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：

D O I：

暂无

中图分类号：

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.

引用

页码：697 / 701

页数：4

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