Inhibition of growth and metastasis of orthotopic human prostate cancer in athymic mice by combination therapy with pegylated interferon-alpha-2b and docetaxel.
Identifieur interne : 003894 ( Main/Exploration ); précédent : 003893; suivant : 003895Inhibition of growth and metastasis of orthotopic human prostate cancer in athymic mice by combination therapy with pegylated interferon-alpha-2b and docetaxel.
Auteurs : Samuel F. Huang [États-Unis] ; Sun-Jin Kim ; Anh T. Lee ; Takashi Karashima ; Cora Bucana ; Daniel Kedar ; Paul Sweeney ; Badar Mian ; Dominic Fan ; David Shepherd ; Isaiah J. Fidler ; Colin P. Dinney ; Jerald J. KillionSource :
- Cancer research [ 0008-5472 ] ; 2002.
Descripteurs français
- KwdFr :
- Animaux (MeSH), Antinéoplasiques d'origine végétale (administration et posologie), Antinéoplasiques d'origine végétale (pharmacologie), Cadhérines (biosynthèse), Division cellulaire (effets des médicaments et des substances chimiques), Docetaxel (MeSH), Facteur de croissance fibroblastique de type 2 (biosynthèse), Humains (MeSH), Immunohistochimie (MeSH), Inhibiteurs de l'angiogenèse (administration et posologie), Inhibiteurs de l'angiogenèse (pharmacologie), Interféron alpha (administration et posologie), Interféron alpha (pharmacologie), Interféron alpha-2 (MeSH), Matrix metalloproteinase 2 (biosynthèse), Matrix metalloproteinase 9 (biosynthèse), Mâle (MeSH), Métastase tumorale (prévention et contrôle), Paclitaxel (administration et posologie), Paclitaxel (analogues et dérivés), Paclitaxel (pharmacologie), Polyéthylène glycols (administration et posologie), Polyéthylène glycols (pharmacologie), Protocoles de polychimiothérapie antinéoplasique (pharmacologie), Protéines recombinantes (MeSH), Relation dose-effet des médicaments (MeSH), Répartition aléatoire (MeSH), Souris (MeSH), Souris nude (MeSH), Synergie des médicaments (MeSH), Taxoïdes (MeSH), Tests d'activité antitumorale sur modèle de xénogreffe (MeSH), Tumeurs de la prostate (anatomopathologie), Tumeurs de la prostate (métabolisme), Tumeurs de la prostate (traitement médicamenteux), Tumeurs de la prostate (vascularisation).
- MESH :
- administration et posologie : Antinéoplasiques d'origine végétale, Inhibiteurs de l'angiogenèse, Interféron alpha, Paclitaxel, Polyéthylène glycols.
- analogues et dérivés : Paclitaxel.
- anatomopathologie : Tumeurs de la prostate.
- biosynthèse : Cadhérines, Facteur de croissance fibroblastique de type 2, Matrix metalloproteinase 2, Matrix metalloproteinase 9.
- effets des médicaments et des substances chimiques : Division cellulaire.
- métabolisme : Tumeurs de la prostate.
- pharmacologie : Antinéoplasiques d'origine végétale, Inhibiteurs de l'angiogenèse, Interféron alpha, Paclitaxel, Polyéthylène glycols, Protocoles de polychimiothérapie antinéoplasique.
- prévention et contrôle : Métastase tumorale.
- traitement médicamenteux : Tumeurs de la prostate.
- vascularisation : Tumeurs de la prostate.
- Animaux, Docetaxel, Humains, Immunohistochimie, Interféron alpha-2, Mâle, Protéines recombinantes, Relation dose-effet des médicaments, Répartition aléatoire, Souris, Souris nude, Synergie des médicaments, Taxoïdes, Tests d'activité antitumorale sur modèle de xénogreffe.
