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. 2015 Jan 22;6:5874. doi: 10.1038/ncomms6874

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Expression of mutant Lef1 results in defective DNA damage response and impairment of SC-specific surveillance mechanisms, including p53 activation. SCs γH2AX carrying high levels of DNA damage undergo apoptosis, mainly by blocking the normal Bcl-2 response. Bulge SCs (BSCs) with lower degree of damaged DNA escape normal control of SC proliferation to maintain the epidermal tissue. Consequently, these proliferative SCs carrying DNA breaks accumulate further mutations, thereby initiating tumour formation.