Antimetastatic effects of blocking PD-1 and the adenosine A2A receptor.
Identifieur interne : 000792 ( PubMed/Checkpoint ); précédent : 000791; suivant : 000793Antimetastatic effects of blocking PD-1 and the adenosine A2A receptor.
Auteurs : Deepak Mittal ; Arabella Young ; Kimberley Stannard ; Michelle Yong ; Michele W L. Teng ; Bertrand Allard [Canada] ; John Stagg [Canada] ; Mark J. Smyth [Australie]Source :
- Cancer research [ 1538-7445 ] ; 2014.
English descriptors
- KwdEn :
- Adenosine A2 Receptor Antagonists (administration & dosage), Adenosine A2 Receptor Antagonists (pharmacology), Animals, Antibodies, Blocking (administration & dosage), Antibodies, Blocking (pharmacology), Antibodies, Monoclonal (administration & dosage), Antibodies, Monoclonal (pharmacology), Antineoplastic Agents (administration & dosage), Antineoplastic Agents (pharmacology), CD8-Positive T-Lymphocytes (immunology), Cell Line, Tumor, Disease Models, Animal, Female, Killer Cells, Natural (immunology), Lung Neoplasms (immunology), Lung Neoplasms (metabolism), Lung Neoplasms (secondary), Melanoma, Experimental, Mice, Neoplasm Metastasis, Neoplasms (drug therapy), Neoplasms (immunology), Neoplasms (metabolism), Neoplasms (mortality), Neoplasms (pathology), Programmed Cell Death 1 Receptor (antagonists & inhibitors), Programmed Cell Death 1 Receptor (metabolism), Receptor, Adenosine A2A (metabolism).
- MESH :
- chemical , administration & dosage : Adenosine A2 Receptor Antagonists, Antibodies, Blocking, Antibodies, Monoclonal, Antineoplastic Agents.
- chemical , antagonists & inhibitors : Programmed Cell Death 1 Receptor.
- chemical , metabolism : Programmed Cell Death 1 Receptor, Receptor, Adenosine A2A.
- chemical , pharmacology : Adenosine A2 Receptor Antagonists, Antibodies, Blocking, Antibodies, Monoclonal, Antineoplastic Agents.
- drug therapy : Neoplasms.
- immunology : CD8-Positive T-Lymphocytes, Killer Cells, Natural, Lung Neoplasms, Neoplasms.
- metabolism : Lung Neoplasms, Neoplasms.
- mortality : Neoplasms.
- pathology : Neoplasms.
- secondary : Lung Neoplasms.
- Animals, Cell Line, Tumor, Disease Models, Animal, Female, Melanoma, Experimental, Mice, Neoplasm Metastasis.
Abstract
Adenosine targeting is an attractive new approach to cancer treatment, but no clinical study has yet examined adenosine inhibition in oncology despite the safe clinical profile of adenosine A2A receptor inhibitors (A2ARi) in Parkinson disease. Metastasis is the main cause of cancer-related deaths worldwide, and therefore we have studied experimental and spontaneous mouse models of melanoma and breast cancer metastasis to demonstrate the efficacy and mechanism of a combination of A2ARi in combination with anti-PD-1 monoclonal antibody (mAb). This combination significantly reduces metastatic burden and prolongs the life of mice compared with either monotherapy alone. Importantly, the combination was only effective when the tumor expressed high levels of CD73, suggesting a tumor biomarker that at a minimum could be used to stratify patients that might receive this combination. The mechanism of the combination therapy was critically dependent on NK cells and IFNγ, and to a lesser extent, CD8(+) T cells and the effector molecule, perforin. Overall, these results provide a strong rationale to use A2ARi with anti-PD-1 mAb for the treatment of minimal residual and metastatic disease.