English descriptors
- KwdEn :
- Angiogenesis Inhibitors (administration & dosage), Angiogenesis Inhibitors (pharmacology), Animals (MeSH), Antineoplastic Agents, Phytogenic (administration & dosage), Antineoplastic Agents, Phytogenic (pharmacology), Antineoplastic Combined Chemotherapy Protocols (pharmacology), Cadherins (biosynthesis), Cell Division (drug effects), Docetaxel (MeSH), Dose-Response Relationship, Drug (MeSH), Drug Synergism (MeSH), Fibroblast Growth Factor 2 (biosynthesis), Humans (MeSH), Immunohistochemistry (MeSH), Interferon alpha-2 (MeSH), Interferon-alpha (administration & dosage), Interferon-alpha (pharmacology), Male (MeSH), Matrix Metalloproteinase 2 (biosynthesis), Matrix Metalloproteinase 9 (biosynthesis), Mice (MeSH), Mice, Nude (MeSH), Neoplasm Metastasis (prevention & control), Paclitaxel (administration & dosage), Paclitaxel (analogs & derivatives), Paclitaxel (pharmacology), Polyethylene Glycols (administration & dosage), Polyethylene Glycols (pharmacology), Prostatic Neoplasms (blood supply), Prostatic Neoplasms (drug therapy), Prostatic Neoplasms (metabolism), Prostatic Neoplasms (pathology), Random Allocation (MeSH), Recombinant Proteins (MeSH), Taxoids (MeSH), Xenograft Model Antitumor Assays (MeSH).
- MESH :
- chemical , administration & dosage : Angiogenesis Inhibitors, Antineoplastic Agents, Phytogenic, Interferon-alpha, Paclitaxel, Polyethylene Glycols.
- chemical , analogs & derivatives : Paclitaxel.
- chemical , biosynthesis : Cadherins, Fibroblast Growth Factor 2, Matrix Metalloproteinase 2, Matrix Metalloproteinase 9.
- chemical , pharmacology : Angiogenesis Inhibitors, Antineoplastic Agents, Phytogenic, Interferon-alpha, Paclitaxel, Polyethylene Glycols.
- blood supply : Prostatic Neoplasms.
- drug effects : Cell Division.
- drug therapy : Prostatic Neoplasms.
- metabolism : Prostatic Neoplasms.
- pathology : Prostatic Neoplasms.
- pharmacology : Antineoplastic Combined Chemotherapy Protocols.
- prevention & control : Neoplasm Metastasis.
- Animals, Docetaxel, Dose-Response Relationship, Drug, Drug Synergism, Humans, Immunohistochemistry, Interferon alpha-2, Male, Mice, Mice, Nude, Random Allocation, Recombinant Proteins, Taxoids, Xenograft Model Antitumor Assays.
Abstract
We evaluated whether treatment of orthotopic human prostate cancer in nude mice with pegylated IFN-alpha-2b (PEG-IFN-alpha-2b) and docetaxel could represent a two-compartment targeting of primary tumor (tumor cells and tumor-associated endothelial cells) and inhibition of regional lymph node metastasis. The antiangiogenic properties of IFN were combined with the cytotoxic properties of docetaxel, resulting in apoptosis of both tumor cells and endothelium and hence significant inhibition of primary tumor growth. We first determined the optimal biological dose of PEG-IFN-alpha-2b (70,000 IU/week) necessary to down-regulate the expression of basic fibroblast growth factor, matrix metalloprotease-9, and matrix metalloprotease-2. The therapeutic dose of docetaxel (10 mg/kg/week) was determined by efficacy and minimal body weight loss. Therapy beginning 3 days after orthotopic implantation of PC3-MM2 prostate cancer cells reduced tumor weight by 37% in mice treated with PEG-IFN-alpha-2b, by 60% in mice treated with docetaxel, and by 83% in those given both drugs. PEG-IFN-alpha-2b also induced apoptosis of tumor-associated endothelial cells and hence a significant decrease in microvessel density. Our data indicate that the combination of PEG-IFN-alpha and docetaxel inhibits neoplastic angiogenesis by inducing a decrease in the local production of proangiogenic molecules by tumor cells, resulting in increased apoptosis of tumor-associated endothelial cells.
