Targeting cancer-derived adenosine: new therapeutic approaches.
Identifieur interne : 000638 ( PubMed/Checkpoint ); précédent : 000637; suivant : 000639Targeting cancer-derived adenosine: new therapeutic approaches.
Auteurs : Arabella Young ; Deepak Mittal ; John Stagg [Canada] ; Mark J. Smyth [Australie]Source :
- Cancer discovery [ 2159-8290 ] ; 2014.
English descriptors
- KwdEn :
- 5'-Nucleotidase (antagonists & inhibitors), 5'-Nucleotidase (immunology), Adenosine (immunology), Adenosine (metabolism), Animals, Antigens, CD (immunology), Apyrase (antagonists & inhibitors), Apyrase (immunology), GPI-Linked Proteins (antagonists & inhibitors), GPI-Linked Proteins (immunology), Humans, Immunosuppressive Agents (therapeutic use), Mice, Molecular Targeted Therapy, Neoplasms (drug therapy), Neoplasms (immunology), Neoplasms (pathology), Purinergic P1 Receptor Antagonists.
- MESH :
- chemical , antagonists & inhibitors : 5'-Nucleotidase, Apyrase, GPI-Linked Proteins.
- chemical , immunology : 5'-Nucleotidase, Adenosine, Antigens, CD, Apyrase, GPI-Linked Proteins.
- chemical , metabolism : Adenosine.
- chemical , therapeutic use : Immunosuppressive Agents.
- drug therapy : Neoplasms.
- immunology : Neoplasms.
- pathology : Neoplasms.
- Animals, Humans, Mice, Molecular Targeted Therapy, Purinergic P1 Receptor Antagonists.
Abstract
CD73 generation of immunosuppressive adenosine within the hypoxic tumor microenvironment causes dysregulation of immune cell infiltrates, resulting in tumor progression, metastases, and poor disease outcomes. Therapies targeted toward the adenosinergic pathway, such as antibodies targeting CD73 and CD39, have proven efficacy in mouse tumor models; however, humanized versions are only in preliminary development. In contrast, A(2A) adenosine receptor antagonists have progressed to late-stage clinical trials in Parkinson disease, yet evidence of their role in oncology is limited. This review will compare the merits and challenges of these therapeutic approaches, identifying tumor indications and combinations that may be fruitful as they progress to the clinic.
DOI: 10.1158/2159-8290.CD-14-0341
PubMed: 25035124
Affiliations:
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Smyth</name><affiliation wicri:level="1"><nlm:affiliation>QIMR Berghofer Medical Research Institute; School of Medicine, University of Queensland, Herston, Queensland, Australia; and mark.smyth@qimrberghofer.edu.au.</nlm:affiliation><country wicri:rule="url">Australie</country><wicri:regionArea>QIMR Berghofer Medical Research Institute; School of Medicine, University of Queensland, Herston, Queensland</wicri:regionArea><wicri:noRegion>Queensland</wicri:noRegion></affiliation></author></analytic><series><title level="j">Cancer discovery</title><idno type="eISSN">2159-8290</idno><imprint><date when="2014" type="published">2014</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>5'-Nucleotidase (antagonists & inhibitors)</term><term>5'-Nucleotidase (immunology)</term><term>Adenosine (immunology)</term><term>Adenosine (metabolism)</term><term>Animals</term><term>Antigens, CD (immunology)</term><term>Apyrase (antagonists & inhibitors)</term><term>Apyrase (immunology)</term><term>GPI-Linked Proteins (antagonists & inhibitors)</term><term>GPI-Linked Proteins (immunology)</term><term>Humans</term><term>Immunosuppressive Agents (therapeutic use)</term><term>Mice</term><term>Molecular Targeted Therapy</term><term>Neoplasms (drug therapy)</term><term>Neoplasms (immunology)</term><term>Neoplasms (pathology)</term><term>Purinergic P1 Receptor Antagonists</term></keywords><keywords scheme="MESH" type="chemical" qualifier="antagonists & inhibitors" xml:lang="en"><term>5'-Nucleotidase</term><term>Apyrase</term><term>GPI-Linked Proteins</term></keywords><keywords scheme="MESH" type="chemical" qualifier="immunology" xml:lang="en"><term>5'-Nucleotidase</term><term>Adenosine</term><term>Antigens, CD</term><term>Apyrase</term><term>GPI-Linked Proteins</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Adenosine</term></keywords><keywords scheme="MESH" type="chemical" qualifier="therapeutic use" xml:lang="en"><term>Immunosuppressive 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>Neoplasms</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Neoplasms</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Humans</term><term>Mice</term><term>Molecular Targeted Therapy</term><term>Purinergic P1 Receptor Antagonists</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">CD73 generation of immunosuppressive adenosine within the