Abstract
The growth and tumorigenicity of murine lung cancer cells transfected with an antisense cyclin D1 construct were evaluated in studies pertaining 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 treatment of human neoplasms of aerodigestive tract origin that either overexpress the cyclin D oncogene or exhibit mutations that influence cell cycle progression via cyclin D-dependent mechanisms.
Publication types
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Animals
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Blotting, Northern
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Cell Cycle
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Cell Division / drug effects
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Cyclin D
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Cyclins / analysis
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Cyclins / drug effects*
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Cyclins / genetics
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Gene Expression Regulation, Neoplastic / drug effects
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Gene Expression Regulation, Neoplastic / genetics
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Genetic Therapy / methods*
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Lung Neoplasms / chemically induced
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Lung Neoplasms / genetics
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Lung Neoplasms / pathology*
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Lung Neoplasms / prevention & control
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Mice
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Mice, Inbred BALB C
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Mice, Nude
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Neoplasm Transplantation
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Oligonucleotides, Antisense / pharmacology*
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Retinoblastoma Protein / analysis
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Suppression, Genetic
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Transfection
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Tumor Cells, Cultured
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Urethane
Substances
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Cyclin D
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Cyclins
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Oligonucleotides, Antisense
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Retinoblastoma Protein
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Urethane