{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Feng L"],"funding":["NHLBI NIH HHS"],"pagination":["206-16"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC3050864"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["13(3)"],"pubmed_abstract":["Extracellular adenosine triphosphate (ATP) is known to boost immune responses in the tumor microenvironment but might also contribute directly to cancer cell death. CD39/ENTPD1 is the dominant ectonucleotidase expressed by endothelial cells and regulatory T cells and catalyzes the sequential hydrolysis of ATP to AMP that is further degraded to adenosine by CD73/ecto-5'-nucleotidase. We have previously shown that deletion of Cd39 results in decreased growth of transplanted tumors in mice, as a result of both defective angiogenesis and heightened innate immune responses (secondary to loss of adenosinergic immune suppression). Whether alterations in local extracellular ATP and adenosine levels as a result of CD39 bioactivity directly affect tumor growth and cytotoxicity has not been investiga"],"journal":["Neoplasia (New York, N.Y.)"],"pubmed_title":["Vascular CD39/ENTPD1 directly promotes tumor cell growth by scavenging extracellular adenosine triphosphate."],"pmcid":["PMC3050864"],"funding_grant_id":["P01-HL076540","R01 HL063972","R01 HL063972-08","R01-HL094400","R01 HL057307-08","R01 HL057307","R01 HL094400-02","P01 HL076540","R01 HL094400"],"pubmed_authors":["Feng L","Bian S","Csizmadia E","Han L","Wang X","Sun X","Murakami T","Wu Y","Robson SC"],"additional_accession":[]},"is_claimable":false,"name":"Vascular CD39/ENTPD1 directly promotes tumor cell growth by scavenging extracellular adenosine triphosphate.","description":"Extracellular adenosine triphosphate (ATP) is known to boost immune responses in the tumor microenvironment but might also contribute directly to cancer cell death. CD39/ENTPD1 is the dominant ectonucleotidase expressed by endothelial cells and regulatory T cells and catalyzes the sequential hydrolysis of ATP to AMP that is further degraded to adenosine by CD73/ecto-5'-nucleotidase. We have previously shown that deletion of Cd39 results in decreased growth of transplanted tumors in mice, as a result of both defective angiogenesis and heightened innate immune responses (secondary to loss of adenosinergic immune suppression). Whether alterations in local extracellular ATP and adenosine levels as a result of CD39 bioactivity directly affect tumor growth and cytotoxicity has not been investiga","dates":{"release":"2011-01-01T00:00:00Z","publication":"2011 Mar","modification":"2025-04-20T04:00:09.02Z","creation":"2019-03-27T00:39:28Z"},"accession":"S-EPMC3050864","cross_references":{"pubmed":["21390184"],"doi":["10.1593/neo.101332"]}}