<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Wang C</submitter><funding>Shanghai Science and Technology Innovation Action Plan</funding><funding>Natural Science Foundation of Shanghai</funding><funding>Natural Science Foundation of Shanghai Municipality</funding><funding>National Natural Science Foundation of China</funding><funding>Shanghai Clinical Research Center for Gynecological Diseases</funding><pagination>747-773</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC12328091</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>45(7)</volume><pubmed_abstract>&lt;h4>Background&lt;/h4>Tumor-associated neutrophils (TANs) play a critical role in modulating immune responses and exhibit significant heterogeneity. Our previous study demonstrated that jagged canonical Notch ligand 2 (JAG2)&lt;sup>+&lt;/sup> TANs were associated with an immunosuppressive microenvironment in high-grade serous ovarian cancer (HGSOC), but the underlying mechanism remains unclear. This study aimed to elucidate the role of JAG2&lt;sup>+&lt;/sup> TANs in tumor immunosuppressive microenvironment in HGSOC.&lt;h4>Methods&lt;/h4>HGSOC samples were collected, with 274 samples constituting two independent cohorts (training and validation cohorts) and an additional 30 samples utilized to establish patient-derived tumor organoids (PDTOs). We characterized the number and phenotype of JAG2&lt;sup>+&lt;/sup> TANs b</pubmed_abstract><journal>Cancer communications (London, England)</journal><pubmed_title>Immunosuppressive JAG2&amp;lt;sup&amp;gt;+&amp;lt;/sup&amp;gt; tumor-associated neutrophils hamper PD-1 blockade response in ovarian cancer by mediating the differentiation of effector regulatory T cells.</pubmed_title><pmcid>PMC12328091</pmcid><funding_grant_id>82072881</funding_grant_id><funding_grant_id>82203665</funding_grant_id><funding_grant_id>23Y11901800</funding_grant_id><funding_grant_id>23ZR1408300</funding_grant_id><funding_grant_id>22MC1940200</funding_grant_id><funding_grant_id>82273205</funding_grant_id><funding_grant_id>82473274</funding_grant_id><funding_grant_id>23Y11909500</funding_grant_id><pubmed_authors>Zhang G</pubmed_authors><pubmed_authors>Liu H</pubmed_authors><pubmed_authors>Cao K</pubmed_authors><pubmed_authors>Huang Y</pubmed_authors><pubmed_authors>Wang C</pubmed_authors><pubmed_authors>Yang M</pubmed_authors><pubmed_authors>Lu J</pubmed_authors><pubmed_authors>He M</pubmed_authors><pubmed_authors>Zhong Y</pubmed_authors><pubmed_authors>Wang X</pubmed_authors><pubmed_authors>Zhang C</pubmed_authors><pubmed_authors>Wang Y</pubmed_authors></additional><is_claimable>false</is_claimable><name>Immunosuppressive JAG2&amp;lt;sup&amp;gt;+&amp;lt;/sup&amp;gt; tumor-associated neutrophils hamper PD-1 blockade response in ovarian cancer by mediating the differentiation of effector regulatory T cells.</name><description>&lt;h4>Background&lt;/h4>Tumor-associated neutrophils (TANs) play a critical role in modulating immune responses and exhibit significant heterogeneity. Our previous study demonstrated that jagged canonical Notch ligand 2 (JAG2)&lt;sup>+&lt;/sup> TANs were associated with an immunosuppressive microenvironment in high-grade serous ovarian cancer (HGSOC), but the underlying mechanism remains unclear. This study aimed to elucidate the role of JAG2&lt;sup>+&lt;/sup> TANs in tumor immunosuppressive microenvironment in HGSOC.&lt;h4>Methods&lt;/h4>HGSOC samples were collected, with 274 samples constituting two independent cohorts (training and validation cohorts) and an additional 30 samples utilized to establish patient-derived tumor organoids (PDTOs). We characterized the number and phenotype of JAG2&lt;sup>+&lt;/sup> TANs b</description><dates><release>2025-01-01T00:00:00Z</release><publication>2025 Jul</publication><modification>2026-07-15T12:45:21.293Z</modification><creation>2026-07-04T03:16:31.229Z</creation></dates><accession>S-EPMC12328091</accession><cross_references><pubmed>40120139</pubmed><doi>10.1002/cac2.70021</doi></cross_references></HashMap>