PubMed: 12384530
Affiliations:
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Le document en format XML
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Anderson Cancer Center, Houston 77030</wicri:regionArea><placeName><settlement type="city">Houston</settlement><region type="state">Texas</region></placeName></affiliation></author><author><name sortKey="Kim, Sun Jin" sort="Kim, Sun Jin" uniqKey="Kim S" first="Sun-Jin" last="Kim">Sun-Jin Kim</name></author><author><name sortKey="Lee, Anh T" sort="Lee, Anh T" uniqKey="Lee A" first="Anh T" last="Lee">Anh T. Lee</name></author><author><name sortKey="Karashima, Takashi" sort="Karashima, Takashi" uniqKey="Karashima T" first="Takashi" last="Karashima">Takashi Karashima</name></author><author><name sortKey="Bucana, Cora" sort="Bucana, Cora" uniqKey="Bucana C" first="Cora" last="Bucana">Cora Bucana</name></author><author><name sortKey="Kedar, Daniel" sort="Kedar, Daniel" uniqKey="Kedar D" first="Daniel" last="Kedar">Daniel Kedar</name></author><author><name sortKey="Sweeney, Paul" sort="Sweeney, Paul" uniqKey="Sweeney P" first="Paul" last="Sweeney">Paul Sweeney</name></author><author><name sortKey="Mian, Badar" sort="Mian, Badar" uniqKey="Mian B" first="Badar" last="Mian">Badar Mian</name></author><author><name sortKey="Fan, Dominic" sort="Fan, Dominic" uniqKey="Fan D" first="Dominic" last="Fan">Dominic Fan</name></author><author><name sortKey="Shepherd, David" sort="Shepherd, David" uniqKey="Shepherd D" first="David" last="Shepherd">David Shepherd</name></author><author><name sortKey="Fidler, Isaiah J" sort="Fidler, Isaiah J" uniqKey="Fidler I" first="Isaiah J" last="Fidler">Isaiah J. 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Killion</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2002">2002</date><idno type="RBID">pubmed:12384530</idno><idno type="pmid">12384530</idno><idno type="wicri:Area/Main/Corpus">003869</idno><idno type="wicri:explorRef" wicri:stream="Main" wicri:step="Corpus" wicri:corpus="PubMed">003869</idno><idno type="wicri:Area/Main/Curation">003869</idno><idno type="wicri:explorRef" wicri:stream="Main" wicri:step="Curation">003869</idno><idno type="wicri:Area/Main/Exploration">003869</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Inhibition of growth and metastasis of orthotopic human prostate cancer in athymic mice by combination therapy with pegylated interferon-alpha-2b and docetaxel.</title><author><name sortKey="Huang, Samuel F" sort="Huang, Samuel F" uniqKey="Huang S" first="Samuel F" last="Huang">Samuel F. Huang</name><affiliation wicri:level="1"><nlm:affiliation>Department of Urology, The University of Texas M. D. Anderson Cancer Center, Houston 77030, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Urology, The University of Texas M. D. Anderson Cancer Center, Houston 77030</wicri:regionArea><placeName><settlement type="city">Houston</settlement><region type="state">Texas</region></placeName></affiliation></author><author><name sortKey="Kim, Sun Jin" sort="Kim, Sun Jin" uniqKey="Kim S" first="Sun-Jin" last="Kim">Sun-Jin Kim</name></author><author><name sortKey="Lee, Anh T" sort="Lee, Anh T" uniqKey="Lee A" first="Anh T" last="Lee">Anh T. Lee</name></author><author><name sortKey="Karashima, Takashi" sort="Karashima, Takashi" uniqKey="Karashima T" first="Takashi" last="Karashima">Takashi Karashima</name></author><author><name sortKey="Bucana, Cora" sort="Bucana, Cora" uniqKey="Bucana C" first="Cora" last="Bucana">Cora Bucana</name></author><author><name sortKey="Kedar, Daniel" sort="Kedar, Daniel" uniqKey="Kedar D" first="Daniel" last="Kedar">Daniel Kedar</name></author><author><name sortKey="Sweeney, Paul" sort="Sweeney, Paul" uniqKey="Sweeney P" first="Paul" last="Sweeney">Paul Sweeney</name></author><author><name sortKey="Mian, Badar" sort="Mian, Badar" uniqKey="Mian B" first="Badar" last="Mian">Badar Mian</name></author><author><name sortKey="Fan, Dominic" sort="Fan, Dominic" uniqKey="Fan D" first="Dominic" last="Fan">Dominic Fan</name></author><author><name sortKey="Shepherd, David" sort="Shepherd, David" uniqKey="Shepherd D" first="David" last="Shepherd">David Shepherd</name></author><author><name sortKey="Fidler, Isaiah J" sort="Fidler, Isaiah J" uniqKey="Fidler I" first="Isaiah