Autophagy Inhibition Delays Early but Not Late-Stage Metastatic Disease.
Identifieur interne : 000342 ( Ncbi/Merge ); précédent : 000341; suivant : 000343Autophagy Inhibition Delays Early but Not Late-Stage Metastatic Disease.
Auteurs : Rebecca A. Barnard ; Daniel P. Regan ; Ryan J. Hansen ; Paola Maycotte ; Andrew Thorburn ; Daniel L. Gustafson [États-Unis]Source :
- The Journal of pharmacology and experimental therapeutics [ 1521-0103 ] ; 2016.
Descripteurs français
- KwdFr :
- Animaux, Antinéoplasiques (pharmacologie), Apoptose (), Autophagie (), Chloroquine (pharmacologie), Cisplatine (pharmacologie), Facteurs temps, Femelle, Lignée cellulaire tumorale, Métastase tumorale, Prolifération cellulaire (), Souris, Stade de la tumeur, Synergie des médicaments, Traitement néoadjuvant, Tréhalose (pharmacologie).
- MESH :
English descriptors
- KwdEn :
- Animals, Antineoplastic Agents (pharmacology), Apoptosis (drug effects), Autophagy (drug effects), Cell Line, Tumor, Cell Proliferation (drug effects), Chloroquine (pharmacology), Cisplatin (pharmacology), Drug Synergism, Female, Mice, Neoadjuvant Therapy, Neoplasm Metastasis, Neoplasm Staging, Time Factors, Trehalose (pharmacology).
- MESH :
- chemical , pharmacology : Antineoplastic Agents, Chloroquine, Cisplatin, Trehalose.
- drug effects : Apoptosis, Autophagy, Cell Proliferation.
- Animals, Cell Line, Tumor, Drug Synergism, Female, Mice, Neoadjuvant Therapy, Neoplasm Metastasis, Neoplasm Staging, Time Factors.
Abstract
The autophagy pathway has been recognized as a mechanism of survival and therapy resistance in cancer, yet the extent of autophagy's function in metastatic progression is still unclear. Therefore, we used murine models of metastatic cancer to investigate the effect of autophagy modulation on metastasis development. Pharmacologic and genetic autophagy inhibition were able to impede cell proliferation in culture, but did not impact the development of experimentally induced 4T1 and B16-F10 metastases. Similarly, autophagy inhibition by adjuvant chloroquine (CQ) treatment did not delay metastasis in an orthotopic 4T1, tumor-resection model. However, neoadjuvant CQ treatment or genetic autophagy inhibition resulted in delayed metastasis development, whereas stimulation of autophagy by trehalose hastened development. Cisplatin was also administered either as a single agent or in combination with CQ. The combination of cisplatin and CQ was antagonistic. The effects of autophagy modulation on metastasis did not appear to be due to alterations in the intrinsic metastatic capability of the cells, as modulating autophagy had no impact on migration, invasion, or anchorage-independent growth in vitro. To explore the possibility of autophagy's influence on the metastatic microenvironment, bone marrow-derived cells (BMDCs), which mediate the establishment of the premetastatic niche, were measured in the lung and in circulation. Trehalose-treated mice had significantly more BMDCs than either vehicle- or CQ-treated mice. Autophagy inhibition may be most useful as a treatment to impede early metastatic development. However, modulating autophagy may also alter the efficacy of platinum-based therapies, requiring caution when considering combination therapies.
