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Tumor cross-talk networks promote growth and support immune evasion in pancreatic cancer

机译:肿瘤串扰网络促进胰腺癌的生长和支持免疫逃避

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摘要

In the event of an injury, normal tissues exit quiescent homeostasis and rapidly engage a complex stromal and immune program. These tissue repair responses are hijacked and become dysregulated in carcinogenesis to form a growth-supportive tumor microenvironment. In pancreatic ductal adenocarcinoma (PDA), which remains one of the deadliest major cancers, the microenvironment is a key driver of tumor maintenance that impedes many avenues of therapy. In this review, we outline recent efforts made to uncover the microenvironmental cross-talk mechanisms that support pancreatic cancer cells, and we detail the strategies that have been undertaken to help overcome these barriers.
机译:如果发生伤害,正常组织出口静态稳态,并迅速接触复杂的基质和免疫计划。 这些组织修复反应被劫持并在致癌物中变得在致癌物中以形成生长支持性肿瘤微环境。 在胰腺导管腺癌(PDA)中,仍然是最致命的主要癌症之一,微环境是肿瘤维持的关键驱动器,其阻碍了许多治疗途径。 在这篇综述中,我们概述了最近努力揭示支持胰腺癌细胞的微环境跨谈机制,我们详细说明了有助于克服这些障碍的策略。

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