J" last="Fidler">Isaiah J. Fidler</name></author><author><name sortKey="Dinney, Colin P" sort="Dinney, Colin P" uniqKey="Dinney C" first="Colin P" last="Dinney">Colin P. Dinney</name></author><author><name sortKey="Killion, Jerald J" sort="Killion, Jerald J" uniqKey="Killion J" first="Jerald J" last="Killion">Jerald J. Killion</name></author></analytic><series><title level="j">Cancer research</title><idno type="ISSN">0008-5472</idno><imprint><date when="2002" type="published">2002</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Angiogenesis Inhibitors (administration & dosage)</term><term>Angiogenesis Inhibitors (pharmacology)</term><term>Animals (MeSH)</term><term>Antineoplastic Agents, Phytogenic (administration & dosage)</term><term>Antineoplastic Agents, Phytogenic (pharmacology)</term><term>Antineoplastic Combined Chemotherapy Protocols (pharmacology)</term><term>Cadherins (biosynthesis)</term><term>Cell Division (drug effects)</term><term>Docetaxel (MeSH)</term><term>Dose-Response Relationship, Drug (MeSH)</term><term>Drug Synergism (MeSH)</term><term>Fibroblast Growth Factor 2 (biosynthesis)</term><term>Humans (MeSH)</term><term>Immunohistochemistry (MeSH)</term><term>Interferon alpha-2 (MeSH)</term><term>Interferon-alpha (administration & dosage)</term><term>Interferon-alpha (pharmacology)</term><term>Male (MeSH)</term><term>Matrix Metalloproteinase 2 (biosynthesis)</term><term>Matrix Metalloproteinase 9 (biosynthesis)</term><term>Mice (MeSH)</term><term>Mice, Nude (MeSH)</term><term>Neoplasm Metastasis (prevention & control)</term><term>Paclitaxel (administration & dosage)</term><term>Paclitaxel (analogs & derivatives)</term><term>Paclitaxel (pharmacology)</term><term>Polyethylene Glycols (administration & dosage)</term><term>Polyethylene Glycols (pharmacology)</term><term>Prostatic Neoplasms (blood supply)</term><term>Prostatic Neoplasms (drug therapy)</term><term>Prostatic Neoplasms (metabolism)</term><term>Prostatic Neoplasms (pathology)</term><term>Random Allocation (MeSH)</term><term>Recombinant Proteins (MeSH)</term><term>Taxoids (MeSH)</term><term>Xenograft Model Antitumor Assays (MeSH)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Animaux (MeSH)</term><term>Antinéoplasiques d'origine végétale (administration et posologie)</term><term>Antinéoplasiques d'origine végétale (pharmacologie)</term><term>Cadhérines (biosynthèse)</term><term>Division cellulaire (effets des médicaments et des substances chimiques)</term><term>Docetaxel (MeSH)</term><term>Facteur de croissance fibroblastique de type 2 (biosynthèse)</term><term>Humains (MeSH)</term><term>Immunohistochimie (MeSH)</term><term>Inhibiteurs de l'angiogenèse (administration et posologie)</term><term>Inhibiteurs de l'angiogenèse (pharmacologie)</term><term>Interféron alpha (administration et posologie)</term><term>Interféron alpha (pharmacologie)</term><term>Interféron alpha-2 (MeSH)</term><term>Matrix metalloproteinase 2 (biosynthèse)</term><term>Matrix metalloproteinase 9 (biosynthèse)</term><term>Mâle (MeSH)</term><term>Métastase tumorale (prévention et contrôle)</term><term>Paclitaxel (administration et posologie)</term><term>Paclitaxel (analogues et dérivés)</term><term>Paclitaxel (pharmacologie)</term><term>Polyéthylène glycols (administration et posologie)</term><term>Polyéthylène glycols (pharmacologie)</term><term>Protocoles de polychimiothérapie antinéoplasique (pharmacologie)</term><term>Protéines recombinantes (MeSH)</term><term>Relation dose-effet des médicaments (MeSH)</term><term>Répartition aléatoire (MeSH)</term><term>Souris (MeSH)</term><term>Souris nude (MeSH)</term><term>Synergie des médicaments (MeSH)</term><term>Taxoïdes (MeSH)</term><term>Tests d'activité antitumorale sur modèle de xénogreffe (MeSH)</term><term>Tumeurs de la prostate (anatomopathologie)</term><term>Tumeurs de la prostate (métabolisme)</term><term>Tumeurs de la prostate (traitement médicamenteux)</term><term>Tumeurs de la prostate (vascularisation)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="administration & dosage" xml:lang="en"><term>Angiogenesis Inhibitors</term><term>Antineoplastic Agents, Phytogenic</term><term>Interferon-alpha</term><term>Paclitaxel</term><term>Polyethylene Glycols</term></keywords><keywords