DOI: 10.1124/jpet.116.233908
PubMed: 27231155
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- to stream PubMed, to step Corpus: 000205
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pubmed:27231155Le document en format XML
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Regan</name><affiliation><nlm:affiliation>Department of Clinical Sciences, Colorado State University, Fort Collins, Colorado (R.A.B., D.P.R., R.J.H., D.L.G.); and Department of Pharmacology, University of Colorado School of Medicine, Aurora, Colorado (P.M., A.T.).</nlm:affiliation><wicri:noCountry code="subField">A.T.).</wicri:noCountry></affiliation></author><author><name sortKey="Hansen, Ryan J" sort="Hansen, Ryan J" uniqKey="Hansen R" first="Ryan J" last="Hansen">Ryan J. Hansen</name><affiliation><nlm:affiliation>Department of Clinical Sciences, Colorado State University, Fort Collins, Colorado (R.A.B., D.P.R., R.J.H., D.L.G.); and Department of Pharmacology, University of Colorado School of Medicine, Aurora, Colorado (P.M., A.T.).</nlm:affiliation><wicri:noCountry code="subField">A.T.).</wicri:noCountry></affiliation></author><author><name sortKey="Maycotte, Paola" sort="Maycotte, Paola" uniqKey="Maycotte P" first="Paola" last="Maycotte">Paola Maycotte</name><affiliation><nlm:affiliation>Department of Clinical Sciences, Colorado State University, Fort Collins, Colorado (R.A.B., D.P.R., R.J.H., D.L.G.); and Department of Pharmacology, University of Colorado School of Medicine, Aurora, Colorado (P.M., A.T.).</nlm:affiliation><wicri:noCountry code="subField">A.T.).</wicri:noCountry></affiliation></author><author><name sortKey="Thorburn, Andrew" sort="Thorburn, Andrew" uniqKey="Thorburn A" first="Andrew" last="Thorburn">Andrew Thorburn</name><affiliation><nlm:affiliation>Department of Clinical Sciences, Colorado State University, Fort Collins, Colorado (R.A.B., D.P.R., R.J.H., D.L.G.); and Department of Pharmacology, University of Colorado School of Medicine, Aurora, Colorado (P.M., A.T.).</nlm:affiliation><wicri:noCountry code="subField">A.T.).</wicri:noCountry></affiliation></author><author><name sortKey="Gustafson, Daniel L" sort="Gustafson, Daniel L" uniqKey="Gustafson D" first="Daniel L" last="Gustafson">Daniel L. 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Barnard</name><affiliation><nlm:affiliation>Department of Clinical Sciences, Colorado State University, Fort Collins, Colorado (R.A.B., D.P.R., R.J.H., D.L.G.); and Department of Pharmacology, University of Colorado School of Medicine, Aurora, Colorado (P.M., A.T.).</nlm:affiliation><wicri:noCountry code="subField">A.T.).</wicri:noCountry></affiliation></author><author><name sortKey="Regan, Daniel P" sort="Regan, Daniel P" uniqKey="Regan D" first="Daniel P" last="Regan">Daniel P. Regan</name><affiliation><nlm:affiliation>Department of Clinical Sciences, Colorado State University, Fort Collins, Colorado (R.A.B., D.P.R., R.J.H., D.L.G.); and Department of Pharmacology, University of Colorado School of Medicine, Aurora, Colorado (P.M., A.T.).</nlm:affiliation><wicri:noCountry code="subField">A.T.).</wicri:noCountry></affiliation></author><author><name sortKey="Hansen, Ryan J" sort="Hansen, Ryan J" uniqKey="Hansen R" first="Ryan J" last="Hansen">Ryan J. Hansen</name><affiliation><nlm:affiliation>Department of Clinical Sciences, Colorado State University, Fort Collins, Colorado (R.A.B., D.P.R., R.J.H., D.L.G.); and Department of Pharmacology, University of Colorado School of Medicine, Aurora, Colorado (P.M., A.T.).</nlm:affiliation><wicri:noCountry code="subField">A.T.).</wicri:noCountry></affiliation></author><author><name sortKey="Maycotte, Paola" sort="Maycotte, Paola" uniqKey="Maycotte P" first="Paola" last="Maycotte">Paola Maycotte</name><affiliation><nlm:affiliation>Department of Clinical Sciences, Colorado State University, Fort Collins, Colorado (R.A.B., D.P.R., R.J.H., D.L.G.); and Department of Pharmacology, University of Colorado School of Medicine, Aurora, Colorado (P.M., A.T.).</nlm:affiliation><wicri:noCountry code="subField">A.T.).</wicri:noCountry></affiliation></author><author><name sortKey="Thorburn, Andrew" sort="Thorburn, Andrew" uniqKey="Thorburn A" first="Andrew" last="Thorburn">Andrew Thorburn</name><affiliation><nlm:affiliation>Department of Clinical Sciences, Colorado State University, Fort Collins, Colorado (R.A.B., D.P.R., R.J.H., D.L.G.); and Department of Pharmacology, University of Colorado School of Medicine, Aurora, Colorado (P.M., A.T.).