Chirurgische Klinik und Poliklinik, Klinikum rechts der Isar, Technische Universität München, Ismaningerstrasse 22, 81675, Munich, Germany.
Langenbecks Arch Surg. 2010 Apr;395(4):295-308. doi: 10.1007/s00423-010-0622-5. Epub 2010 Mar 18.
The purpose of this review is to highlight the molecular mechanisms leading to the development and progression of pancreatic ductal adenocarcinoma (PDAC) with particular emphasis on tumor cell proliferation, local invasion, and metastasis. Recent advances in the field of PDAC biology have shed light on the molecular events that trigger PDAC initiation and maintenance.
It is now clear that apart from the genetic alterations within the tumor cells, interactions of the tumor with its environment are necessary for proliferation and invasion. Interestingly, a number of developmental signaling pathways are reactivated in PDAC. Progress has also been made in the understanding of the molecular events that govern the process of metastasis.
Although our understanding of the mechanisms underlying PDAC pathobiology are more advanced than ever, little progress has been made in the clinical treatment of PDAC, and successful bench-to-bedside transfer of knowledge to boost new treatment options is still unsatisfying.
本文旨在强调导致胰腺导管腺癌 (PDAC) 发生和进展的分子机制,特别强调肿瘤细胞增殖、局部侵袭和转移。PDAC 生物学领域的最新进展揭示了触发 PDAC 起始和维持的分子事件。
现在很明显,除了肿瘤细胞内的遗传改变外,肿瘤与其环境的相互作用对于增殖和侵袭是必需的。有趣的是,许多发育信号通路在 PDAC 中被重新激活。在理解控制转移过程的分子事件方面也取得了进展。
尽管我们对 PDAC 病理生物学机制的理解比以往任何时候都更加深入,但在 PDAC 的临床治疗方面几乎没有取得进展,成功地将知识从实验室转移到临床以增加新的治疗选择仍然令人不满意。