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Tumour suppressors

Selective justice

Nature Reviews Cancer volume 11, pages 4–5 (2011)Cite this article

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Both groups used a slightly different mouse model of lung cancer that each expresses oncogenically activated KrasG12D. They also used different strategies to restore p53. Tyler Jacks and colleagues used lox-stop-lox Trp53 knock-in alleles and a ubiquitously expressed Cre recombinase fused to a modified version of the oestrogen receptor (CreERT2). Tamoxifen was used to activate Cre, which removes the stop cassette and enables the transcription of Trp53. Gerard Evan and colleagues also used knock-in alleles of Trp53, but these alleles produce p53 fused to a different modified version of the oestrogen receptor (ERTAM), making the p53 protein, but not the gene, dependent on tamoxifen. Importantly, both models enable the transcription and expression of the exogenous Trp53 alleles from the endogenous Trp53 promoter.

both groups found that p53 expression had no effect on the development of low-grade lesions such as adenomas. p53 only made its presence felt as the tumours progressed to carcinomas

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ORIGINAL RESEARCH PAPERS

  1. Junttila, M. R. et al. Selective activation of p53-mediated tumour suppression in high grade tumours. Nature 468, 567–571 (2010)

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  2. Feldser, D. M. et al. Stage-specific sensitivity to p53 restoration during lung cancer progression. Nature 468, 572–575 (2010)

    Article  CAS  Google Scholar 

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  1. Nicola McCarthy
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McCarthy, N. Selective justice. Nat Rev Cancer 11, 4–5 (2011). https://doi.org/10.1038/nrc2987

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