<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Tabasum S</submitter><funding>Melanoma Research Alliance</funding><funding>NCI NIH HHS</funding><funding>National Institutes of Health</funding><pagination>1493-1507</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC10618652</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>11(11)</volume><pubmed_abstract>Immune checkpoint blockade (ICB) has become the standard of care for several solid tumors. Multiple combinatorial approaches have been studied to improve therapeutic efficacy. The combination of antiangiogenic agents and ICB has demonstrated efficacy in several cancers. To improve the mechanistic understanding of synergies with these treatment modalities, we performed screens of sera from long-term responding patients treated with ipilimumab and bevacizumab. We discovered a high-titer antibody response against EGF-like repeats and discoidin I-like domains protein 3 (EDIL3) that correlated with favorable clinical outcomes. EDIL3 is an extracellular protein, previously identified as a marker of poor prognosis in various malignancies. Our Tumor Immune Dysfunction and Exclusion analysis predic</pubmed_abstract><journal>Cancer immunology research</journal><pubmed_title>EDIL3 as an Angiogenic Target of Immune Exclusion Following Checkpoint Blockade.</pubmed_title><pmcid>PMC10618652</pmcid><funding_grant_id>R21 CA143832</funding_grant_id><funding_grant_id>CA143832</funding_grant_id><pubmed_authors>Li X</pubmed_authors><pubmed_authors>Li J</pubmed_authors><pubmed_authors>Yoon CH</pubmed_authors><pubmed_authors>Weirather JL</pubmed_authors><pubmed_authors>Campisi M</pubmed_authors><pubmed_authors>Schol PJ</pubmed_authors><pubmed_authors>Tabasum S</pubmed_authors><pubmed_authors>Manos MP</pubmed_authors><pubmed_authors>Thapa D</pubmed_authors><pubmed_authors>Giobbie-Hurder A</pubmed_authors><pubmed_authors>Hodi FS</pubmed_authors><pubmed_authors>Barbie DA</pubmed_authors></additional><is_claimable>false</is_claimable><name>EDIL3 as an Angiogenic Target of Immune Exclusion Following Checkpoint Blockade.</name><description>Immune checkpoint blockade (ICB) has become the standard of care for several solid tumors. Multiple combinatorial approaches have been studied to improve therapeutic efficacy. The combination of antiangiogenic agents and ICB has demonstrated efficacy in several cancers. To improve the mechanistic understanding of synergies with these treatment modalities, we performed screens of sera from long-term responding patients treated with ipilimumab and bevacizumab. We discovered a high-titer antibody response against EGF-like repeats and discoidin I-like domains protein 3 (EDIL3) that correlated with favorable clinical outcomes. EDIL3 is an extracellular protein, previously identified as a marker of poor prognosis in various malignancies. Our Tumor Immune Dysfunction and Exclusion analysis predic</description><dates><release>2023-01-01T00:00:00Z</release><publication>2023 Nov</publication><modification>2026-06-04T16:32:12.957Z</modification><creation>2025-04-06T03:02:55.091Z</creation></dates><accession>S-EPMC10618652</accession><cross_references><pubmed>37728484</pubmed><doi>10.1158/2326-6066.CIR-23-0171</doi></cross_references></HashMap>