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Neuroendocrine carcinoma arising in a hepatitis C virus-infected liver: mechanism of the tumor development may be similar to that of development of pancreatic neuroendocrine cells.

机译:在C型肝炎病毒感染的肝脏中发生的神经内分泌癌:肿瘤的发生机制可能与胰腺神经内分泌细胞的发生机制相似。

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摘要

We experienced a case of neuroendocrine carcinoma (NC). The tumor developed in the cirrhotic liver of a 62-year-old Japanese man who had been infected with hepatitis C virus. The tumor cells showed high N/C ratio, formed many rosettes, and expressed CD56, synaptophysin, HepPar1 and pancreatic and duodenal homeobox 1. MIB1 expression was 65%. Because both liver and pancreas are derived from a common endodermal layer during fetal development, we speculated that the tumor may have formed via the interaction of neurogenin 3, insulinoma-associated 1 gene and NeuroD/beta2, which are involved in the stage at which some pancreatic cells commit to becoming endocrine cells. Molecular analysis revealed that the NC had higher relative expression levels of mRNA of the three molecules than did the nontumorous liver. The results indicate that the NC in this patient may have formed via the same mechanism that acts in the development of pancreatic neuroendocrine cells.
机译:我们经历了一例神经内分泌癌(NC)。该肿瘤在一名感染了丙型肝炎病毒的62岁日本男子的肝硬化肝脏中发展。肿瘤细胞显示高N / C比,形成许多玫瑰花结,并表达CD56,突触素,HepPar1和胰腺和十二指肠同源盒1。MIB1表达为65%。由于肝脏和胰腺均来自胎儿发育过程中的共同内胚层,因此我们推测该肿瘤可能是由于神经生成素3,胰岛素瘤相关的1基因和NeuroD / beta2的相互作用而形成的,它们参与了某些阶段胰腺细胞致力于成为内分泌细胞。分子分析表明,与非肿瘤肝相比,NC具有较高的三个分子mRNA相对表达水平。结果表明,该患者的NC可能是通过与胰腺神经内分泌细胞发育相同的机制形成的。

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