" content="review-article" /> <meta name="HW.identifier" content="/anticanres/24/5A/2783.atom" /> <meta name="HW.pisa" content="anticanres;24/5A/2783" /> <meta name="DC.Format" content="text/html" /> <meta name="DC.Language" content="en" /> <meta name="DC.Title" content="Role of Resveratrol in Prevention and Therapy of Cancer: Preclinical and Clinical Studies" /> <meta name="DC.Date" content="2004-09-01" /> <meta name="DC.Publisher" content="International Institute of Anticancer Research" /> <meta name="DC.Rights" content="Copyright© 2004 International Institute of Anticancer Research (Dr. John G. Delinassios), All rights reserved" /> <meta name="DC.AccessRights" content="restricted" /> <meta name="DC.Description" content="Resveratrol, trans-3,5,4’-trihydroxystilbene, was first isolated in 1940 as a constituent of the roots of white hellebore (Veratrum grandiflorum O. Loes), but has since been found in various plants, including grapes, berries and peanuts. Besides cardioprotective effects, resveratrol exhibits anticancer properties, as suggested by its ability to suppress proliferation of a wide variety of tumor cells, including lymphoid and myeloid cancers; multiple myeloma; cancers of the breast, prostate, stomach, colon, pancreas, and thyroid; melanoma; head and neck squamous cell carcinoma; ovarian carcinoma; and cervical carcinoma. The growth-inhibitory effects of resveratrol are mediated through cell-cycle arrest; up-regulation of p21Cip1/WAF1, p53 and Bax; down-regulation of survivin, cyclin D1, cyclin E, Bcl-2, Bcl-xL and cIAPs; and activation of caspases. Resveratrol has been shown to suppress the activation of several transcription factors, including NF-Î B, AP-1 and Egr-1; to inhibit protein kinases including IÎ Bα kinase, JNK, MAPK, Akt, PKC, PKD and casein kinase II; and to down-regulate products of genes such as COX-2, 5-LOX, VEGF, IL-1, IL-6, IL-8, AR and PSA. These activities account for the suppression of angiogenesis by this stilbene. Resveratrol also has been shown to potentiate the apoptotic effects of cytokines (e.g., TRAIL), chemotherapeutic agents and γ-radiation. Phamacokinetic studies revealed that the target organs of resveratrol are liver and kidney, where it is concentrated after absorption and is mainly converted to a sulfated form and a glucuronide conjugate. In vivo, resveratrol blocks the multistep process of carcinogenesis at various stages: it blocks carcinogen activation by inhibiting aryl hydrocarbon-induced CYP1A1 expression and activity, and suppresses tumor initiation, promotion and progression. Besides chemopreventive effects, resveratrol appears to exhibit therapeutic effects against cancer. Limited data in humans have revealed that resveratrol is pharmacologically quite safe. Currently, structural analogues of resveratrol with improved bioavailability are being pursued as potential therapeutic agents for cancer." /> <meta name="DC.Contributor" content="BHARAT B. AGGARWAL" /> <meta name="DC.Contributor" content="ANJANA BHARDWAJ" /> <meta name="DC.Contributor" content="RISHI S. AGGARWAL" /> <meta name="DC.Contributor" content="NAVINDRA P. SEERAM" /> <meta name="DC.Contributor" content="SHISHIR SHISHODIA" /> <meta name="DC.Contributor" content="YASUNARI TAKADA" /> <meta name="article:published_time" content="2004-09-01" /> <meta name="article:section" content="Experimental Studies" /> <meta name="citation_title" content="Role of Resveratrol in Prevention and Therapy of Cancer: Preclinical and Clinical Studies" /> <meta name="citation_abstract" lang="en" content="<p>Resveratrol, trans-3,5,4’-trihydroxystilbene, was first isolated in 1940 as a constituent of the roots of white hellebore (Veratrum grandiflorum O. Loes), but has since been found in various plants, including grapes, berries