Using a model where K - ras
acts as an oncogene and initiates tumor formation, mice that were bred to not have Notch1 function showed an almost uniform distribution of about two cancerous lesions per mouse after 6 weeks, compared with approximately 14 tumors / mouse for those with Notch1 function still remaining.
In response to cellular stress such
as DNA damage,
oncogene activation, transcriptional inhibition, and hypoxia, tumor suppressor p53 is activated and expressed, and
acts as a transcription factor to induce its target genes [1], thereby playing a central role in the regulation of DNA repair, cell cycle, apoptosis, senescence, and angiogenesis [2 - 4].