中国科学院机构知识库网格
Chinese Academy of Sciences Institutional Repositories Grid
CDKN2B deletion is essential for pancreatic cancer development instead of unmeaningful co-deletion due to juxtaposition to CDKN2A

文献类型:期刊论文

作者Shi P*4; Jiao B4; Chen C2; Zhou X2,3; Lai R2; Tu Q2,3; Hao J4; Sun B2,3; Yang D2,3; An S2,3
刊名Oncogene
出版日期2017
卷号**期号:**页码:publication online
英文摘要Pancreatic cancer is among the deadliest malignancies; however, the genetic events that lead to pancreatic carcinogenesis in adults remain unclear. In vivo models in which these genetic alterations occur in adult animals may more accurately reflect the features of human cancer. In this study, we demonstrate that inactivation of Cdkn2b (p15ink4b) is necessary for induction of pancreatic cancer by oncogenic KRASG12D expression and inactivation of Tp53 and Cdkn2a in adult mouse pancreatic ductal cells (P60 or older). KRASG12D overexpression in these cells activated transforming growth factor-β signaling and expression of CDKN2B, which, along with CDKN2A, led to cellular senescence and protected cells from KRAS-mediated transformation via inhibition of retinoblastoma phosphorylation. These results show a critical role of CDKN2B inactivation in pancreatic carcinogenesis, and provide a useful adult animal model by genetic engineering via lentiviral delivery.
语种英语
资助机构This work was supported by by the ‘Strategic Priority Research Program’ of the Chinese Academy of Sciences (grant no. XDB13020400 to PS and XDA 01040403 to XZ), the National Natural Science Foundation of China (NSFC, 81472862) and the Top Talents Program of Yunnan Province, China (2012HA014) to XZ. ; This work was supported by by the ‘Strategic Priority Research Program’ of the Chinese Academy of Sciences (grant no. XDB13020400 to PS and XDA 01040403 to XZ), the National Natural Science Foundation of China (NSFC, 81472862) and the Top Talents Program of Yunnan Province, China (2012HA014) to XZ. ; This work was supported by by the ‘Strategic Priority Research Program’ of the Chinese Academy of Sciences (grant no. XDB13020400 to PS and XDA 01040403 to XZ), the National Natural Science Foundation of China (NSFC, 81472862) and the Top Talents Program of Yunnan Province, China (2012HA014) to XZ. ; This work was supported by by the ‘Strategic Priority Research Program’ of the Chinese Academy of Sciences (grant no. XDB13020400 to PS and XDA 01040403 to XZ), the National Natural Science Foundation of China (NSFC, 81472862) and the Top Talents Program of Yunnan Province, China (2012HA014) to XZ.
源URL[http://159.226.149.26:8080/handle/152453/12040]  
专题昆明动物研究所_动物模型与人类重大疾病机理重点实验室
昆明动物研究所_遗传资源与进化国家重点实验室
昆明动物研究所_动物毒素室
昆明动物研究所_进化与功能基因组学
昆明动物研究所_肿瘤生物学
昆明动物研究所_肿瘤干细胞生物学
昆明动物研究所_发育的印迹调控与进化学
昆明动物研究所_中国科学院昆明灵长类研究中心
通讯作者ship@mail.kiz.ac.cn; zhaoxudong@mail.kiz.ac.cn
作者单位1.Kunming Primate Research Center, Chinese Academy of Sciences, Kunming, China
2.Key Laboratory of Animal Models and Human Disease Mechanisms of Chinese Academy of Sciences/Key Laboratory of Bioactive Peptides of Yunnan Province, Kunming Institute of Zoology, Kunming, China;
3.Kunming College of Life Science, University of Chinese Academy of Sciences, Kunming, China
4.State Key Laboratory of Genetic Resources and Evolution, Laboratory of Evolutionary and Functional Genomics, Kunming Institute of Zoology, Chinese Academy of Sciences, Kunming, China
5.KIZ-SU Joint Laboratory of Animal Model and Drug Development, College of Pharmaceutical Sciences, Soochow University, Suzhou, China
推荐引用方式
GB/T 7714
Shi P*,Jiao B,Chen C,et al. CDKN2B deletion is essential for pancreatic cancer development instead of unmeaningful co-deletion due to juxtaposition to CDKN2A[J]. Oncogene,2017,**(**):publication online.
APA Shi P*.,Jiao B.,Chen C.,Zhou X.,Lai R.,...&Zhao X*.(2017).CDKN2B deletion is essential for pancreatic cancer development instead of unmeaningful co-deletion due to juxtaposition to CDKN2A.Oncogene,**(**),publication online.
MLA Shi P*,et al."CDKN2B deletion is essential for pancreatic cancer development instead of unmeaningful co-deletion due to juxtaposition to CDKN2A".Oncogene **.**(2017):publication online.

入库方式: OAI收割

来源:昆明动物研究所

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