and peanuts. Besides cardioprotective effects, resveratrol exhibits anticancer properties, as suggested by its ability to suppress proliferation of a wide variety of tumor cells, including lymphoid and myeloid cancers; multiple myeloma; cancers of the breast, prostate, stomach, colon, pancreas, and thyroid; melanoma; head and neck squamous cell carcinoma; ovarian carcinoma; and cervical carcinoma. The growth-inhibitory effects of resveratrol are mediated through cell-cycle arrest; up-regulation of p21<sup>Cip1/WAF1</sup>, p53 and Bax; down-regulation of survivin, cyclin D1, cyclin E, Bcl-2, Bcl-x<sub>L</sub> and cIAPs; and activation of caspases. Resveratrol has been shown to suppress the activation of several transcription factors, including NF-Î B, AP-1 and Egr-1; to inhibit protein kinases including IÎ Bα kinase, JNK, MAPK, Akt, PKC, PKD and casein kinase II; and to down-regulate products of genes such as COX-2, 5-LOX, VEGF, IL-1, IL-6, IL-8, AR and PSA. These activities account for the suppression of angiogenesis by this stilbene. Resveratrol also has been shown to potentiate the apoptotic effects of cytokines (e.g., TRAIL), chemotherapeutic agents and γ-radiation. Phamacokinetic studies revealed that the target organs of resveratrol are liver and kidney, where it is concentrated after absorption and is mainly converted to a sulfated form and a glucuronide conjugate. In vivo, resveratrol blocks the multistep process of carcinogenesis at various stages: it blocks carcinogen activation by inhibiting aryl hydrocarbon-induced CYP1A1 expression and activity, and suppresses tumor initiation, promotion and progression. Besides chemopreventive effects, resveratrol appears to exhibit therapeutic effects against cancer. Limited data in humans have revealed that resveratrol is pharmacologically quite safe. Currently, structural analogues of resveratrol with improved bioavailability are being pursued as potential therapeutic agents for cancer.</p>" /> <meta name="citation_journal_title" content="Anticancer Research" /> <meta name="citation_publisher" content="International Institute of Anticancer Research" /> <meta name="citation_publication_date" content="2004/09/01" /> <meta name="citation_mjid" content="anticanres;24/5A/2783" /> <meta name="citation_id" content="24/5A/2783" /> <meta name="citation_public_url" content="https://ar.iiarjournals.org/content/24/5A/2783" /> <meta name="citation_abstract_html_url" content="https://ar.iiarjournals.org/content/24/5A/2783.abstract" /> <meta name="citation_full_html_url" content="https://ar.iiarjournals.org/content/24/5A/2783.full" /> <meta name="citation_pdf_url" content="https://ar.iiarjournals.org/content/anticanres/24/5A/2783.full.pdf" /> <meta name="citation_issn" content="0250-7005" /> <meta name="citation_issn" content="1791-7530" /> <meta name="citation_pmid" content="15517885" /> <meta name="citation_volume" content="24" /> <meta name="citation_issue" content="5A" /> <meta name="citation_article_type" content="Review Article" /> <meta name="citation_section" content="Experimental Studies" /> <meta name="citation_firstpage" content="2783" /> <meta name="citation_lastpage" content="2840" /> <meta name="citation_author" content="BHARAT B. AGGARWAL" /> <meta name="citation_author" content="ANJANA BHARDWAJ" /> <meta name="citation_author" content="RISHI S. AGGARWAL" /> <meta name="citation_author" content="NAVINDRA P. SEERAM" /> <meta name="citation_author" content="SHISHIR SHISHODIA" /> <meta name="citation_author" content="YASUNARI TAKADA" /> <meta name="twitter:title" content="Role of Resveratrol in Prevention and Therapy of Cancer: Preclinical and Clinical Studies" /> <meta name="twitter:card" content="summary_large_image" /> <meta