Novel in vivo imaging shows up-regulation of death receptors by paclitaxel and correlates with enhanced antitumor effects of receptor agonist antibodies.
Identifieur interne : 002958 ( Main/Exploration ); précédent : 002957; suivant : 002959Novel in vivo imaging shows up-regulation of death receptors by paclitaxel and correlates with enhanced antitumor effects of receptor agonist antibodies.
Auteurs : RBID : pubmed:17148761English descriptors
- KwdEn :
- Animals, Antibodies, Monoclonal (pharmacokinetics), Antibodies, Monoclonal (pharmacology), Antineoplastic Combined Chemotherapy Protocols (pharmacology), Apoptosis (drug effects), Apoptosis (genetics), Colorectal Neoplasms (drug therapy), Colorectal Neoplasms (genetics), Colorectal Neoplasms (metabolism), Colorectal Neoplasms (radionuclide imaging), Drug Synergism, Female, Humans, Indium Radioisotopes (diagnostic use), Mice, Mice, Nude, Mitogen-Activated Protein Kinase 1 (biosynthesis), Mitogen-Activated Protein Kinase 1 (metabolism), Mitogen-Activated Protein Kinase 3 (biosynthesis), Mitogen-Activated Protein Kinase 3 (metabolism), Paclitaxel (pharmacology), Phosphorylation, Radionuclide Imaging (methods), Receptors, TNF-Related Apoptosis-Inducing Ligand (agonists), Receptors, TNF-Related Apoptosis-Inducing Ligand (biosynthesis), Receptors, TNF-Related Apoptosis-Inducing Ligand (genetics), Technetium (diagnostic use), Tumor Suppressor Protein p53 (biosynthesis), Tumor Suppressor Protein p53 (metabolism), Up-Regulation (drug effects), Xenograft Model Antitumor Assays.
- MESH :
- chemical , agonists : Receptors, TNF-Related Apoptosis-Inducing Ligand.
- chemical , biosynthesis : Mitogen-Activated Protein Kinase 1, Mitogen-Activated Protein Kinase 3, Receptors, TNF-Related Apoptosis-Inducing Ligand, Tumor Suppressor Protein p53.
- chemical , diagnostic use : Indium Radioisotopes, Technetium.
- chemical , genetics : Receptors, TNF-Related Apoptosis-Inducing Ligand.
- chemical , metabolism : Mitogen-Activated Protein Kinase 1, Mitogen-Activated Protein Kinase 3, Tumor Suppressor Protein p53.
- chemical , pharmacokinetics : Antibodies, Monoclonal.
- chemical , pharmacology : Antibodies, Monoclonal, Paclitaxel.
- drug effects : Apoptosis, Up-Regulation.
- drug therapy : Colorectal Neoplasms.
- genetics : Apoptosis, Colorectal Neoplasms.
- metabolism : Colorectal Neoplasms.
- methods : Radionuclide Imaging.
- pharmacology : Antineoplastic Combined Chemotherapy Protocols.
- radionuclide imaging : Colorectal Neoplasms.
- Animals, Drug Synergism, Female, Humans, Mice, Mice, Nude, Phosphorylation, Xenograft Model Antitumor Assays.
Abstract
Susceptibility to apoptosis by tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) is mediated through cognate death receptor signaling. We hypothesized that auto-amplification of this apparatus would enhance antitumor effects in vivo and could be optimized using the results obtained from novel imaging techniques. We therefore imaged mice bearing human colorectal cancer (Colo205) tumor xenografts with HGS-ETR1 and HGS-ETR2 agonist antibodies to TRAIL receptor-1 (TRAIL-R1) and TRAIL-R2, respectively, after radiolabeling the antibodies. Paclitaxel significantly increased in vivo expression of TRAIL-R1 and TRAIL-R2 in a time-dependent manner. The imaging results were confirmed by immunoblots for steady-state protein levels (>20-fold increase in TRAIL-R1 and TRAIL-R2 levels in tumor xenografts by 48 h after paclitaxel administration). TRAIL-R1 and TRAIL-R2 mRNA expression did not change, suggesting that these effects were posttranscriptional. Sequential treatment with paclitaxel followed by HGS-ETR1 or HGS-ETR2 after 48 h resulted in markedly enhanced antitumor activity against Colo205 mouse xenografts. Our experiments suggest that sequential taxane treatment followed by TRAIL-R agonist antibodies could be applied in the clinic, and that novel imaging techniques using radiolabeled receptor antibodies may be exploitable to optimize sequence timing and patient selection.
