<P> One study found that p53 and Myc proteins were key to the survival of Chronic Myeloid Leukaemia (CML) cells . Targeting p53 and Myc proteins with drugs gave positive results on mice with CML . </P> <P> Most p53 mutations are detected by DNA sequencing . However, it is known that single missense mutations can have a large spectrum from rather mild to very severe functional affects . </P> <P> The large spectrum of cancer phenotypes due to mutations in the TP53 gene is also supported by the fact that different isoforms of p53 proteins have different cellular mechanisms for prevention against cancer . Mutations in TP53 can give rise to different isoforms, preventing their overall functionality in different cellular mechanisms and thereby extending the cancer phenotype from mild to severe . Recents studies show that p53 isoforms are differentially expressed in different human tissues, and the loss - of - function or gain - of - function mutations within the isoforms can cause tissue - specific cancer or provides cancer stem cell potential in different tissues . TP53 mutation also hits energy metabolism and increases glycolysis in breast cancer cells . </P> <P> The dynamics of p53 proteins, along with its antagonist Mdm2, indicate that the levels of p53, in units of concentration, oscillate as a function of time . This "damped" oscillation is both clinically documented and mathematically modelled . Mathematical models also indicate that the p53 concentration oscillates much faster once teratogens, such as double - stranded breaks (DSB) or UV radiation, are introduced to the system . This supports and models the current understanding of p53 dynamics, where DNA damage induces p53 activation (see p53 regulation for more information). Current models can also be useful for modelling the mutations in p53 isoforms and their effects on p53 oscillation, thereby promoting de novo tissue - specific pharmacological drug discovery . </P>

What does a mutation in p53 lead to