name="twitter:image" content="https://ar.iiarjournals.org/sites/default/files/highwire/default/covers/acr_default_cover_0.gif" /> <meta name="twitter:description" content="Resveratrol, trans-3,5,4’-trihydroxystilbene, was first isolated in 1940 as a constituent of the roots of white hellebore (Veratrum grandiflorum O. Loes), but has since been found in various plants, including grapes, berries and peanuts. Besides cardioprotective effects, resveratrol exhibits anticancer properties, as suggested by its ability to suppress proliferation of a wide variety of tumor cells, including lymphoid and myeloid cancers; multiple myeloma; cancers of the breast, prostate, stomach, colon, pancreas, and thyroid; melanoma; head and neck squamous cell carcinoma; ovarian carcinoma; and cervical carcinoma. The growth-inhibitory effects of resveratrol are mediated through cell-cycle arrest; up-regulation of p21Cip1/WAF1, p53 and Bax; down-regulation of survivin, cyclin D1, cyclin E, Bcl-2, Bcl-xL and cIAPs; and activation of caspases. Resveratrol has been shown to suppress the activation of several transcription factors, including NF-Î B, AP-1 and Egr-1; to inhibit protein kinases including IÎ Bα kinase, JNK, MAPK, Akt, PKC, PKD and casein kinase II; and to down-regulate products of genes such as COX-2, 5-LOX, VEGF, IL-1, IL-6, IL-8, AR and PSA. These activities account for the suppression of angiogenesis by this stilbene. Resveratrol also has been shown to potentiate the apoptotic effects of cytokines (e.g., TRAIL), chemotherapeutic agents and γ-radiation. Phamacokinetic studies revealed that the target organs of resveratrol are liver and kidney, where it is concentrated after absorption and is mainly converted to a sulfated form and a glucuronide conjugate. In vivo, resveratrol blocks the multistep process of carcinogenesis at various stages: it blocks carcinogen activation by inhibiting aryl hydrocarbon-induced CYP1A1 expression and activity, and suppresses tumor initiation, promotion and progression. Besides chemopreventive effects, resveratrol appears to exhibit therapeutic effects against cancer. Limited data in humans have revealed that resveratrol is pharmacologically quite safe. Currently, structural analogues of resveratrol with improved bioavailability are being pursued as potential therapeutic agents for cancer." /> <meta name="og-title" property="og:title" content="Role of Resveratrol in Prevention and Therapy of Cancer: Preclinical and Clinical Studies" /> <meta name="og-url" property="og:url" content="https://ar.iiarjournals.org/content/24/5A/2783" /> <meta name="og-site-name" property="og:site_name" content="Anticancer Research" /> <meta name="og-description" property="og:description" content="Resveratrol, trans-3,5,4’-trihydroxystilbene, was first isolated in 1940 as a constituent of the roots of white hellebore (Veratrum grandiflorum O. Loes), but has since been found in various plants, including grapes, berries and peanuts. Besides cardioprotective effects, resveratrol exhibits anticancer properties, as suggested by its ability to suppress proliferation of a wide variety of tumor cells, including lymphoid and myeloid cancers; multiple myeloma; cancers of the breast, prostate, stomach, colon, pancreas, and thyroid; melanoma; head and neck squamous cell carcinoma; ovarian carcinoma; and cervical carcinoma. The growth-inhibitory effects of resveratrol are mediated through cell-cycle arrest; up-regulation of p21Cip1/WAF1, p53 and Bax; down-regulation of survivin, cyclin D1, cyclin E, Bcl-2, Bcl-xL and cIAPs; and activation of caspases. Resveratrol has been shown to suppress the activation of several transcription factors, including NF-Î B, AP-1 and Egr-1; to inhibit protein kinases including IÎ Bα kinase, JNK, MAPK, Akt, PKC, PKD and casein kinase II; and to down-regulate products