Identification of Sox9-Dependent Acinar-to-Ductal Reprogramming as the Principal Mechanism for Initiation of Pancreatic Ductal Adenocarcinoma

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Identification of Sox9-Dependent Acinar-to-Ductal Reprogramming as the Principal Mechanism for Initiation of Pancreatic Ductal Adenocarcinoma

机译：依赖Sox9的从腺到口腔的重编程是胰腺导管腺癌起始的主要机制。

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Tumors are largely classified by histologic appearance, yet morphologic features do not necessarily predict cellular origin. To determine the origin of pancreatic ductal adenocarcinoma (PDA), we labeled and traced pancreatic cell populations after induction of a PDA-initiating Kras mutation. Our studies reveal that ductal and stem-like centroacinar cells are surprisingly refractory to oncogenic transformation, whereas acinar cells readily form PDA precursor lesions with ductal features. We show that formation of acinar-derived premalignant lesions depends on ectopic induction of the ductal gene Sox9. Moreover, when concomitantly expressed with oncogenic Kras, Sox9 accelerates formation of premalignant lesions. These results provide insight into the cellular origin of PDA and suggest that its precursors arise via induction of a duct-like state in acinar cells.

机译：肿瘤在很大程度上根据组织学外观分类，但是形态学特征不一定能预测细胞起源。为了确定胰腺导管腺癌（PDA）的起源，我们在诱导PDA启动的Kras突变后标记和追踪胰腺细胞群。我们的研究表明，导管和干细胞样的中央棘突细胞对致癌转化具有令人惊讶的抵抗力，而腺泡细胞容易形成具有导管特征的PDA前体病变。我们表明腺泡来源的癌前病变的形成取决于导管基因Sox9的异位诱导。此外，当与致癌性Kras一起表达时，Sox9会加速癌前病变的形成。这些结果提供了对PDA细胞起源的洞察力，并暗示了其前体是通过在腺泡细胞中诱导导管样状态而产生的。

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《Cancer Cell》 |2012年第6期|共14页
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正文语种 eng
中图分类肿瘤学;
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1. Identification of Sox9-Dependent Acinar-to-Ductal Reprogramming as the Principal Mechanism for Initiation of Pancreatic Ductal Adenocarcinoma [J] . Cancer Cell . 2012,第6期

机译：依赖Sox9的从腺到口腔的重编程是胰腺导管腺癌起始的主要机制。
2. KLF4 Is Essential for Induction of Cellular Identity Change and Acinar-to-Ductal Reprogramming during Early Pancreatic Carcinogenesis [J] . Wei Daoyan, Wang Liang, Yan Yongmin, Cancer Cell . 2016,第3期

机译：KLF4是早期胰腺癌发生过程中诱导细胞身份变化和腺泡至牙齿重编程的关键。
3. Telomeres are shortened in acinar-to-ductal metaplasia lesions associated with pancreatic intraepithelial neoplasia but not in isolated acinar-to-ductal metaplasias [J] . Seung-Mo Hong, Christopher M Heaphy, Chanjuan Shi, Modern Pathology . 2011,第2期

机译：在与胰腺上皮内瘤变相关的腺泡到导管化生病变中端粒缩短，但在孤立的腺泡到导管化生中则不缩短
4. Cell surface proteomics-driven identification of pancreatic ductal adenocarcinoma subtypes [C] . Laura Postolache, Christian Eisen, Martin Sprick, American Society for Mass Spectrometry Conference on Mass Spectrometry and Allied Topics . 2012

机译：细胞表面蛋白质组学驱动的胰腺导管腺癌亚型的鉴定
5. Molecular Mechanisms of Resistance of Pancreatic Ductal Adenocarcinoma Cells to Oncolytic Vesicular Stomatitis Virus. [D] . Felt, Sebastien Alexandre. 2017

机译：胰导管腺癌细胞对溶瘤性水疱性口炎病毒的抗性分子机制。
6. Identification of Sox9-dependent acinar-to-ductal reprogramming as the principal mechanism for initiation of pancreatic ductal adenocarcinoma [O] . Janel L. Kopp, Guido von Figura, Erin Mayes, -1

机译：的识别sox9的依赖性腺泡到导管重编程为胰腺导管腺癌的开始时的主要机制
7. Identification of Sox9-Dependent Acinar-to-Ductal Reprogramming as the Principal Mechanism for Initiation of Pancreatic Ductal Adenocarcinoma [O] . Kopp Janel L., von Figura Guido, Mayes Erin, 2012

机译：确定Sox9依赖腺泡到口腔重编程为胰腺导管腺癌起始的主要机制。

Identification of Sox9-Dependent Acinar-to-Ductal Reprogramming as the Principal Mechanism for Initiation of Pancreatic Ductal Adenocarcinoma

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