{"title":"在胰腺癌中,抗bag3治疗对肿瘤相关巨噬细胞的消耗是对PD-1阻断的补充","authors":"Yi Sun, R. Torphy, Yuwen Zhu","doi":"10.21037/APC.2018.10.01","DOIUrl":null,"url":null,"abstract":"New literature published in Gut has shown that combined treatment of anti-BAG3 mAb and anti-PD-1 mAb in pancreatic cancer can eliminate tumor-associated macrophages (TAMs), increase tumor infiltrating CD8+ T cells and result in tumor growth suppression (1). These findings highlight the potential of BAG3 (Bcl-2-associated athanogene 3) as a therapeutic target in conjunction with immune checkpoint blockade in the treatment of pancreatic cancer.","PeriodicalId":8372,"journal":{"name":"Annals of Pancreatic Cancer","volume":null,"pages":null},"PeriodicalIF":0.0000,"publicationDate":"2018-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Depletion of tumor associated macrophages by anti-BAG3 treatment complements PD-1 blockade in pancreatic cancer\",\"authors\":\"Yi Sun, R. Torphy, Yuwen Zhu\",\"doi\":\"10.21037/APC.2018.10.01\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"New literature published in Gut has shown that combined treatment of anti-BAG3 mAb and anti-PD-1 mAb in pancreatic cancer can eliminate tumor-associated macrophages (TAMs), increase tumor infiltrating CD8+ T cells and result in tumor growth suppression (1). These findings highlight the potential of BAG3 (Bcl-2-associated athanogene 3) as a therapeutic target in conjunction with immune checkpoint blockade in the treatment of pancreatic cancer.\",\"PeriodicalId\":8372,\"journal\":{\"name\":\"Annals of Pancreatic Cancer\",\"volume\":null,\"pages\":null},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2018-10-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Annals of Pancreatic Cancer\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.21037/APC.2018.10.01\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Annals of Pancreatic Cancer","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.21037/APC.2018.10.01","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
Depletion of tumor associated macrophages by anti-BAG3 treatment complements PD-1 blockade in pancreatic cancer
New literature published in Gut has shown that combined treatment of anti-BAG3 mAb and anti-PD-1 mAb in pancreatic cancer can eliminate tumor-associated macrophages (TAMs), increase tumor infiltrating CD8+ T cells and result in tumor growth suppression (1). These findings highlight the potential of BAG3 (Bcl-2-associated athanogene 3) as a therapeutic target in conjunction with immune checkpoint blockade in the treatment of pancreatic cancer.