<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Wen RM</submitter><funding>NIH, DoD</funding><funding>NCRR NIH HHS</funding><funding>NCI NIH HHS</funding><funding>NIGMS NIH HHS</funding><pagination>e180282</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC11645153</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>134(24)</volume><pubmed_abstract>Prostate cancer is the second leading cause of male cancer death in the U.S. Current immune checkpoint inhibitor-based immunotherapies have improved survival for many malignancies; however, they have failed to prolong survival for prostate cancer. Siglecs (sialic acid-binding immunoglobulin-like lectins) are expressed on immune cells and regulate their function. Siglec-7 and Siglec-9 contribute to immune evasion in cancer by interacting with sialic acid-containing glycoprotein ligands on cancer cells. However, the role of Siglec-7/9 receptors and their ligands in prostate cancer remains poorly understood. Here, we find that Siglec-7 and Siglec-9 are associated with poor prognosis in patients with prostate cancer and are highly expressed in myeloid cells, including macrophages, in prostate </pubmed_abstract><journal>The Journal of clinical investigation</journal><pubmed_title>Sialylated glycoproteins suppress immune cell killing by binding to Siglec-7 and Siglec-9 in prostate cancer.</pubmed_title><pmcid>PMC11645153</pmcid><funding_grant_id>F32 CA250324</funding_grant_id><funding_grant_id>S10 RR025518</funding_grant_id><funding_grant_id>W81XWH2110195,1F32CA250324-01,PF-20-143-01-LIB,R01CA227942,NIH K99 GM147304,U01CA226051,S10RR025518-01,S10RR027431-01</funding_grant_id><funding_grant_id>P30 CA014051</funding_grant_id><funding_grant_id>U01 CA226051</funding_grant_id><funding_grant_id>K99 GM147304</funding_grant_id><funding_grant_id>R01 CA227942</funding_grant_id><funding_grant_id>S10 RR027431</funding_grant_id><pubmed_authors>Brooks JD</pubmed_authors><pubmed_authors>Garcia Marques FJ</pubmed_authors><pubmed_authors>Pitteri SJ</pubmed_authors><pubmed_authors>Fan Z</pubmed_authors><pubmed_authors>Engleman EG</pubmed_authors><pubmed_authors>Totten SM</pubmed_authors><pubmed_authors>Bertozzi CR</pubmed_authors><pubmed_authors>Wen RM</pubmed_authors><pubmed_authors>Fong L</pubmed_authors><pubmed_authors>Lyu A</pubmed_authors><pubmed_authors>Stark JC</pubmed_authors><pubmed_authors>Riley NM</pubmed_authors><pubmed_authors>Zhang X</pubmed_authors><pubmed_authors>Bermudez A</pubmed_authors><pubmed_authors>Marti GEW</pubmed_authors><pubmed_authors>Nolley R</pubmed_authors><pubmed_authors>Zhao H</pubmed_authors></additional><is_claimable>false</is_claimable><name>Sialylated glycoproteins suppress immune cell killing by binding to Siglec-7 and Siglec-9 in prostate cancer.</name><description>Prostate cancer is the second leading cause of male cancer death in the U.S. Current immune checkpoint inhibitor-based immunotherapies have improved survival for many malignancies; however, they have failed to prolong survival for prostate cancer. Siglecs (sialic acid-binding immunoglobulin-like lectins) are expressed on immune cells and regulate their function. Siglec-7 and Siglec-9 contribute to immune evasion in cancer by interacting with sialic acid-containing glycoprotein ligands on cancer cells. However, the role of Siglec-7/9 receptors and their ligands in prostate cancer remains poorly understood. Here, we find that Siglec-7 and Siglec-9 are associated with poor prognosis in patients with prostate cancer and are highly expressed in myeloid cells, including macrophages, in prostate </description><dates><release>2024-01-01T00:00:00Z</release><publication>2024 Oct</publication><modification>2026-06-02T10:45:57.252Z</modification><creation>2025-04-04T01:54:59.075Z</creation></dates><accession>S-EPMC11645153</accession><cross_references><pubmed>39436703</pubmed><doi>10.1172/JCI180282</doi></cross_references></HashMap>