of genes such as COX-2, 5-LOX, VEGF, IL-1, IL-6, IL-8, AR and PSA. These activities account for the suppression of angiogenesis by this stilbene. Resveratrol also has been shown to potentiate the apoptotic effects of cytokines (e.g., TRAIL), chemotherapeutic agents and γ-radiation. Phamacokinetic studies revealed that the target organs of resveratrol are liver and kidney, where it is concentrated after absorption and is mainly converted to a sulfated form and a glucuronide conjugate. In vivo, resveratrol blocks the multistep process of carcinogenesis at various stages: it blocks carcinogen activation by inhibiting aryl hydrocarbon-induced CYP1A1 expression and activity, and suppresses tumor initiation, promotion and progression. Besides chemopreventive effects, resveratrol appears to exhibit therapeutic effects against cancer. Limited data in humans have revealed that resveratrol is pharmacologically quite safe. Currently, structural analogues of resveratrol with improved bioavailability are being pursued as potential therapeutic agents for cancer." /> <meta name="og-type" property="og:type" content="article" /> <meta name="og-image" property="og:image" content="https://ar.iiarjournals.org/sites/default/files/highwire/default/covers/acr_default_cover_0.gif" /> <link rel="shortlink" href="/node/6178" /> <link rel="shortcut icon" href="https://ar.iiarjournals.org/sites/default/files/images/favicon.ico" type="image/vnd.microsoft.icon" /> <meta name="viewport" content="width=device-width, initial-scale=1" /> <title>Role of Resveratrol in Prevention and Therapy of Cancer: Preclinical and Clinical Studies | Anticancer Research</title> <link type="text/css" rel="stylesheet" href="/sites/default/files/advagg_css/css__QEy_BpbtMcsqv3xURK855GSs2fFjOibU10yA758Mn4c__NucWi_bEk5E3BNVDtTt2nhiPtE1A5I24YwRDQ2fojJ0__M8F9fri-b1QX8RwJbNRiWvN_bqCXCQEG9-9ZZDMJpyg.css" media="all" /> <link type="text/css" 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class="highwire-cite-authors"><span class="highwire-citation-authors"><span class="highwire-citation-author first" data-delta="0">BHARAT B. AGGARWAL</span>, <span class="highwire-citation-author" data-delta="1">ANJANA BHARDWAJ</span>, <span class="highwire-citation-author" data-delta="2">RISHI S. AGGARWAL</span>, <span class="highwire-citation-author" data-delta="3">NAVINDRA P. SEERAM</span>, <span class="highwire-citation-author" data-delta="4">SHISHIR SHISHODIA</span> and <span class="highwire-citation-author" data-delta="5">YASUNARI TAKADA</span></span></div> <div class="highwire-cite-metadata"><span class="highwire-cite-metadata-journal highwire-cite-metadata">Anticancer Research </span><span class="highwire-cite-metadata-date highwire-cite-metadata">September 2004, </span><span class="highwire-cite-metadata-volume highwire-cite-metadata">24 </span><span class="highwire-cite-metadata-issue highwire-cite-metadata">(5A) </span><span class="highwire-cite-metadata-pages highwire-cite-metadata">2783-2840; </span></div> <div class="highwire-cite-extras"><span class="highwire-foxycart-add-to-cart-ahah highwire-foxycart-add-to-cart-ahah" data-text="Add to Cart (%short-price)" data-apath="/anticanres/24/5A/2783.atom" data-type="link" data-font-icon="" data-parent-id="5377"></span></div> </div> <div id="hw-article-author-popups-top-node-6178--2985315924" style="display: none;"><div class="author-tooltip-0"><div class="author-tooltip-name">BHARAT B. 