scheme="MESH" type="chemical" qualifier="analogs & derivatives" xml:lang="en"><term>Paclitaxel</term></keywords><keywords scheme="MESH" type="chemical" qualifier="biosynthesis" xml:lang="en"><term>Cadherins</term><term>Fibroblast Growth Factor 2</term><term>Matrix Metalloproteinase 2</term><term>Matrix Metalloproteinase 9</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Angiogenesis Inhibitors</term><term>Antineoplastic Agents, Phytogenic</term><term>Interferon-alpha</term><term>Paclitaxel</term><term>Polyethylene Glycols</term></keywords><keywords scheme="MESH" qualifier="administration et posologie" xml:lang="fr"><term>Antinéoplasiques d'origine végétale</term><term>Inhibiteurs de l'angiogenèse</term><term>Interféron alpha</term><term>Paclitaxel</term><term>Polyéthylène glycols</term></keywords><keywords scheme="MESH" qualifier="analogues et dérivés" xml:lang="fr"><term>Paclitaxel</term></keywords><keywords scheme="MESH" qualifier="anatomopathologie" xml:lang="fr"><term>Tumeurs de la prostate</term></keywords><keywords scheme="MESH" qualifier="biosynthèse" xml:lang="fr"><term>Cadhérines</term><term>Facteur de croissance fibroblastique de type 2</term><term>Matrix metalloproteinase 2</term><term>Matrix metalloproteinase 9</term></keywords><keywords scheme="MESH" qualifier="blood supply" xml:lang="en"><term>Prostatic Neoplasms</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Cell Division</term></keywords><keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Prostatic Neoplasms</term></keywords><keywords scheme="MESH" qualifier="effets des médicaments et des substances chimiques" xml:lang="fr"><term>Division cellulaire</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Prostatic Neoplasms</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Tumeurs de la prostate</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Prostatic Neoplasms</term></keywords><keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Antinéoplasiques d'origine végétale</term><term>Inhibiteurs de l'angiogenèse</term><term>Interféron alpha</term><term>Paclitaxel</term><term>Polyéthylène glycols</term><term>Protocoles de polychimiothérapie antinéoplasique</term></keywords><keywords scheme="MESH" qualifier="pharmacology" xml:lang="en"><term>Antineoplastic Combined Chemotherapy Protocols</term></keywords><keywords scheme="MESH" qualifier="prevention & control" xml:lang="en"><term>Neoplasm Metastasis</term></keywords><keywords scheme="MESH" qualifier="prévention et contrôle" xml:lang="fr"><term>Métastase tumorale</term></keywords><keywords scheme="MESH" qualifier="traitement médicamenteux" xml:lang="fr"><term>Tumeurs de la prostate</term></keywords><keywords scheme="MESH" qualifier="vascularisation" xml:lang="fr"><term>Tumeurs de la prostate</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Docetaxel</term><term>Dose-Response Relationship, Drug</term><term>Drug Synergism</term><term>Humans</term><term>Immunohistochemistry</term><term>Interferon alpha-2</term><term>Male</term><term>Mice</term><term>Mice, Nude</term><term>Random Allocation</term><term>Recombinant Proteins</term><term>Taxoids</term><term>Xenograft Model Antitumor Assays</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Docetaxel</term><term>Humains</term><term>Immunohistochimie</term><term>Interféron alpha-2</term><term>Mâle</term><term>Protéines recombinantes</term><term>Relation dose-effet des médicaments</term><term>Répartition aléatoire</term><term>Souris</term><term>Souris nude</term><term>Synergie des médicaments</term><term>Taxoïdes</term><term>Tests d'activité antitumorale sur modèle de xénogreffe</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">We evaluated whether treatment of orthotopic human prostate cancer in nude mice with pegylated IFN-alpha-2b (PEG-IFN-alpha-2b) and docetaxel could represent a two-compartment targeting of primary tumor (tumor cells and tumor-associated endothelial cells) and inhibition of regional lymph node metastasis. The antiangiogenic properties of IFN were combined with the cytotoxic properties of docetaxel, resulting in apoptosis of both tumor cells and endothelium and hence significant inhibition of primary tumor growth. We first determined the optimal biological dose of