胰腺癌是一種無情的病癥，通常能夠在幾個月的時間內(nèi)致人死亡,。如今,，科學家報告說，一種新的療法能夠點燃某些免疫細胞,，從而使胰腺癌患者的生命延長30%,。盡管病人的生命僅僅延長了兩個月，但癌癥研究人員對這一結果充滿了熱情,。
美國賓夕法尼亞大學埃布拉姆森癌癥中心的腫瘤免疫學家Robert Vonderheide和同事,，通過激發(fā)CD40來使免疫系統(tǒng)對抗癌癥，CD40是一種攜帶了幾種免疫細胞的蛋白質,。最終結果顯示,，接受治療的病人壽命平均達到7.4個月,。Vonderheide表示：“這是一個很有希望的研究結果，需要在未來更大規(guī)模的研究中加以擴大和測試,。”研究人員日前在美國《科學》雜志網(wǎng)絡版上報告了這一研究成果,。（生物谷Bioon.com）
生物谷推薦原文出處：
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.