DOI: 10.1158/0008-5472.CAN-14-0957
PubMed: 24986517
Affiliations:
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Smyth</name><affiliation wicri:level="1"><nlm:affiliation>Authors' Affiliations: Immunology in Cancer and Infection Laboratory and Cancer Immunoregulation and Immunotherapy Laboratories, QIMR Berghofer Medical Research Institute, Herston; School of Medicine, University of Queensland, Queensland, Australia; and mark.smyth@qimrberghofer.edu.au.</nlm:affiliation><country wicri:rule="url">Australie</country><wicri:regionArea>Authors' Affiliations: Immunology in Cancer and Infection Laboratory and Cancer Immunoregulation and Immunotherapy Laboratories, QIMR Berghofer Medical Research Institute, Herston; School of Medicine, University of Queensland, Queensland</wicri:regionArea><wicri:noRegion>Queensland</wicri:noRegion></affiliation></author></analytic><series><title level="j">Cancer research</title><idno type="eISSN">1538-7445</idno><imprint><date when="2014" type="published">2014</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adenosine A2 Receptor Antagonists (administration & dosage)</term><term>Adenosine A2 Receptor Antagonists (pharmacology)</term><term>Animals</term><term>Antibodies, Blocking (administration & dosage)</term><term>Antibodies, Blocking (pharmacology)</term><term>Antibodies, Monoclonal (administration & dosage)</term><term>Antibodies, Monoclonal (pharmacology)</term><term>Antineoplastic Agents (administration & dosage)</term><term>Antineoplastic Agents (pharmacology)</term><term>CD8-Positive T-Lymphocytes (immunology)</term><term>Cell Line, Tumor</term><term>Disease Models, Animal</term><term>Female</term><term>Killer Cells, Natural (immunology)</term><term>Lung Neoplasms (immunology)</term><term>Lung Neoplasms (metabolism)</term><term>Lung Neoplasms (secondary)</term><term>Melanoma, Experimental</term><term>Mice</term><term>Neoplasm Metastasis</term><term>Neoplasms (drug therapy)</term><term>Neoplasms (immunology)</term><term>Neoplasms (metabolism)</term><term>Neoplasms (mortality)</term><term>Neoplasms (pathology)</term><term>Programmed Cell Death 1 Receptor (antagonists & inhibitors)</term><term>Programmed Cell Death 1 Receptor (metabolism)</term><term>Receptor, Adenosine A2A (metabolism)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="administration & dosage" xml:lang="en"><term>Adenosine A2 Receptor Antagonists</term><term>Antibodies, Blocking</term><term>Antibodies, Monoclonal</term><term>Antineoplastic Agents</term></keywords><keywords scheme="MESH" type="chemical" qualifier="antagonists & inhibitors" xml:lang="en"><term>Programmed Cell Death 1 Receptor</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Programmed Cell Death 1 Receptor</term><term>Receptor, Adenosine A2A</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Adenosine A2 Receptor Antagonists</term><term>Antibodies, Blocking</term><term>Antibodies, Monoclonal</term><term>Antineoplastic Agents</term></keywords><keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Neoplasms</term></keywords><keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>CD8-Positive T-Lymphocytes</term><term>Killer Cells, Natural</term><term>Lung Neoplasms</term><term>Neoplasms</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Lung Neoplasms</term><term>Neoplasms</term></keywords><keywords scheme="MESH" qualifier="mortality" xml:lang="en"><term>Neoplasms</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Neoplasms</term></keywords><keywords scheme="MESH" qualifier="secondary" xml:lang="en"><term>Lung Neoplasms</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Cell Line, Tumor</term><term>Disease Models, Animal</term><term>Female</term><term>Melanoma, Experimental</term><term>Mice</term><term>Neoplasm Metastasis</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Adenosine targeting is an attractive new approach to cancer treatment, but no clinical study has yet examined adenosine inhibition in oncology despite the safe clinical profile of adenosine A2A receptor inhibitors (A2ARi) in Parkinson disease. Metastasis is the main cause of cancer-related deaths worldwide, and therefore we have studied experimental and spontaneous mouse models of melanoma and breast cancer metastasis to demonstrate the efficacy and mechanism of a combination of A2ARi in combination with anti-PD-1 