The growth and tumorigenicity of murine lung cancer cells transfected
with an antisense cyclin D1 construct were evaluated in studies pertai
ning to mouse lung carcinogenesis. This antisense construct inhibited
the expression of cyclin D in these cells, significantly reducing both
their in vitro proliferation and tumorigenicity in nude mice relative
to control cells. These data may have implications regarding the trea
tment of human neoplasms of aerodigestive tract origin that either ove
rexpress the cyclin D oncogene or exhibit mutations that influence cel
l cycle progression via cyclin D-dependent mechanisms.