PDF(Pubmed)
Abstract：
Pancreatic ductal adenocarcinomas are distinguished by their robust desmoplasia, or fibroinflammatory response. Dominated by non-malignant cells, the mutated epithelium must therefore combat, cooperate with or co-opt the surrounding cells and signalling processes in its microenvironment. It is proposed that an invasive pancreatic ductal adenocarcinoma represents the coordinated evolution of malignant and non-malignant cells and mechanisms that subvert and repurpose normal tissue composition, architecture and physiology to foster tumorigenesis. The complex kinetics and stepwise development of pancreatic cancer suggests that it is governed by a discrete set of organizing rules and principles, and repeated attempts to target specific components within the microenvironment reveal self-regulating mechanisms of resistance. The histopathological and genetic progression models of the transforming ductal epithelium must therefore be considered together with a programme of stromal progression to create a comprehensive picture of pancreatic cancer evolution. Understanding the underlying organizational logic of the tumour to anticipate and pre-empt the almost inevitable compensatory mechanisms will be essential to eradicate the disease.
摘要：
胰腺导管腺癌的特点是其强烈的血管增生，或纤维炎症反应。由非恶性细胞主导，因此，突变的上皮必须对抗，在其微环境中与周围的细胞和信号过程合作或共同选择。有人提出，浸润性胰腺导管腺癌代表了恶性和非恶性细胞的协调演变以及破坏和重新利用正常组织组成的机制，促进肿瘤发生的结构和生理学。胰腺癌的复杂动力学和逐步发展表明，它受一组离散的组织规则和原则的支配。并反复尝试靶向微环境中的特定成分，揭示了抵抗的自我调节机制。因此，必须将转化导管上皮的组织病理学和遗传进展模型与基质进展程序一起考虑，以创建胰腺癌演变的全面图片。了解肿瘤的潜在组织逻辑以预测和预防几乎不可避免的代偿机制对于根除疾病至关重要。
