一個(gè)國際研究團(tuán)隊(duì)在近日出版的《科學(xué)》雜志上宣稱,，由于胰腺癌的腫瘤大部分與血管無關(guān),，針對胰腺癌癥的傳統(tǒng)藥物比如美國禮來公司的健擇（Gemza）很難接近腫瘤并殺死腫瘤細(xì)胞,，導(dǎo)致這些藥物失效,。
英國癌癥研究所劍橋研究院的大衛(wèi)·圖文森領(lǐng)導(dǎo)了該項(xiàng)研究,。研究人員讓經(jīng)過基因改造的老鼠患上胰腺癌,，他們發(fā)現(xiàn),，老鼠體內(nèi)只有很少的腫瘤與血管,，人類也同樣如此。這表明,，胰腺癌可能同其他癌癥不同,，不需要給腫瘤供應(yīng)豐富的血液，所以,，通過限制血液供應(yīng)以殺死腫瘤的血管內(nèi)皮生長因子（VEGF）抑制劑對胰腺癌腫瘤不起作用,。
研究人員同時(shí)發(fā)現(xiàn)，在老鼠和胰腺癌癥病人身上進(jìn)行的研究表明,，將Gemza同美國無限制藥公司的藥物IPI-926結(jié)合,，可能更好地戰(zhàn)勝胰腺癌。不過,，還需要進(jìn)行進(jìn)一步的安全測試,。
全世界每年有23萬人被診斷出患上胰腺癌，只有3%的人能活過5年,。而且,，胰腺癌擴(kuò)散很快，當(dāng)很多人被診斷出身患該癌癥時(shí),，已無力回天,。（生物谷Bioon.com）
生物谷推薦原始出處：
Science May 21, 2009 DOI: 10.1126/science.1171362
Inhibition of Hedgehog Signaling Enhances Delivery of Chemotherapy in a Mouse Model of Pancreatic Cancer
Kenneth P. Olive 1, Michael A. Jacobetz 1, Christian J. Davidson 2, Aarthi Gopinathan 3, Dominick McIntyre 1, Davina Honess 1, Basetti Madhu 1, Mae A. Goldgraben 1, Meredith E. Caldwell 1, David Allard 1, Kristopher K. Frese 1, Gina DeNicola 3, Christine Feig 1, Chelsea Combs 2, Stephen P. Winter 1, Heather Ireland 1, Stefanie Reichelt 1, William J. Howat 1, Alex Chang 4, Mousumi Dhara 4, Lifu Wang 5, Felix Rückert 6, Robert Grützmann 6, Christian Pilarsky 6, Kamel Izeradjene 7, Sunil R. Hingorani 7, Pearl Huang 8, Susan E. Davies 9, William Plunkett 10, Merrill Egorin 11, Ralph H. Hruban 4, Nigel Whitebread 12, Karen McGovern 12, Julian Adams 12, Christine Iacobuzio-Donahue 4, John Griffiths 1, David A. Tuveson 1*
1 Cancer Research UK, Cambridge Research Institute, The Li Ka Shing Centre, Robinson Way, Cambridge, CB2 ORE, UK.
2 Abramson Family Cancer Research Institute, University of Pennsylvania, Philadelphia, PA 19104, USA.
3 Cancer Research UK, Cambridge Research Institute, The Li Ka Shing Centre, Robinson Way, Cambridge, CB2 ORE, UK.; Abramson Family Cancer Research Institute, University of Pennsylvania, Philadelphia, PA 19104, USA.
4 Departments of Oncology and Pathology, The Sol Goldman Pancreatic Cancer Research Center, Sidney Cancer Center and Johns Hopkins University, Baltimore, MD 21287, USA.
5 Abramson Family Cancer Research Institute, University of Pennsylvania, Philadelphia, PA 19104, USA.; Department of Gastroenterology, Ruijin Hospital, Shanghai Jiaotong University School of Medicine, Shanghai 200025, China.
6 Department of Surgery, University Hospital Dresden, Fetscherstr. 74, 01307 Dresden, Germany.
7 Clinical Research and Public Health Sciences Division, Fred Hutchinson Cancer Research Center, and University of Washington, Seattle, WA 98109, USA.
8 Oncology Franchise, Merck and Co, North Wales, PA 19454, USA.
9 Department of Histopathology, Addenbrooke’s Hospital, Cambridge University Hospitals NHS Foundation Trust, Cambridge, CB2 2QQ, UK.
10 Univ. of Texas MD Anderson Cancer Center, Houston, TX 77030, USA.
11 Division of Hematology and Oncology, University of Pittsburgh Medical Center, Pittsburgh, PA 15213, USA.
12 Infinity Pharmaceuticals Inc, Cambridge, MA 01239, USA.
Pancreatic ductal adenocarcinoma (PDA) is among the most lethal human cancers, in part because it is insensitive to many chemotherapeutic drugs. Studying a mouse model of PDA that is refractory to the clinically used drug gemcitabine, we found that the tumors in this model were poorly perfused and poorly vascularized, properties that are shared with human PDA. We tested whether the delivery and efficacy of gemcitabine in the mice could be improved by coadministration of IPI-926, a drug that depletes tumor-associated stromal tissue by inhibiting the Hedgehog cellular signaling pathway. The combination therapy produced a transient increase in intratumoral vascular density and intratumoral concentration of gemcitabine, leading to transient stabilization of disease. Thus, inefficient drug delivery may be an important contributor to chemoresistance in pancreatic cancer.
