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A previous study comparing the conditional mutations of p53 LSL-R270H , p53 LSL-R172H and the p53 fl/fl allele in the Kras LSL-G12D/+ mouse model of LUAD revealed that while for all alterations the LOF effects were sufficient to promote Kras -initiated LUAD and drive metastasis to regional lymph nodes and distant organ sites, such as kidney in a small number of mice, the transcriptional processes governed by p53 to elicit this metastatic phenotype is however poorly understood

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