DOI: 10.1158/1535-7163.MCT-06-0188
PubMed: 17148761
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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Novel in vivo imaging shows up-regulation of death receptors by paclitaxel and correlates with enhanced antitumor effects of receptor agonist antibodies.</title><author><name sortKey="Gong, Jing" uniqKey="Gong J">Jing Gong</name><affiliation wicri:level="1"><nlm:affiliation>Department of Experimental Therapeutics, University of Texas M.D. Anderson Cancer Center, Box 4221515, Holcombe Boulevard, Houston, TX 77230-1402, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Experimental Therapeutics, University of Texas M.D. Anderson Cancer Center, Box 4221515, Holcombe Boulevard, Houston, TX 77230-1402</wicri:regionArea></affiliation></author><author><name sortKey="Yang, David" uniqKey="Yang D">David Yang</name></author><author><name sortKey="Kohanim, Saady" uniqKey="Kohanim S">Saady Kohanim</name></author><author><name sortKey="Humphreys, Robin" uniqKey="Humphreys R">Robin Humphreys</name></author><author><name sortKey="Broemeling, Lyle" uniqKey="Broemeling L">Lyle Broemeling</name></author><author><name sortKey="Kurzrock, Razelle" uniqKey="Kurzrock R">Razelle Kurzrock</name></author></titleStmt><publicationStmt><date when="2006">2006</date><idno type="doi">10.1158/1535-7163.MCT-06-0188</idno><idno type="RBID">pubmed:17148761</idno><idno type="pmid">17148761</idno><idno type="wicri:Area/Main/Corpus">002963</idno><idno type="wicri:Area/Main/Curation">002963</idno><idno type="wicri:Area/Main/Exploration">002958</idno></publicationStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Antibodies, Monoclonal (pharmacokinetics)</term><term>Antibodies, Monoclonal (pharmacology)</term><term>Antineoplastic Combined Chemotherapy Protocols (pharmacology)</term><term>Apoptosis (drug effects)</term><term>Apoptosis (genetics)</term><term>Colorectal Neoplasms (drug therapy)</term><term>Colorectal Neoplasms (genetics)</term><term>Colorectal Neoplasms (metabolism)</term><term>Colorectal Neoplasms (radionuclide imaging)</term><term>Drug Synergism</term><term>Female</term><term>Humans</term><term>Indium Radioisotopes (diagnostic use)</term><term>Mice</term><term>Mice, Nude</term><term>Mitogen-Activated Protein Kinase 1 (biosynthesis)</term><term>Mitogen-Activated Protein Kinase 1 (metabolism)</term><term>Mitogen-Activated Protein Kinase 3 (biosynthesis)</term><term>Mitogen-Activated Protein Kinase 3 (metabolism)</term><term>Paclitaxel (pharmacology)</term><term>Phosphorylation</term><term>Radionuclide Imaging (methods)</term><term>Receptors, TNF-Related Apoptosis-Inducing Ligand (agonists)</term><term>Receptors, TNF-Related Apoptosis-Inducing Ligand (biosynthesis)</term><term>Receptors, TNF-Related Apoptosis-Inducing Ligand (genetics)</term><term>Technetium (diagnostic use)</term><term>Tumor Suppressor Protein p53 (biosynthesis)</term><term>Tumor Suppressor Protein p53 (metabolism)</term><term>Up-Regulation (drug effects)</term><term>Xenograft Model Antitumor Assays</term></keywords><keywords scheme="MESH" type="chemical" qualifier="agonists" xml:lang="en"><term>Receptors, TNF-Related Apoptosis-Inducing Ligand</term></keywords><keywords scheme="MESH" type="chemical" qualifier="biosynthesis" xml:lang="en"><term>Mitogen-Activated Protein Kinase 1</term><term>Mitogen-Activated Protein Kinase 3</term><term>Receptors, TNF-Related Apoptosis-Inducing Ligand</term><term>Tumor Suppressor Protein p53</term></keywords><keywords scheme="MESH" type="chemical" qualifier="diagnostic use" xml:lang="en"><term>Indium Radioisotopes</term><term>Technetium</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Receptors, TNF-Related Apoptosis-Inducing Ligand</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Mitogen-Activated Protein Kinase 1</term><term>Mitogen-Activated Protein Kinase 3</term><term>Tumor Suppressor Protein p53</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacokinetics" xml:lang="en"><term>Antibodies, Monoclonal</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Antibodies, Monoclonal</term><term>Paclitaxel</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Apoptosis</term><term>Up-Regulation</term></keywords><keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Colorectal Neoplasms</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Apoptosis</term><term>Colorectal Neoplasms</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Colorectal Neoplasms</term></keywords><keywords scheme="MESH" qualifier="methods" xml:lang="en"><term>Radionuclide Imaging</term></keywords><keywords scheme="MESH" qualifier="pharmacology" xml:lang="en"><term>Antineoplastic Combined Chemotherapy Protocols</term></keywords><keywords scheme="MESH" qualifier="radionuclide imaging" xml:lang="en"><term>Colorectal Neoplasms</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Drug Synergism</term><term>Female</term><term>Humans</term><term>Mice</term><term>Mice, Nude</term><term>Phosphorylation</term><term>Xenograft Model Antitumor Assays</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Susceptibility