TP53 loss creates therapeutic vulnerability in colorectal cancer

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 and Xiongbin Lu ()
Additional contact information
Yunhua Liu: The University of Texas MD Anderson Cancer Center
Xinna Zhang: The University of Texas MD Anderson Cancer Center
Cecil Han: The University of Texas MD Anderson Cancer Center
Guohui Wan: The University of Texas MD Anderson Cancer Center
Xingxu Huang: School of Life Science and Technology, ShanghaiTech University
Cristina Ivan: The University of Texas MD Anderson Cancer Center
Dahai Jiang: The University of Texas MD Anderson Cancer Center
Cristian Rodriguez-Aguayo: Center for RNA Interference and Non-coding RNAs, The University of Texas MD Anderson Cancer Center
Gabriel Lopez-Berestein: Center for RNA Interference and Non-coding RNAs, The University of Texas MD Anderson Cancer Center
Pulivarthi H. Rao: Baylor College of Medicine
Dipen M. Maru: The University of Texas MD Anderson Cancer Center
Andreas Pahl: Heidelberg Pharma GmbH
Xiaoming He: The Ohio State University
Anil K. Sood: The University of Texas MD Anderson Cancer Center
Lee M. Ellis: The University of Texas MD Anderson Cancer Center
Jan Anderl: Heidelberg Pharma GmbH
Xiongbin Lu: The University of Texas MD Anderson Cancer Center

Nature, 2015, vol. 520, issue 7549, 697-701

Abstract: 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.

Date: 2015
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DOI: 10.1038/nature14418

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