Inflammation and de-differentiation in pancreatic carcinogenesis
Inflammation and de-differentiation in pancreatic carcinogenesis
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DOI：
10.12998/wjcc.v6.i15.882
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发表时间：
2018-12
影响因子：
1.1
通讯作者：
Takahiro Seimiya;M. Otsuka;Takuma Iwata;Eri Tanaka;Tatsunori Suzuki;Kazuma Sekiba;M. Yamagami;Rei Ishibashi;K. Koike
中科院分区：
文献类型：
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作者：
Takahiro Seimiya;M. Otsuka;Takuma Iwata;Eri Tanaka;Tatsunori Suzuki;Kazuma Sekiba;M. Yamagami;Rei Ishibashi;K. Koike
胰腺癌是一种预后极差的恶性肿瘤。慢性胰腺炎是众所周知的胰腺癌的危险因素。炎症被认为通过DNA损伤和细胞内信号通路的激活来影响癌症的发生。在胰腺器官发生和细胞分化的每个阶段，许多转录因子和信号通路共同决定和维持细胞的特性。最近的研究表明，癌症的发生是通过抑制与分化相关的转录因子来促进的。胰腺炎还表现出转录变化，提示多因素表观遗传变化导致分化受损。综上所述，这些因素可能构成胰腺癌发生的重要框架。在这篇综述中，我们讨论了炎症和去分化在胰腺癌发展中的作用，以及新的治疗应用的未来。
Pancreatic cancer is a malignancy with an extremely poor prognosis. Chronic pancreatitis is a well-known risk factor for pancreatic cancer. Inflammation is thought to influence carcinogenesis through DNA damage and activation of intracellular signaling pathways. Many transcription factors and signaling pathways co-operate to determine and maintain cell identity at each phase of pancreatic organogenesis and cell differentiation. Recent studies have shown that carcinogenesis is promoted through the suppression of transcription factors related to differentiation. Pancreatitis also demonstrates transcriptional changes, suggesting that multifactorial epigenetic changes lead to impaired differentiation. Taken together, these factors may constitute an important framework for pancreatic carcinogenesis. In this review, we discuss the role of inflammation and de-differentiation in the development of pancreatic cancer, as well as the future of novel therapeutic applications.