PEG-IFN-alpha-2b (70,000 IU/week) necessary to down-regulate the expression of basic fibroblast growth factor, matrix metalloprotease-9, and matrix metalloprotease-2. The therapeutic dose of docetaxel (10 mg/kg/week) was determined by efficacy and minimal body weight loss. Therapy beginning 3 days after orthotopic implantation of PC3-MM2 prostate cancer cells reduced tumor weight by 37% in mice treated with PEG-IFN-alpha-2b, by 60% in mice treated with docetaxel, and by 83% in those given both drugs. PEG-IFN-alpha-2b also induced apoptosis of tumor-associated endothelial cells and hence a significant decrease in microvessel density. Our data indicate that the combination of PEG-IFN-alpha and docetaxel inhibits neoplastic angiogenesis by inducing a decrease in the local production of proangiogenic molecules by tumor cells, resulting in increased apoptosis of tumor-associated endothelial cells.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">12384530</PMID><DateCompleted><Year>2002</Year><Month>11</Month><Day>29</Day></DateCompleted><DateRevised><Year>2019</Year><Month>12</Month><Day>10</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0008-5472</ISSN><JournalIssue CitedMedium="Print"><Volume>62</Volume><Issue>20</Issue><PubDate><Year>2002</Year><Month>Oct</Month><Day>15</Day></PubDate></JournalIssue><Title>Cancer research</Title><ISOAbbreviation>Cancer Res</ISOAbbreviation></Journal><ArticleTitle>Inhibition of growth and metastasis of orthotopic human prostate cancer in athymic mice by combination therapy with pegylated interferon-alpha-2b and docetaxel.</ArticleTitle><Pagination><MedlinePgn>5720-6</MedlinePgn></Pagination><Abstract><AbstractText>We evaluated whether treatment of orthotopic human prostate cancer in nude mice with pegylated IFN-alpha-2b (PEG-IFN-alpha-2b) and docetaxel could represent a two-compartment targeting of primary tumor (tumor cells and tumor-associated endothelial cells) and inhibition of regional lymph node metastasis. The antiangiogenic properties of IFN were combined with the cytotoxic properties of docetaxel, resulting in apoptosis of both tumor cells and endothelium and hence significant inhibition of primary tumor growth. We first determined the optimal biological dose of PEG-IFN-alpha-2b (70,000 IU/week) necessary to down-regulate the expression of basic fibroblast growth factor, matrix metalloprotease-9, and matrix metalloprotease-2. The therapeutic dose of docetaxel (10 mg/kg/week) was determined by efficacy and minimal body weight loss. Therapy beginning 3 days after orthotopic implantation of PC3-MM2 prostate cancer cells reduced tumor weight by 37% in mice treated with PEG-IFN-alpha-2b, by 60% in mice treated with docetaxel, and by 83% in those given both drugs. PEG-IFN-alpha-2b also induced apoptosis of tumor-associated endothelial cells and hence a significant decrease in microvessel density. Our data indicate that the combination of PEG-IFN-alpha and docetaxel inhibits neoplastic angiogenesis by inducing a decrease in the local production of proangiogenic molecules by tumor cells, resulting in increased apoptosis of tumor-associated endothelial cells.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Huang</LastName><ForeName>Samuel F</ForeName><Initials>SF</Initials><AffiliationInfo><Affiliation>Department of Urology, The University of Texas M. D. Anderson Cancer Center, Houston 77030, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Kim</LastName><ForeName>Sun-Jin</ForeName><Initials>SJ</Initials></Author><Author ValidYN="Y"><LastName>Lee</LastName><ForeName>Anh T</ForeName><Initials>AT</Initials></Author><Author ValidYN="Y"><LastName>Karashima</LastName><ForeName>Takashi</ForeName><Initials>T</Initials></Author><Author ValidYN="Y"><LastName>Bucana</LastName><ForeName>Cora</ForeName><Initials>C</Initials></Author><Author ValidYN="Y"><LastName>Kedar</LastName><ForeName>Daniel</ForeName><Initials>D</Initials></Author><Author ValidYN="Y"><LastName>Sweeney</LastName><ForeName>Paul</ForeName><Initials>P</Initials></Author><Author ValidYN="Y"><LastName>Mian</LastName><ForeName>Badar</ForeName><Initials>B</Initials></Author><Author ValidYN="Y"><LastName>Fan</LastName><ForeName>Dominic</ForeName><Initials>D</Initials></Author><Author