Abstract
Cytotoxic nucleoside analogues are widely used in treatment of patients with hematological malignancies as well as for some solid tumors. Resistance developed against these molecules limit their clinical use. Many studies on cell models and clinical samples have identified cellular mechanisms involved in this phenomenon. Here, we describe the available data concerning the proteins involved in the metabolism and the mechanism of action of nucleoside analogues, as well as the clinical studies showing their implication in the resistance to these drugs.
Publication types
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English Abstract
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Research Support, Non-U.S. Gov't
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Review
MeSH terms
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Antimetabolites, Antineoplastic / metabolism*
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Antimetabolites, Antineoplastic / therapeutic use
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Apoptosis
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Cladribine / metabolism
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Cladribine / therapeutic use
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Cytarabine / metabolism
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Cytarabine / therapeutic use
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Deoxycytidine / analogs & derivatives*
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Deoxycytidine / metabolism
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Deoxycytidine / therapeutic use
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Deoxycytidine Kinase / metabolism
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Drug Resistance, Neoplasm / physiology*
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Gemcitabine
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Humans
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Nucleoside Transport Proteins / metabolism*
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Nucleosides / metabolism*
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Phosphorylation
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Vidarabine / analogs & derivatives*
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Vidarabine / metabolism
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Vidarabine / therapeutic use
Substances
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Antimetabolites, Antineoplastic
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Nucleoside Transport Proteins
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Nucleosides
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Cytarabine
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Deoxycytidine
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Cladribine
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Deoxycytidine Kinase
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Vidarabine
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fludarabine
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Gemcitabine