Tumor microenvironment participates in metastasis of pancreatic cancer.

Tumor microenvironment participates in metastasis of pancreatic cancer.
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肿瘤微环境参与胰腺癌转移

DOI:
10.1186/s12943-018-0858-1
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发表时间:
2018-07-30
期刊:
影响因子:
37.3
通讯作者:
Zhao Y
Zhao Y
中科院分区:
医学1区
文献类型:
--
作者:
Ren B;Cui M;Yang G;Wang H;Feng M;You L;Zhao Y

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胰腺癌是一种致死性疾病,由于其早期诊断和转移的困难,死亡率很高。由胰腺上皮/癌细胞和基质细胞之间的相互作用诱导的肿瘤微环境对于胰腺癌进展至关重要,并且与化疗、放疗和免疫治疗的失败有关。微环境的形成需要胰腺癌细胞和基质细胞之间的相互作用。胰腺癌微环境中促进结缔组织增生和免疫抑制的成分与患者预后不良相关。这些组分可以促进原发和转移部位的结缔组织增生和免疫抑制,或者可以通过刺激血管生成/淋巴管生成、上皮-间质转化、侵袭/迁移和转移前小生境形成来促进转移。一些分子参与微环境形成和转移。在这篇综述中,我们专注于胰腺癌微环境形成的机制,并讨论胰腺癌微环境如何参与转移,代表了联合治疗以提高总生存率的潜在靶点。
Pancreatic cancer is a deadly disease with high mortality due to difficulties in its early diagnosis and metastasis. The tumor microenvironment induced by interactions between pancreatic epithelial/cancer cells and stromal cells is critical for pancreatic cancer progression and has been implicated in the failure of chemotherapy, radiation therapy and immunotherapy. Microenvironment formation requires interactions between pancreatic cancer cells and stromal cells. Components of the pancreatic cancer microenvironment that contribute to desmoplasia and immunosuppression are associated with poor patient prognosis. These components can facilitate desmoplasia and immunosuppression in primary and metastatic sites or can promote metastasis by stimulating angiogenesis/lymphangiogenesis, epithelial-mesenchymal transition, invasion/migration, and pre-metastatic niche formation. Some molecules participate in both microenvironment formation and metastasis. In this review, we focus on the mechanisms of pancreatic cancer microenvironment formation and discuss how the pancreatic cancer microenvironment participates in metastasis, representing a potential target for combination therapy to enhance overall survival.
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