胰腺癌是一种无情的病症，通常能够在几个月的时间内致人死亡。如今，科学家报告说，一种新的疗法能够点燃某些免疫细胞，从而使胰腺癌患者的生命延长30%。尽管病人的生命仅仅延长了两个月，但癌症研究人员对这一结果充满了热情。
美国宾夕法尼亚大学埃布拉姆森癌症中心的肿瘤免疫学家Robert Vonderheide和同事，通过激发CD40来使免疫系统对抗癌症，CD40是一种携带了几种免疫细胞的蛋白质。最终结果显示，接受治疗的病人寿命平均达到7.4个月。Vonderheide表示：“这是一个很有希望的研究结果，需要在未来更大规模的研究中加以扩大和测试。”研究人员日前在美国《科学》杂志网络版上报告了这一研究成果。（生物谷Bioon.com）
生物谷推荐原文出处：
Science DOI: 10.1126/science.1198443
CD40 Agonists Alter Tumor Stroma and Show Efficacy Against Pancreatic Carcinoma in Mice and Humans
Gregory L. Beatty1,2,6, Elena G. Chiorean3, Matthew P. Fishman1, Babak Saboury5, Ursina R. Teitelbaum2,6, Weijing Sun2,6, Richard D. Huhn4, Wenru Song4, Dongguang Li4, Leslie L. Sharp4, Drew A. Torigian2,5, Peter J. O’Dwyer2,6, and Robert H. Vonderheide1,2,6,*
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.