</nlm:affiliation><wicri:noCountry code="subField">A.T.).</wicri:noCountry></affiliation></author><author><name sortKey="Gustafson, Daniel L" sort="Gustafson, Daniel L" uniqKey="Gustafson D" first="Daniel L" last="Gustafson">Daniel L. Gustafson</name><affiliation wicri:level="1"><nlm:affiliation>Department of Clinical Sciences, Colorado State University, Fort Collins, Colorado (R.A.B., D.P.R., R.J.H., D.L.G.); and Department of Pharmacology, University of Colorado School of Medicine, Aurora, Colorado (P.M., A.T.) Daniel.Gustafson@colostate.edu.</nlm:affiliation><country wicri:rule="url">États-Unis</country></affiliation></author></analytic><series><title level="j">The Journal of pharmacology and experimental therapeutics</title><idno type="eISSN">1521-0103</idno><imprint><date when="2016" type="published">2016</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Antineoplastic Agents (pharmacology)</term><term>Apoptosis (drug effects)</term><term>Autophagy (drug effects)</term><term>Cell Line, Tumor</term><term>Cell Proliferation (drug effects)</term><term>Chloroquine (pharmacology)</term><term>Cisplatin (pharmacology)</term><term>Drug Synergism</term><term>Female</term><term>Mice</term><term>Neoadjuvant Therapy</term><term>Neoplasm Metastasis</term><term>Neoplasm Staging</term><term>Time Factors</term><term>Trehalose (pharmacology)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Animaux</term><term>Antinéoplasiques (pharmacologie)</term><term>Apoptose ()</term><term>Autophagie ()</term><term>Chloroquine (pharmacologie)</term><term>Cisplatine (pharmacologie)</term><term>Facteurs temps</term><term>Femelle</term><term>Lignée cellulaire tumorale</term><term>Métastase tumorale</term><term>Prolifération cellulaire ()</term><term>Souris</term><term>Stade de la tumeur</term><term>Synergie des médicaments</term><term>Traitement néoadjuvant</term><term>Tréhalose (pharmacologie)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Antineoplastic Agents</term><term>Chloroquine</term><term>Cisplatin</term><term>Trehalose</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Apoptosis</term><term>Autophagy</term><term>Cell Proliferation</term></keywords><keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Antinéoplasiques</term><term>Chloroquine</term><term>Cisplatine</term><term>Tréhalose</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Cell Line, Tumor</term><term>Drug Synergism</term><term>Female</term><term>Mice</term><term>Neoadjuvant Therapy</term><term>Neoplasm Metastasis</term><term>Neoplasm Staging</term><term>Time Factors</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Apoptose</term><term>Autophagie</term><term>Facteurs temps</term><term>Femelle</term><term>Lignée cellulaire tumorale</term><term>Métastase tumorale</term><term>Prolifération cellulaire</term><term>Souris</term><term>Stade de la tumeur</term><term>Synergie des médicaments</term><term>Traitement néoadjuvant</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The autophagy pathway has been recognized as a mechanism of survival and therapy resistance in cancer, yet the extent of autophagy's function in metastatic progression is still unclear. Therefore, we used murine models of metastatic cancer to investigate the effect of autophagy modulation on metastasis development. Pharmacologic and genetic autophagy inhibition were able to impede cell proliferation in culture, but did not impact the development of experimentally induced 4T1 and B16-F10 metastases. Similarly, autophagy inhibition by adjuvant chloroquine (CQ) treatment did not delay metastasis in an orthotopic 4T1, tumor-resection model. However, neoadjuvant CQ treatment or genetic autophagy inhibition resulted in delayed metastasis development, whereas stimulation of autophagy by trehalose hastened development. Cisplatin was also administered either as a single agent or in combination with CQ. The combination of cisplatin and CQ was antagonistic. The effects of autophagy modulation on metastasis did not appear to be due to alterations in the intrinsic metastatic capability of the cells, as modulating autophagy had no impact on migration, invasion, or anchorage-independent growth in vitro. To explore the possibility of autophagy's influence on the metastatic microenvironment, bone marrow-derived cells (BMDCs), which mediate the establishment of the premetastatic niche, were measured in the lung and in circulation. Trehalose-treated mice had significantly more BMDCs than either vehicle- or CQ-treated mice. Autophagy inhibition may be most useful as a treatment to impede early metastatic development. However, modulating autophagy may also alter the efficacy of platinum-based therapies, requiring caution when considering combination therapies.