<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Feng L</submitter><funding>NHLBI NIH HHS</funding><pagination>206-16</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC3050864</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>13(3)</volume><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</pubmed_abstract><journal>Neoplasia (New York, N.Y.)</journal><pubmed_title>Vascular CD39/ENTPD1 directly promotes tumor cell growth by scavenging extracellular adenosine triphosphate.</pubmed_title><pmcid>PMC3050864</pmcid><funding_grant_id>P01-HL076540</funding_grant_id><funding_grant_id>R01 HL063972</funding_grant_id><funding_grant_id>R01 HL063972-08</funding_grant_id><funding_grant_id>R01-HL094400</funding_grant_id><funding_grant_id>R01 HL057307-08</funding_grant_id><funding_grant_id>R01 HL057307</funding_grant_id><funding_grant_id>R01 HL094400-02</funding_grant_id><funding_grant_id>P01 HL076540</funding_grant_id><funding_grant_id>R01 HL094400</funding_grant_id><pubmed_authors>Feng L</pubmed_authors><pubmed_authors>Bian S</pubmed_authors><pubmed_authors>Csizmadia E</pubmed_authors><pubmed_authors>Han L</pubmed_authors><pubmed_authors>Wang X</pubmed_authors><pubmed_authors>Sun X</pubmed_authors><pubmed_authors>Murakami T</pubmed_authors><pubmed_authors>Wu Y</pubmed_authors><pubmed_authors>Robson SC</pubmed_authors></additional><is_claimable>false</is_claimable><name>Vascular CD39/ENTPD1 directly promotes tumor cell growth by scavenging extracellular adenosine triphosphate.</name><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</description><dates><release>2011-01-01T00:00:00Z</release><publication>2011 Mar</publication><modification>2025-04-20T04:00:09.02Z</modification><creation>2019-03-27T00:39:28Z</creation></dates><accession>S-EPMC3050864</accession><cross_references><pubmed>21390184</pubmed><doi>10.1593/neo.101332</doi></cross_references></HashMap>