چکیده (انگلیسی):

Neural cell adhesion molecule (NCAM/CD56) expression in acute myeloid leukemia (AML) has
been associated with extramedullary leukemia, multidrug resistance, shorter remission and
survival. Recently, Bloomfield et al. published a succinct review of issues surrounding the
AML prognostication and current therapeutics. However, we want to reiterate the prognostic
value and therapeutic potential of CD56 that is frequently expressed in AML as was also
reported by their own group earlier. In addition, novel RUNX1 isoforms contribute in controlling
CD56 expression in AML cells. Anti-CD56 antibody therapy deserves exploration as an arsenal
against AML patients expressing CD56. Relevantly, targeting RNA splicing machinery or RUNX1
isoform-specific siRNA may also become part of future therapeutic strategies for AML with CD56
overexpression.