<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Jain S</submitter><funding>Clinical Translational Science Center</funding><funding>Cure, New York Community Trust, Cancer Research and Treatment Fund</funding><funding>NCATS NIH HHS</funding><funding>NCRR NIH HHS</funding><funding>Berman Fund</funding><funding>Anne Moore Breast Cancer Research Fund, Stephen and Madeline Anbinder Foundation, Rozaliya Kosmandel Research Fund</funding><pagination>1491-8</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC3707432</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>24(6)</volume><pubmed_abstract>&lt;h4>Background&lt;/h4>Bone marrow-derived endothelial progenitor cells (EPCs) are critical for metastatic progression. This study explores the effect of tetrathiomolybdate (TM), an anti-angiogenic copper chelator, on EPCs in patients at high risk for breast cancer recurrence.&lt;h4>Patients and methods&lt;/h4>This phase 2 study enrolled breast cancer patients with stage 3 and stage 4 without evidence of disease (NED), and stage 2 if triple-negative. TM 100 mg orally was administered to maintain ceruloplasmin &lt;17 mg/dl for 2 years or until relapse. The primary end point was change in EPCs.&lt;h4>Results&lt;/h4>Forty patients (28 stage 2/3, 12 stage 4 NED) were enrolled. Seventy-five percent patients achieved the copper depletion target by 1 month. Ninety-one percent of triple-negative patients copper-depl</pubmed_abstract><journal>Annals of oncology : official journal of the European Society for Medical Oncology</journal><pubmed_title>Tetrathiomolybdate-associated copper depletion decreases circulating endothelial progenitor cells in women with breast cancer at high risk of relapse.</pubmed_title><pmcid>PMC3707432</pmcid><funding_grant_id>UL1 TR000457</funding_grant_id><funding_grant_id>UL1-RR024996</funding_grant_id><pubmed_authors>Kornhauser N</pubmed_authors><pubmed_authors>Jain S</pubmed_authors><pubmed_authors>Warren JD</pubmed_authors><pubmed_authors>Cobham MV</pubmed_authors><pubmed_authors>Schneider S</pubmed_authors><pubmed_authors>Vahdat LT</pubmed_authors><pubmed_authors>Chuang E</pubmed_authors><pubmed_authors>Lam C</pubmed_authors><pubmed_authors>Donovan D</pubmed_authors><pubmed_authors>Cigler T</pubmed_authors><pubmed_authors>Zelkowitz R</pubmed_authors><pubmed_authors>Lane ME</pubmed_authors><pubmed_authors>Mathijsen Greenwood C</pubmed_authors><pubmed_authors>Mittal V</pubmed_authors><pubmed_authors>Rafii S</pubmed_authors><pubmed_authors>Moore A</pubmed_authors><pubmed_authors>Cohen J</pubmed_authors><pubmed_authors>Ward MM</pubmed_authors><pubmed_authors>Hurtado Rua SM</pubmed_authors><pubmed_authors>Benkert S</pubmed_authors></additional><is_claimable>false</is_claimable><name>Tetrathiomolybdate-associated copper depletion decreases circulating endothelial progenitor cells in women with breast cancer at high risk of relapse.</name><description>&lt;h4>Background&lt;/h4>Bone marrow-derived endothelial progenitor cells (EPCs) are critical for metastatic progression. This study explores the effect of tetrathiomolybdate (TM), an anti-angiogenic copper chelator, on EPCs in patients at high risk for breast cancer recurrence.&lt;h4>Patients and methods&lt;/h4>This phase 2 study enrolled breast cancer patients with stage 3 and stage 4 without evidence of disease (NED), and stage 2 if triple-negative. TM 100 mg orally was administered to maintain ceruloplasmin &lt;17 mg/dl for 2 years or until relapse. The primary end point was change in EPCs.&lt;h4>Results&lt;/h4>Forty patients (28 stage 2/3, 12 stage 4 NED) were enrolled. Seventy-five percent patients achieved the copper depletion target by 1 month. Ninety-one percent of triple-negative patients copper-depl</description><dates><release>2013-01-01T00:00:00Z</release><publication>2013 Jun</publication><modification>2026-05-30T10:38:20.537Z</modification><creation>2026-04-08T07:01:19.597Z</creation></dates><accession>S-EPMC3707432</accession><cross_references><pubmed>23406736</pubmed><doi>10.1093/annonc/mds654</doi></cross_references></HashMap>