hypoxic tumor microenvironment causes dysregulation of immune cell infiltrates, resulting in tumor progression, metastases, and poor disease outcomes. Therapies targeted toward the adenosinergic pathway, such as antibodies targeting CD73 and CD39, have proven efficacy in mouse tumor models; however, humanized versions are only in preliminary development. In contrast, A(2A) adenosine receptor antagonists have progressed to late-stage clinical trials in Parkinson disease, yet evidence of their role in oncology is limited. This review will compare the merits and challenges of these therapeutic approaches, identifying tumor indications and combinations that may be fruitful as they progress to the clinic.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">25035124</PMID><DateCreated><Year>2014</Year><Month>08</Month><Day>05</Day></DateCreated><DateCompleted><Year>2015</Year><Month>03</Month><Day>31</Day></DateCompleted><DateRevised><Year>2014</Year><Month>08</Month><Day>05</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">2159-8290</ISSN><JournalIssue CitedMedium="Internet"><Volume>4</Volume><Issue>8</Issue><PubDate><Year>2014</Year><Month>Aug</Month></PubDate></JournalIssue><Title>Cancer discovery</Title><ISOAbbreviation>Cancer Discov</ISOAbbreviation></Journal><ArticleTitle>Targeting cancer-derived adenosine: new therapeutic approaches.</ArticleTitle><Pagination><MedlinePgn>879-88</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1158/2159-8290.CD-14-0341</ELocationID><Abstract><AbstractText Label="UNLABELLED">CD73 generation of immunosuppressive adenosine within the hypoxic tumor microenvironment causes dysregulation of immune cell infiltrates, resulting in tumor progression, metastases, and poor disease outcomes. Therapies targeted toward the adenosinergic pathway, such as antibodies targeting CD73 and CD39, have proven efficacy in mouse tumor models; however, humanized versions are only in preliminary development. In contrast, A(2A) adenosine receptor antagonists have progressed to late-stage clinical trials in Parkinson disease, yet evidence of their role in oncology is limited. This review will compare the merits and challenges of these therapeutic approaches, identifying tumor indications and combinations that may be fruitful as they progress to the clinic.</AbstractText><AbstractText Label="SIGNIFICANCE" NlmCategory="CONCLUSIONS">High concentrations of immunosuppressive adenosine have been reported in cancers, and adenosine is implicated in the growth of tumors. This brief review delineates the current treatment strategies and tumor subtypes that will benefit from targeting adenosinergic pathways, alone or in combination with contemporary approaches to cancer treatment.</AbstractText><CopyrightInformation>©2014 American Association for Cancer Research.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Young</LastName><ForeName>Arabella</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>QIMR Berghofer Medical Research Institute; School of Medicine, University of Queensland, Herston, Queensland, Australia; and.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Mittal</LastName><ForeName>Deepak</ForeName><Initials>D</Initials><AffiliationInfo><Affiliation>QIMR Berghofer Medical Research Institute; School of Medicine, University of Queensland, Herston, Queensland, Australia; and.</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>QIMR Berghofer Medical Research Institute; School of Medicine, University of Queensland, Herston, 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><PublicationType 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PubStatus="entrez"><Year>2014</Year><Month>7</Month><Day>19</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2014</Year><Month>7</Month><Day>19</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2015</Year><Month>4</Month><Day>1</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">25035124</ArticleId><ArticleId IdType="pii">2159-8290.CD-14-0341</ArticleId><ArticleId IdType="doi">10.1158/2159-8290.CD-14-0341</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="Young, Arabella" sort="Young, Arabella" uniqKey="Young A" first="Arabella" last="Young">Arabella Young</name></noCountry><country name="Canada"><noRegion><name sortKey="Stagg, John" sort="Stagg, John" uniqKey="Stagg J" first="John" last="Stagg">John Stagg</name></noRegion></country><country name="Australie"><noRegion><name sortKey="Smyth, Mark J" sort="Smyth, Mark J" uniqKey="Smyth M" first="Mark J" last="Smyth">Mark J. 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