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A Phase I Study of FOLFIRINOX Plus IPI-926, a Hedgehog Pathway Inhibitor, for Advanced Pancreatic Adenocarcinoma.一项关于FOLFIRINOX联合Hedgehog信号通路抑制剂IPI-926用于晚期胰腺腺癌的I期研究。
Pancreas. 2016 Mar;45(3):370-5. doi: 10.1097/MPA.0000000000000458.
2
Antiproliferative effects of curcumin analog L49H37 in pancreatic stellate cells: a comparative study.姜黄素类似物L49H37对胰腺星状细胞的抗增殖作用:一项比较研究。
Ann Gastroenterol. 2015 Jul-Sep;28(3):391-398.
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Alternatively activated macrophages promote pancreatic fibrosis in chronic pancreatitis.交替活化的巨噬细胞促进慢性胰腺炎中的胰腺纤维化。
Nat Commun. 2015 May 18;6:7158. doi: 10.1038/ncomms8158.
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Microenvironmental hCAP-18/LL-37 promotes pancreatic ductal adenocarcinoma by activating its cancer stem cell compartment.微环境 hCAP-18/LL-37 通过激活其癌症干细胞隔室促进胰腺导管腺癌。
Gut. 2015 Dec;64(12):1921-35. doi: 10.1136/gutjnl-2014-308935. Epub 2015 Apr 3.
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The future of immune checkpoint therapy.免疫检查点疗法的未来。
Science. 2015 Apr 3;348(6230):56-61. doi: 10.1126/science.aaa8172.
6
Actin cytoskeletal control during epithelial to mesenchymal transition: focus on the pancreas and intestinal tract.上皮-间质转化过程中的肌动蛋白细胞骨架调控:聚焦于胰腺和肠道
Br J Cancer. 2015 Feb 17;112(4):613-20. doi: 10.1038/bjc.2014.658. Epub 2015 Jan 22.
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Organoid models of human and mouse ductal pancreatic cancer.人类和小鼠胰腺导管癌的类器官模型
Cell. 2015 Jan 15;160(1-2):324-38. doi: 10.1016/j.cell.2014.12.021. Epub 2014 Dec 31.
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A next-generation dual-recombinase system for time- and host-specific targeting of pancreatic cancer.一种用于胰腺癌的时间和宿主特异性靶向的新一代双重组酶系统。
Nat Med. 2014 Nov;20(11):1340-1347. doi: 10.1038/nm.3646. Epub 2014 Oct 19.
9
Pathology of pancreatic ductal adenocarcinoma: facts, challenges and future developments.胰腺导管腺癌的病理学:事实、挑战与未来发展
World J Gastroenterol. 2014 Oct 14;20(38):13833-41. doi: 10.3748/wjg.v20.i38.13833.
10
α-Smooth muscle actin expression and desmoplastic stromal reaction in pancreatic cancer: results from the CONKO-001 study.胰腺癌中α平滑肌肌动蛋白的表达及促纤维增生性间质反应:CONKO-001研究结果
Br J Cancer. 2014 Nov 11;111(10):1917-23. doi: 10.1038/bjc.2014.495. Epub 2014 Oct 14.

胰腺癌-基质相互作用中的关键参与者:癌症相关成纤维细胞、内皮细胞和炎症细胞。

Key players in pancreatic cancer-stroma interaction: Cancer-associated fibroblasts, endothelial and inflammatory cells.

作者信息

Nielsen Michael Friberg Bruun, Mortensen Michael Bau, Detlefsen Sönke

机构信息

Michael Friberg Bruun Nielsen, Sönke Detlefsen, Department of Pathology, Odense University Hospital, University of Southern Denmark, 5000 Odense, Denmark.

出版信息

World J Gastroenterol. 2016 Mar 7;22(9):2678-700. doi: 10.3748/wjg.v22.i9.2678.

DOI:10.3748/wjg.v22.i9.2678
PMID:26973408
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4777992/
Abstract

Pancreatic cancer (PC) is the most aggressive type of common cancers, and in 2014, nearly 40000 patients died from the disease in the United States. Pancreatic ductal adenocarcinoma, which accounts for the majority of PC cases, is characterized by an intense stromal desmoplastic reaction surrounding the cancer cells. Cancer-associated fibroblasts (CAFs) are the main effector cells in the desmoplastic reaction, and pancreatic stellate cells are the most important source of CAFs. However, other important components of the PC stroma are inflammatory cells and endothelial cells. The aim of this review is to describe the complex interplay between PC cells and the cellular and non-cellular components of the tumour stroma. Published data have indicated that the desmoplastic stroma protects PC cells against chemotherapy and radiation therapy and that it might promote the proliferation and migration of PC cells. However, in animal studies, experimental depletion of the desmoplastic stroma and CAFs has led to more aggressive cancers. Hence, the precise role of the tumour stroma in PC remains to be elucidated. However, it is likely that a context-dependent therapeutic modification, rather than pure depletion, of the PC stroma holds potential for the development of new treatment strategies for PC patients.

摘要

胰腺癌(PC)是常见癌症中侵袭性最强的类型,2014年在美国,近40000名患者死于该疾病。占PC病例大多数的胰腺导管腺癌的特征是癌细胞周围有强烈的间质促纤维增生反应。癌症相关成纤维细胞(CAF)是促纤维增生反应中的主要效应细胞,胰腺星状细胞是CAF的最重要来源。然而,PC间质的其他重要成分是炎症细胞和内皮细胞。本综述的目的是描述PC细胞与肿瘤间质的细胞和非细胞成分之间复杂的相互作用。已发表的数据表明,促纤维增生性间质可保护PC细胞免受化疗和放疗,并且可能促进PC细胞的增殖和迁移。然而,在动物研究中,促纤维增生性间质和CAF的实验性清除导致了更具侵袭性的癌症。因此,肿瘤间质在PC中的精确作用仍有待阐明。然而,对PC间质进行依赖于具体情况的治疗性修饰,而非单纯清除,可能为PC患者开发新的治疗策略带来潜力。