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Current treatment strategy for chronic myeloid leukemia (CML) mainly includesinhibition of tyrosine kinase activity, which has dramatically improved theprognosis of the disease but without cure. In addition some patients may becomedrug resistant. Thus there is still the need for other therapies to avoidresistance and if possible to cure the disease. Loss of p53 is known to play animportant role in the disease progression of CML and causes drug resistance.Here I propose that in CML, inositol requiring enzyme 1 alpha (IRE1 alpha) maycause abnormal degradation of p53 mRNA resulting in inhibition of apoptosis inleukemic clonal cells, which has not been elucidated before. Hence, I proposethat inhibition of endoribonuclease activity of IRE1 alpha with small moleculeinhibitors may provide a novel strategy to enhance p53 function in CML leukemicclones to overcome the limitations of current treatment regimens.

IRE1 alpha may be causing abnormal loss of p53 at post transcriptional level in chronic myeloid leukemia