to apoptosis by tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) is mediated through cognate death receptor signaling. We hypothesized that auto-amplification of this apparatus would enhance antitumor effects in vivo and could be optimized using the results obtained from novel imaging techniques. We therefore imaged mice bearing human colorectal cancer (Colo205) tumor xenografts with HGS-ETR1 and HGS-ETR2 agonist antibodies to TRAIL receptor-1 (TRAIL-R1) and TRAIL-R2, respectively, after radiolabeling the antibodies. Paclitaxel significantly increased in vivo expression of TRAIL-R1 and TRAIL-R2 in a time-dependent manner. The imaging results were confirmed by immunoblots for steady-state protein levels (>20-fold increase in TRAIL-R1 and TRAIL-R2 levels in tumor xenografts by 48 h after paclitaxel administration). TRAIL-R1 and TRAIL-R2 mRNA expression did not change, suggesting that these effects were posttranscriptional. Sequential treatment with paclitaxel followed by HGS-ETR1 or HGS-ETR2 after 48 h resulted in markedly enhanced antitumor activity against Colo205 mouse xenografts. Our experiments suggest that sequential taxane treatment followed by TRAIL-R agonist antibodies could be applied in the clinic, and that novel imaging techniques using radiolabeled receptor antibodies may be exploitable to optimize sequence timing and patient selection.</div></front></TEI><pubmed><MedlineCitation Owner="NLM" Status="MEDLINE"><PMID Version="1">17148761</PMID><DateCreated><Year>2006</Year><Month>12</Month><Day>18</Day></DateCreated><DateCompleted><Year>2007</Year><Month>06</Month><Day>07</Day></DateCompleted><DateRevised><Year>2009</Year><Month>11</Month><Day>19</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Print">1535-7163</ISSN><JournalIssue CitedMedium="Print"><Volume>5</Volume><Issue>12</Issue><PubDate><Year>2006</Year><Month>Dec</Month></PubDate></JournalIssue><Title>Molecular cancer therapeutics</Title><ISOAbbreviation>Mol. Cancer Ther.</ISOAbbreviation></Journal><ArticleTitle>Novel in vivo imaging shows up-regulation of death receptors by paclitaxel and correlates with enhanced antitumor effects of receptor agonist antibodies.</ArticleTitle><Pagination><MedlinePgn>2991-3000</MedlinePgn></Pagination><Abstract><AbstractText>Susceptibility to apoptosis by tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) is mediated through cognate death receptor signaling. We hypothesized that auto-amplification of this apparatus would enhance antitumor effects in vivo and could be optimized using the results obtained from novel imaging techniques. We therefore imaged mice bearing human colorectal cancer (Colo205) tumor xenografts with HGS-ETR1 and HGS-ETR2 agonist antibodies to TRAIL receptor-1 (TRAIL-R1) and TRAIL-R2, respectively, after radiolabeling the antibodies. Paclitaxel significantly increased in vivo expression of TRAIL-R1 and TRAIL-R2 in a time-dependent manner. The imaging results were confirmed by immunoblots for steady-state protein levels (>20-fold increase in TRAIL-R1 and TRAIL-R2 levels in tumor xenografts by 48 h after paclitaxel administration). TRAIL-R1 and TRAIL-R2 mRNA expression did not change, suggesting that these effects were posttranscriptional. Sequential treatment with paclitaxel followed by HGS-ETR1 or HGS-ETR2 after 48 h resulted in markedly enhanced antitumor activity against Colo205 mouse xenografts. Our experiments suggest that sequential taxane treatment followed by TRAIL-R agonist antibodies could be applied in the clinic, and that novel imaging techniques using radiolabeled receptor antibodies may be exploitable to optimize sequence timing and patient selection.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Gong</LastName><ForeName>Jing</ForeName><Initials>J</Initials><Affiliation>Department of Experimental Therapeutics, University of Texas M.D. Anderson Cancer Center, Box 4221515, Holcombe Boulevard, Houston, TX 77230-1402, USA.</Affiliation></Author><Author ValidYN="Y"><LastName>Yang</LastName><ForeName>David</ForeName><Initials>D</Initials></Author><Author ValidYN="Y"><LastName>Kohanim</LastName><ForeName>Saady</ForeName><Initials>S</Initials></Author><Author ValidYN="Y"><LastName>Humphreys</LastName><ForeName>Robin</ForeName><Initials>R</Initials></Author><Author ValidYN="Y"><LastName>Broemeling</LastName><ForeName>Lyle</ForeName><Initials>L</Initials></Author><Author ValidYN="Y"><LastName>Kurzrock</LastName><ForeName>Razelle</ForeName><Initials>R</Initials></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>CA-16672</GrantID><Acronym>CA</Acronym><Agency>NCI NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType>Journal Article</PublicationType><PublicationType>Research Support, N.I.H., Extramural</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2006</Year><Month>12</Month><Day>05</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Mol Cancer Ther</MedlineTA><NlmUniqueID>101132535</NlmUniqueID><ISSNLinking>1535-7163</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance>Antibodies, 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