Abstract
We have previously demonstrated that BDS.1 cells are a minimal deviation rat hepatoma cell line that is hypersensitive to the anti-proliferative effects of glucocorticoids in vitro. When transplanted into athymic mice, exposure to dexamethasone reduced the initial growth rate and increased the latency time before detection of palpable BDS.1-derived tumors but did not affect the maximal growth rate, size and histology of the tumor. After collagenase dissociation, the in vitro growth of BDS.1-derived tumor cells was fully suppressed by dexamethasone. Exposure to insulin prevented the glucocorticoid inhibition of anchorage-independent growth of BDS.1 cell colonies in vitro and may therefore be one of the systemic factors that masks the long term in vivo growth response of glucocorticoids.
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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Body Weight / drug effects
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Carcinoma, Hepatocellular / drug therapy*
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Cell Adhesion / drug effects
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Cell Division / drug effects
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Cell Line
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Dexamethasone / pharmacology*
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Dose-Response Relationship, Drug
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Drug Antagonism
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Insulin / pharmacology
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Insulin-Like Growth Factor I / pharmacology
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Insulin-Like Growth Factor II / pharmacology
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Liver Neoplasms / drug therapy*
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Mammary Neoplasms, Animal / drug therapy
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Mice
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Mice, Nude
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Neoplasm Transplantation
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Neoplasms, Experimental
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Platelet-Derived Growth Factor / pharmacology
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Rats
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Transforming Growth Factor alpha / pharmacology
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Tumor Cells, Cultured
Substances
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Insulin
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Platelet-Derived Growth Factor
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Transforming Growth Factor alpha
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Insulin-Like Growth Factor I
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Insulin-Like Growth Factor II
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Dexamethasone