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">27231155</PMID><DateCompleted><Year>2017</Year><Month>05</Month><Day>26</Day></DateCompleted><DateRevised><Year>2019</Year><Month>02</Month><Day>20</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1521-0103</ISSN><JournalIssue CitedMedium="Internet"><Volume>358</Volume><Issue>2</Issue><PubDate><Year>2016</Year><Month>08</Month></PubDate></JournalIssue><Title>The Journal of pharmacology and experimental therapeutics</Title><ISOAbbreviation>J. Pharmacol. Exp. Ther.</ISOAbbreviation></Journal><ArticleTitle>Autophagy Inhibition Delays Early but Not Late-Stage Metastatic Disease.</ArticleTitle><Pagination><MedlinePgn>282-93</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1124/jpet.116.233908</ELocationID><Abstract><AbstractText>The autophagy pathway has been recognized as a mechanism of survival and therapy resistance in cancer, yet the extent of autophagy's function in metastatic progression is still unclear. Therefore, we used murine models of metastatic cancer to investigate the effect of autophagy modulation on metastasis development. Pharmacologic and genetic autophagy inhibition were able to impede cell proliferation in culture, but did not impact the development of experimentally induced 4T1 and B16-F10 metastases. Similarly, autophagy inhibition by adjuvant chloroquine (CQ) treatment did not delay metastasis in an orthotopic 4T1, tumor-resection model. However, neoadjuvant CQ treatment or genetic autophagy inhibition resulted in delayed metastasis development, whereas stimulation of autophagy by trehalose hastened development. Cisplatin was also administered either as a single agent or in combination with CQ. The combination of cisplatin and CQ was antagonistic. The effects of autophagy modulation on metastasis did not appear to be due to alterations in the intrinsic metastatic capability of the cells, as modulating autophagy had no impact on migration, invasion, or anchorage-independent growth in vitro. To explore the possibility of autophagy's influence on the metastatic microenvironment, bone marrow-derived cells (BMDCs), which mediate the establishment of the premetastatic niche, were measured in the lung and in circulation. Trehalose-treated mice had significantly more BMDCs than either vehicle- or CQ-treated mice. Autophagy inhibition may be most useful as a treatment to impede early metastatic development. However, modulating autophagy may also alter the efficacy of platinum-based therapies, requiring caution when considering combination therapies.</AbstractText><CopyrightInformation>Copyright © 2016 by The American Society for Pharmacology and Experimental Therapeutics.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Barnard</LastName><ForeName>Rebecca A</ForeName><Initials>RA</Initials><AffiliationInfo><Affiliation>Department of Clinical Sciences, Colorado State University, Fort Collins, Colorado (R.A.B., D.P.R., R.J.H., D.L.G.); and Department of Pharmacology, University of Colorado School of Medicine, Aurora, Colorado (P.M., A.T.).</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Regan</LastName><ForeName>Daniel P</ForeName><Initials>DP</Initials><AffiliationInfo><Affiliation>Department of Clinical Sciences, Colorado State University, Fort Collins, Colorado (R.A.B., D.P.R., R.J.H., D.L.G.); and Department of Pharmacology, University of Colorado School of Medicine, Aurora, Colorado (P.M., A.T.).</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Hansen</LastName><ForeName>Ryan J</ForeName><Initials>RJ</Initials><AffiliationInfo><Affiliation>Department of Clinical Sciences, Colorado State University, Fort Collins, Colorado (R.A.B., D.P.R., R.J.H., D.L.G.); and Department of Pharmacology, University of Colorado School of Medicine, Aurora, Colorado (P.M., A.T.).</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Maycotte</LastName><ForeName>Paola</ForeName><Initials>P</Initials><AffiliationInfo><Affiliation>Department of Clinical Sciences, Colorado State University, Fort Collins, Colorado (R.A.B., D.P.R., R.J.H., D.L.G.); and Department of Pharmacology, University of Colorado School of Medicine, Aurora, Colorado (P.M., A.T.).