TP53 loss creates therapeutic vulnerability in colorectal cancer

被引：0
|
作者：
Yunhua Liu
Xinna Zhang
Cecil Han
Guohui Wan
Xingxu Huang
Cristina Ivan
Dahai Jiang
Cristian Rodriguez-Aguayo
Gabriel Lopez-Berestein
Pulivarthi H. Rao
Dipen M. Maru
Andreas Pahl
Xiaoming He
Anil K. Sood
Lee M. Ellis
Jan Anderl
Xiongbin Lu
机构：
[1] The University of Texas MD Anderson Cancer Center,Department of Cancer Biology
[2] The University of Texas MD Anderson Cancer Center,Department of Gynaecologic Oncology and Reproductive Medicine
[3] Center for RNA Interference and Non-coding RNAs,Department of Experimental Therapeutics
[4] The University of Texas MD Anderson Cancer Center,Department of Paediatrics
[5] School of Life Science and Technology,Department of Pathology
[6] ShanghaiTech University,Department of Biomedical Engineering
[7] The University of Texas MD Anderson Cancer Center,Department of Surgical Oncology
[8] Baylor College of Medicine,undefined
[9] The University of Texas MD Anderson Cancer Center,undefined
[10] Heidelberg Pharma GmbH,undefined
[11] The Ohio State University,undefined
[12] The University of Texas MD Anderson Cancer Center,undefined
来源：
Nature | 2015年 / 520卷
关键词：
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学科分类号：
摘要：
Genomic deletion of the tumour suppressor TP53 frequently includes other neighbouring genes, such as the POLR2A housekeeping gene that encodes a crucial RNA polymerase II subunit; suppression of POLR2A with α-amanitin or by RNA interference selectively inhibits the tumorigenic potential of cancer cells, and in mouse models of cancer, tumours can be selectively targeted with α-amanitin coupled to antibodies, suggesting new therapeutic approaches for human cancers.
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页码：697 / 701
页数：4
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