<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Fu C</submitter><funding>"Financial Support for Selected Researchers Back from Abroad (2012)" from Liaoning Province</funding><pagination>1011-1025</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC7935791</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>112(3)</volume><pubmed_abstract>Myeloid-derived suppressor cells (MDSCs) are responsible for antitumor immunodeficiency in tumor-bearing hosts. Primarily, MDSCs are classified into 2 groups: monocytic (M)-MDSCs and polymorphonuclear (PMN)-MDSCs. In most cancers, PMN-MDSCs (CD11b&lt;sup>+&lt;/sup> Ly6C&lt;sup>low&lt;/sup> Ly6G&lt;sup>+&lt;/sup> cells) represent the most abundant MDSC subpopulation. However, the functional and phenotypic heterogeneities of PMN-MDSC remain elusive, which delays clinical therapeutic targeting decisions. In the 4T1 murine tumor model, CD11b&lt;sup>+&lt;/sup> Ly6G&lt;sup>low&lt;/sup> PMN-MDSCs were sensitive to surgical and pharmacological interventions. By comprehensively analyzing 64 myeloid cell-related surface molecule expression profiles, cell density, nuclear morphology, and immunosuppressive activity, the PMN-MDSC p</pubmed_abstract><journal>Cancer science</journal><pubmed_title>CD205&lt;sup>+&lt;/sup> polymorphonuclear myeloid-derived suppressor cells suppress antitumor immunity by overexpressing GLUT3.</pubmed_title><pmcid>PMC7935791</pmcid><funding_grant_id>88030312004</funding_grant_id><pubmed_authors>Zheng K</pubmed_authors><pubmed_authors>Fu C</pubmed_authors><pubmed_authors>Ma S</pubmed_authors><pubmed_authors>Gu X</pubmed_authors><pubmed_authors>Zhang Y</pubmed_authors><pubmed_authors>Fu Z</pubmed_authors><pubmed_authors>Tang S</pubmed_authors><pubmed_authors>Zhou D</pubmed_authors><pubmed_authors>Jiang C</pubmed_authors><pubmed_authors>Xia C</pubmed_authors><pubmed_authors>Lyu S</pubmed_authors></additional><is_claimable>false</is_claimable><name>CD205&lt;sup>+&lt;/sup> polymorphonuclear myeloid-derived suppressor cells suppress antitumor immunity by overexpressing GLUT3.</name><description>Myeloid-derived suppressor cells (MDSCs) are responsible for antitumor immunodeficiency in tumor-bearing hosts. Primarily, MDSCs are classified into 2 groups: monocytic (M)-MDSCs and polymorphonuclear (PMN)-MDSCs. In most cancers, PMN-MDSCs (CD11b&lt;sup>+&lt;/sup> Ly6C&lt;sup>low&lt;/sup> Ly6G&lt;sup>+&lt;/sup> cells) represent the most abundant MDSC subpopulation. However, the functional and phenotypic heterogeneities of PMN-MDSC remain elusive, which delays clinical therapeutic targeting decisions. In the 4T1 murine tumor model, CD11b&lt;sup>+&lt;/sup> Ly6G&lt;sup>low&lt;/sup> PMN-MDSCs were sensitive to surgical and pharmacological interventions. By comprehensively analyzing 64 myeloid cell-related surface molecule expression profiles, cell density, nuclear morphology, and immunosuppressive activity, the PMN-MDSC p</description><dates><release>2021-01-01T00:00:00Z</release><publication>2021 Mar</publication><modification>2025-04-04T18:37:22.527Z</modification><creation>2025-04-04T18:37:22.527Z</creation></dates><accession>S-EPMC7935791</accession><cross_references><pubmed>33368883</pubmed><doi>10.1111/cas.14783</doi></cross_references></HashMap>