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Colorectal cancer

POLR2A deletion with TP53 opens a window of opportunity for therapy

Nature Reviews Clinical Oncology volume 12, page 374 (2015)Cite this article

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Inactivation of the guardian of the genome, the tumour suppressor protein p53, is common in most human tumours. Despite tremendous efforts, no effective therapy aimed at restoring p53 activity has been successfully translated into the clinic. Now, Xiongbin Lu and colleagues highlight that co-depletion of TP53 and one of its neighbouring genes, POLR2A, renders cancer cells highly vulnerable to POLR2A inhibition, providing a new treatment strategy for tumours containing such genomic changes.

Copy-number losses targeting tumour suppressors often involve neighbouring genes that do not contribute to cancer development per se, but nevertheless generate a vulnerability that is exploitable for therapeutic development.

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References

  1. Liu, Y. et al. TP53 loss creates therapeutic vulnerability in colorectal cancer. Nature 520, 697–701 (2015)

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Authors
  1. Alessia Errico
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Errico, A. POLR2A deletion with TP53 opens a window of opportunity for therapy. Nat Rev Clin Oncol 12, 374 (2015). https://doi.org/10.1038/nrclinonc.2015.94

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