</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Thorburn</LastName><ForeName>Andrew</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Department of Clinical Sciences, Colorado State University, Fort Collins, Colorado (R.A.B., D.P.R., R.J.H., D.L.G.); and Department of Pharmacology, University of Colorado School of Medicine, Aurora, Colorado (P.M., A.T.).</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Gustafson</LastName><ForeName>Daniel L</ForeName><Initials>DL</Initials><AffiliationInfo><Affiliation>Department of Clinical Sciences, Colorado State University, Fort Collins, Colorado (R.A.B., D.P.R., R.J.H., D.L.G.); and Department of Pharmacology, University of Colorado School of Medicine, Aurora, Colorado (P.M., A.T.) Daniel.Gustafson@colostate.edu.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>P30 CA046934</GrantID><Acronym>CA</Acronym><Agency>NCI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 CA150925</GrantID><Acronym>CA</Acronym><Agency>NCI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 CA190170</GrantID><Acronym>CA</Acronym><Agency>NCI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>T32 OD010437</GrantID><Acronym>OD</Acronym><Agency>NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D052061">Research Support, N.I.H., Extramural</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2016</Year><Month>05</Month><Day>26</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>J Pharmacol Exp Ther</MedlineTA><NlmUniqueID>0376362</NlmUniqueID><ISSNLinking>0022-3565</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000970">Antineoplastic Agents</NameOfSubstance></Chemical><Chemical><RegistryNumber>886U3H6UFF</RegistryNumber><NameOfSubstance UI="D002738">Chloroquine</NameOfSubstance></Chemical><Chemical><RegistryNumber>B8WCK70T7I</RegistryNumber><NameOfSubstance UI="D014199">Trehalose</NameOfSubstance></Chemical><Chemical><RegistryNumber>Q20Q21Q62J</RegistryNumber><NameOfSubstance UI="D002945">Cisplatin</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000970" MajorTopicYN="N">Antineoplastic Agents</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="Y">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D017209" MajorTopicYN="N">Apoptosis</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D001343" MajorTopicYN="N">Autophagy</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="Y">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D045744" MajorTopicYN="N">Cell Line, Tumor</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D049109" MajorTopicYN="N">Cell Proliferation</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002738" MajorTopicYN="N">Chloroquine</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002945" MajorTopicYN="N">Cisplatin</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D004357" MajorTopicYN="N">Drug Synergism</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D020360" MajorTopicYN="N">Neoadjuvant Therapy</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D009362" MajorTopicYN="N">Neoplasm Metastasis</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D009367" MajorTopicYN="N">Neoplasm Staging</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D013997" MajorTopicYN="N">Time Factors</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D014199" MajorTopicYN="N">Trehalose</DescriptorName><QualifierName UI="Q000494" 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Barnard</name><name sortKey="Hansen, Ryan J" sort="Hansen, Ryan J" uniqKey="Hansen R" first="Ryan J" last="Hansen">Ryan J. Hansen</name><name sortKey="Maycotte, Paola" sort="Maycotte, Paola" uniqKey="Maycotte P" first="Paola" last="Maycotte">Paola Maycotte</name><name sortKey="Regan, Daniel P" sort="Regan, Daniel P" uniqKey="Regan D" first="Daniel P" last="Regan">Daniel P. Regan</name><name sortKey="Thorburn, Andrew" sort="Thorburn, Andrew" uniqKey="Thorburn A" first="Andrew" last="Thorburn">Andrew Thorburn</name></noCountry><country name="États-Unis"><noRegion><name sortKey="Gustafson, Daniel L" sort="Gustafson, Daniel L" uniqKey="Gustafson D" first="Daniel L" last="Gustafson">Daniel L. Gustafson</name></noRegion></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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