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xmlns:xhtml="http://www.w3.org/1999/xhtml"><div class="article abstract-view"><span class="highwire-journal-article-marker-start"></span><div class="section abstract" id="abstract-1"><h2>Abstract</h2> <p id="P1">Resveratrol, trans-3,5,4’-trihydroxystilbene, was first isolated in 1940 as a constituent of the roots of white hellebore (Veratrum grandiflorum O. Loes), but has since been found in various plants, including grapes, berries and peanuts. Besides cardioprotective effects, resveratrol exhibits anticancer properties, as suggested by its ability to suppress proliferation of a wide variety of tumor cells, including lymphoid and myeloid cancers; multiple myeloma; cancers of the breast, prostate, stomach, colon, pancreas, and thyroid; melanoma; head and neck squamous cell carcinoma; ovarian carcinoma; and cervical carcinoma. The growth-inhibitory effects of resveratrol are mediated through cell-cycle arrest; up-regulation of p21<sup>Cip1/WAF1</sup>, p53 and Bax; down-regulation of survivin, cyclin D1, cyclin E, Bcl-2, Bcl-x<sub>L</sub> and cIAPs; and activation of caspases. Resveratrol has been shown to suppress the activation of several transcription factors, including NF-Î B, AP-1 and Egr-1; to inhibit protein kinases including IÎ Bα kinase, JNK, MAPK, Akt, PKC, PKD and casein kinase II; and to down-regulate products of genes such as COX-2, 5-LOX, VEGF, IL-1, IL-6, IL-8, AR and PSA. These activities account for the suppression of angiogenesis by this stilbene. Resveratrol also has been shown to potentiate the apoptotic effects of cytokines (e.g., TRAIL), chemotherapeutic agents and γ-radiation. Phamacokinetic studies revealed that the target organs of resveratrol are liver and kidney, where it is concentrated after absorption and is mainly converted to a sulfated form and a glucuronide conjugate. In vivo, resveratrol blocks the multistep process of carcinogenesis at various stages: it blocks carcinogen activation by inhibiting aryl hydrocarbon-induced CYP1A1 expression and activity, and suppresses tumor initiation, promotion and progression. Besides chemopreventive effects, resveratrol appears to exhibit therapeutic effects against cancer. Limited data in humans have revealed that resveratrol is pharmacologically quite safe. Currently, structural analogues of resveratrol with improved bioavailability are being pursued as potential therapeutic agents for cancer.</p> </div><div class="section fn-group" id="fn-group-1"><h2>Footnotes</h2><ul><li class="history" id="history-1"><ul class="history-list"><li xmlns:hwp="http://schema.highwire.org/Journal" class="received" hwp:start="2004-04-07"><span class="received-label">Received </span>April 7, 2004.</li><li xmlns:hwp="http://schema.highwire.org/Journal" class="accepted" hwp:start="2004-07-01"><span class="accepted-label">Accepted </span>July 1, 2004.</li></ul></li></ul></div><ul><li class="copyright-statement" id="copyright-statement-1">Copyright© 2004 International Institute of Anticancer Research (Dr. John G. 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data-delta="2"><span class="nlm-given-names">RISHI S.</span> <span class="nlm-surname">AGGARWAL</span></span>, <span class="highwire-citation-author" data-delta="3"><span class="nlm-given-names">NAVINDRA P.</span> <span class="nlm-surname">SEERAM</span></span>, <span class="highwire-citation-author" data-delta="4"><span class="nlm-given-names">SHISHIR</span> <span class="nlm-surname">SHISHODIA</span></span>, <span class="highwire-citation-author" data-delta="5"><span class="nlm-given-names">YASUNARI</span> <span class="nlm-surname">TAKADA</span></span></span></div> <div class="highwire-cite-metadata"><span class="highwire-cite-metadata-journal highwire-cite-metadata">Anticancer Research </span><span class="highwire-cite-metadata-date highwire-cite-metadata">Sep 2004, </span><span class="highwire-cite-metadata-volume highwire-cite-metadata">24 </span><span class="highwire-cite-metadata-issue highwire-cite-metadata">(5A) </span><span class="highwire-cite-metadata-pages 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