monoclonal antibody (mAb). This combination significantly reduces metastatic burden and prolongs the life of mice compared with either monotherapy alone. Importantly, the combination was only effective when the tumor expressed high levels of CD73, suggesting a tumor biomarker that at a minimum could be used to stratify patients that might receive this combination. The mechanism of the combination therapy was critically dependent on NK cells and IFNγ, and to a lesser extent, CD8(+) T cells and the effector molecule, perforin. Overall, these results provide a strong rationale to use A2ARi with anti-PD-1 mAb for the treatment of minimal residual and metastatic disease.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">24986517</PMID><DateCreated><Year>2014</Year><Month>07</Month><Day>16</Day></DateCreated><DateCompleted><Year>2014</Year><Month>09</Month><Day>26</Day></DateCompleted><DateRevised><Year>2014</Year><Month>07</Month><Day>16</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1538-7445</ISSN><JournalIssue CitedMedium="Internet"><Volume>74</Volume><Issue>14</Issue><PubDate><Year>2014</Year><Month>Jul</Month><Day>15</Day></PubDate></JournalIssue><Title>Cancer research</Title><ISOAbbreviation>Cancer Res.</ISOAbbreviation></Journal><ArticleTitle>Antimetastatic effects of blocking PD-1 and the adenosine A2A receptor.</ArticleTitle><Pagination><MedlinePgn>3652-8</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1158/0008-5472.CAN-14-0957</ELocationID><Abstract><AbstractText>Adenosine targeting is an attractive new approach to cancer treatment, but no clinical study has yet examined adenosine inhibition in oncology despite the safe clinical profile of adenosine A2A receptor inhibitors (A2ARi) in Parkinson disease. Metastasis is the main cause of cancer-related deaths worldwide, and therefore we have studied experimental and spontaneous mouse models of melanoma and breast cancer metastasis to demonstrate the efficacy and mechanism of a combination of A2ARi in combination with anti-PD-1 monoclonal antibody (mAb). This combination significantly reduces metastatic burden and prolongs the life of mice compared with either monotherapy alone. Importantly, the combination was only effective when the tumor expressed high levels of CD73, suggesting a tumor biomarker that at a minimum could be used to stratify patients that might receive this combination. The mechanism of the combination therapy was critically dependent on NK cells and IFNγ, and to a lesser extent, CD8(+) T cells and the effector molecule, perforin. Overall, these results provide a strong rationale to use A2ARi with anti-PD-1 mAb for the treatment of minimal residual and metastatic disease.</AbstractText><CopyrightInformation>©2014 American Association for Cancer Research.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Mittal</LastName><ForeName>Deepak</ForeName><Initials>D</Initials><AffiliationInfo><Affiliation>Authors' Affiliations: Immunology in Cancer and Infection Laboratory and Cancer Immunoregulation and Immunotherapy Laboratories, QIMR Berghofer Medical Research Institute, Herston; School of Medicine, University of Queensland, Queensland, Australia; and.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Young</LastName><ForeName>Arabella</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Authors' Affiliations: Immunology in Cancer and Infection Laboratory and Cancer Immunoregulation and Immunotherapy Laboratories, QIMR Berghofer Medical Research Institute, Herston; School of Medicine, University of Queensland, Queensland, Australia; and.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Stannard</LastName><ForeName>Kimberley</ForeName><Initials>K</Initials><AffiliationInfo><Affiliation>Authors' Affiliations: Immunology in Cancer and Infection Laboratory and Cancer Immunoregulation and Immunotherapy Laboratories, QIMR Berghofer Medical Research Institute, Herston;</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Yong</LastName><ForeName>Michelle</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Authors' Affiliations: Immunology in Cancer and Infection Laboratory and Cancer Immunoregulation and Immunotherapy Laboratories, QIMR Berghofer Medical Research Institute, Herston;</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Teng</LastName><ForeName>Michele W L</ForeName><Initials>MW</Initials><AffiliationInfo><Affiliation>Authors' Affiliations: Immunology in Cancer and Infection Laboratory and Cancer Immunoregulation and Immunotherapy Laboratories, QIMR Berghofer Medical Research Institute, Herston; School of Medicine, University of Queensland, Queensland, Australia; and.