ValidYN="Y"><LastName>Shepherd</LastName><ForeName>David</ForeName><Initials>D</Initials></Author><Author ValidYN="Y"><LastName>Fidler</LastName><ForeName>Isaiah J</ForeName><Initials>IJ</Initials></Author><Author ValidYN="Y"><LastName>Dinney</LastName><ForeName>Colin P</ForeName><Initials>CP</Initials></Author><Author ValidYN="Y"><LastName>Killion</LastName><ForeName>Jerald J</ForeName><Initials>JJ</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D023362">Evaluation Study</PublicationType><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Cancer Res</MedlineTA><NlmUniqueID>2984705R</NlmUniqueID><ISSNLinking>0008-5472</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D020533">Angiogenesis 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control</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D017239" MajorTopicYN="N">Paclitaxel</DescriptorName><QualifierName UI="Q000008" MajorTopicYN="N">administration & dosage</QualifierName><QualifierName UI="Q000031" MajorTopicYN="Y">analogs & derivatives</QualifierName><QualifierName UI="Q000494" MajorTopicYN="Y">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D011092" MajorTopicYN="N">Polyethylene Glycols</DescriptorName><QualifierName UI="Q000008" MajorTopicYN="N">administration & dosage</QualifierName><QualifierName UI="Q000494" MajorTopicYN="Y">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D011471" MajorTopicYN="N">Prostatic Neoplasms</DescriptorName><QualifierName UI="Q000098" MajorTopicYN="N">blood supply</QualifierName><QualifierName UI="Q000188" MajorTopicYN="Y">drug therapy</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D011897" MajorTopicYN="N">Random Allocation</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D011994" MajorTopicYN="N">Recombinant Proteins</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D043823" MajorTopicYN="Y">Taxoids</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D023041" MajorTopicYN="N">Xenograft Model Antitumor Assays</DescriptorName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>2002</Year><Month>10</Month><Day>18</Day><Hour>4</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2002</Year><Month>11</Month><Day>30</Day><Hour>4</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2002</Year><Month>10</Month><Day>18</Day><Hour>4</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">12384530</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>États-Unis</li></country><region><li>Texas</li></region><settlement><li>Houston</li></settlement></list><tree><noCountry><name sortKey="Bucana, Cora" sort="Bucana, Cora" uniqKey="Bucana C" first="Cora" last="Bucana">Cora Bucana</name><name sortKey="Dinney, Colin P" sort="Dinney, Colin P" uniqKey="Dinney C" first="Colin P" last="Dinney">Colin P. Dinney</name><name sortKey="Fan, Dominic" sort="Fan, Dominic" uniqKey="Fan D" first="Dominic" last="Fan">Dominic Fan</name><name sortKey="Fidler, Isaiah J" sort="Fidler, Isaiah J" uniqKey="Fidler I" first="Isaiah J" last="Fidler">Isaiah J. Fidler</name><name sortKey="Karashima, Takashi" sort="Karashima, Takashi" uniqKey="Karashima T" first="Takashi" last="Karashima">Takashi Karashima</name><name sortKey="Kedar, Daniel" sort="Kedar, Daniel" uniqKey="Kedar D" first="Daniel" last="Kedar">Daniel Kedar</name><name sortKey="Killion, Jerald J" sort="Killion, Jerald J" uniqKey="Killion J" first="Jerald J" last="Killion">Jerald J. Killion</name><name sortKey="Kim, Sun Jin" sort="Kim, Sun Jin" uniqKey="Kim S" first="Sun-Jin" last="Kim">Sun-Jin Kim</name><name sortKey="Lee, Anh T" sort="Lee, Anh T" uniqKey="Lee A" first="Anh T" last="Lee">Anh T. Lee</name><name sortKey="Mian, Badar" sort="Mian, Badar" uniqKey="Mian B" first="Badar" last="Mian">Badar Mian</name><name sortKey="Shepherd, David" sort="Shepherd, David" uniqKey="Shepherd D" first="David" last="Shepherd">David Shepherd</name><name sortKey="Sweeney, Paul" sort="Sweeney, Paul" uniqKey="Sweeney P" first="Paul" last="Sweeney">Paul Sweeney</name></noCountry><country name="États-Unis"><region name="Texas"><name sortKey="Huang, Samuel F" sort="Huang, Samuel F" uniqKey="Huang S" first="Samuel F" last="Huang">Samuel F. Huang</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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