| Literature DB >> 21436454 |
Gregory L Beatty1, Elena G Chiorean, Matthew P Fishman, Babak Saboury, Ursina R Teitelbaum, Weijing Sun, Richard D Huhn, Wenru Song, Dongguang Li, Leslie L Sharp, Drew A Torigian, Peter J O'Dwyer, Robert H Vonderheide.
Abstract
Immunosuppressive tumor microenvironments can restrain antitumor immunity, particularly in pancreatic ductal adenocarcinoma (PDA). Because CD40 activation can reverse immune suppression and drive antitumor T cell responses, we tested the combination of an agonist CD40 antibody with gemcitabine chemotherapy in a small cohort of patients with surgically incurable PDA and observed tumor regressions in some patients. We reproduced this treatment effect in a genetically engineered mouse model of PDA and found unexpectedly that tumor regression required macrophages but not T cells or gemcitabine. CD40-activated macrophages rapidly infiltrated tumors, became tumoricidal, and facilitated the depletion of tumor stroma. Thus, cancer immune surveillance does not necessarily depend on therapy-induced T cells; rather, our findings demonstrate a CD40-dependent mechanism for targeting tumor stroma in the treatment of cancer.Entities:
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Year: 2011 PMID: 21436454 PMCID: PMC3406187 DOI: 10.1126/science.1198443
Source DB: PubMed Journal: Science ISSN: 0036-8075 Impact factor: 47.728