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Allard</LastName><ForeName>Bertrand</ForeName><Initials>B</Initials><AffiliationInfo><Affiliation>Centre de Recherche du Centre Hospitalier de l'Université de Montréal, Faculté de Pharmacie et Institut du Cancer de Montréal, Montréal, Québec, Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Stagg</LastName><ForeName>John</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Centre de Recherche du Centre Hospitalier de l'Université de Montréal, Faculté de Pharmacie et Institut du Cancer de Montréal, Montréal, Québec, Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Smyth</LastName><ForeName>Mark J</ForeName><Initials>MJ</Initials><AffiliationInfo><Affiliation>Authors' Affiliations: Immunology in Cancer and Infection Laboratory and Cancer Immunoregulation and Immunotherapy Laboratories, QIMR Berghofer Medical Research Institute, Herston; School of Medicine, University of Queensland, Queensland, Australia; and mark.smyth@qimrberghofer.edu.au.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><Agency>Canadian Institutes of Health Research</Agency><Country>Canada</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2014</Year><Month>07</Month><Day>01</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Cancer 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MajorTopicYN="N">immunology</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000556" MajorTopicYN="N">secondary</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008546" MajorTopicYN="N">Melanoma, Experimental</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D009362" MajorTopicYN="N">Neoplasm Metastasis</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D009369" MajorTopicYN="N">Neoplasms</DescriptorName><QualifierName UI="Q000188" MajorTopicYN="N">drug therapy</QualifierName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName><QualifierName UI="Q000401" MajorTopicYN="N">mortality</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D061026" MajorTopicYN="N">Programmed Cell Death 1 Receptor</DescriptorName><QualifierName UI="Q000037" MajorTopicYN="Y">antagonists & inhibitors</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D043705" MajorTopicYN="N">Receptor, Adenosine A2A</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="entrez"><Year>2014</Year><Month>7</Month><Day>3</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2014</Year><Month>7</Month><Day>6</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2014</Year><Month>9</Month><Day>27</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">24986517</ArticleId><ArticleId IdType="pii">0008-5472.CAN-14-0957</ArticleId><ArticleId IdType="doi">10.1158/0008-5472.CAN-14-0957</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>Australie</li><li>Canada</li></country></list><tree><noCountry><name sortKey="Mittal, Deepak" sort="Mittal, Deepak" uniqKey="Mittal D" first="Deepak" last="Mittal">Deepak Mittal</name><name sortKey="Stannard, Kimberley" sort="Stannard, Kimberley" uniqKey="Stannard K" first="Kimberley" last="Stannard">Kimberley Stannard</name><name sortKey="Teng, Michele W L" sort="Teng, Michele W L" uniqKey="Teng M" first="Michele W L" last="Teng">Michele W L. Teng</name><name sortKey="Yong, Michelle" sort="Yong, Michelle" uniqKey="Yong M" first="Michelle" last="Yong">Michelle Yong</name><name sortKey="Young, Arabella" sort="Young, Arabella" uniqKey="Young A" first="Arabella" last="Young">Arabella Young</name></noCountry><country name="Canada"><noRegion><name sortKey="Allard, Bertrand" sort="Allard, Bertrand" uniqKey="Allard B" first="Bertrand" last="Allard">Bertrand Allard</name></noRegion><name sortKey="Stagg, John" sort="Stagg, John" uniqKey="Stagg J" first="John" last="Stagg">John Stagg</name></country><country name="Australie"><noRegion><name sortKey="Smyth, Mark J" sort="Smyth, Mark J" uniqKey="Smyth M" first="Mark J" last="Smyth">Mark J. Smyth</name></noRegion></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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