Abstract
Lovastatin (LOV), until now largely used for the treatment of hypercholesterolemia is a new promising drug in multiple myeloma (MM), however, the precise mechanism of its antitumor activity is not clear yet. It is probable that this effect is mediated by down-regulation of BCL-2 expression. In this study, we analyzed BCL-2 and BAX expression in cells of MM patients exposed to LOV in short-term culture. The obtained results indicate an increase in susceptibility to apoptosis both in CD138+ malignant cells and CD8+ T lymphocytes. Interestingly, such a tendency was confirmed in vivo in MM patient subjected to 3 cycles of LOV therapy.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Apoptosis / drug effects*
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Bone Marrow
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CD4-Positive T-Lymphocytes / drug effects
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CD8-Positive T-Lymphocytes / drug effects
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Gene Expression / drug effects
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Gene Expression Regulation, Neoplastic / drug effects*
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Genes, bcl-2 / drug effects*
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Humans
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Hydroxymethylglutaryl-CoA Reductase Inhibitors / pharmacology*
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Lovastatin / pharmacology*
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Multiple Myeloma / genetics
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Multiple Myeloma / metabolism*
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Plasma Cells / drug effects
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Proto-Oncogene Proteins c-bcl-2 / biosynthesis*
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bcl-2-Associated X Protein
Substances
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BAX protein, human
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Hydroxymethylglutaryl-CoA Reductase Inhibitors
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Proto-Oncogene Proteins c-bcl-2
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bcl-2-Associated X Protein
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Lovastatin