Acyclovir (ACV), a nucleoside analog, has been demonstrated previously
to suppress selectively the proliferation of NIH3T3 fibroblastic cell
s transformed by either v-abl or bcr-abl gene transfection. From a vie
wpoint of clinical application of ACV, we investigated whether ACV inh
ibited the growth of leukemia cells expressing either p210(BCR-ABL) or
p185(BCR-ABL). Acyclovir exerted an inhibitory effect on OM9;22 cells
, p185(BCR-ABL) expressing cells, in a dose-dependent manner. Despite
no down-modulation of a BCR-ABL tyrosine kinase activity or its expres
sion was observed after treatment with ACV, cell cycle analysis demons
trated synchronization of OM9;22 cells at the G0/G1 phase. This sugges
ts that, although ACV does not directly act on BCR-ABL tyrosine kinase
, ACV may exert its inhibitory effect on some leukemia cell lines via
alterations of the cell cycle. Although selective inhibition of Philad
elphia chromosome-positive leukemia cell growth was not apparent, our
data provides a therapeutic possibility for ACV in the treatment for l
eukemia. Copyright (C) 1996 Elsevier Science Ltd.