Abstract
In multiple myeloma the duration of plateau is an important clinical and biological determinant of quality of life and survival. During plateau phase, the tumour is in an indolent state, as manifested by a low labelling index of plasma cells and other proliferative markers, e.g. the thymidine kinase level. The mechanism by which plasma cells escape from this indolent phase to a more aggressive phase of this disease is unknown, but a number of possible mechanisms have been postulated. These include loss of immunoregulation, clonal evolution, cytokine dysfunction and oncogene activation or tumour suppressor gene dysfunction. As current chemotherapy protocols do not appear to be able to eradicate the malignant clone, understanding the nature of the indolent phase of the malignant clone and the reasons for its escape from this phase are very important and may provide new options for disease control.
MeSH terms
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Antibodies, Anti-Idiotypic / immunology
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Antineoplastic Combined Chemotherapy Protocols / pharmacology
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Antineoplastic Combined Chemotherapy Protocols / therapeutic use
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Carrier Proteins / metabolism
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Cell Division
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Drug Resistance
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Gene Expression Regulation, Neoplastic
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Humans
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Immunity, Cellular
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Interleukin-6 / physiology
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Membrane Proteins / metabolism
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Multiple Myeloma / drug therapy
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Multiple Myeloma / genetics
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Multiple Myeloma / immunology
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Multiple Myeloma / pathology*
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Mutation
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Myeloma Proteins / biosynthesis
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Neoplastic Stem Cells / pathology
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Nucleoside Transport Proteins
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Nucleosides / metabolism
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Oncogenes
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Prognosis
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Receptors, Interleukin / physiology
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Receptors, Interleukin-6
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Receptors, Lymphocyte Homing / metabolism
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Remission Induction
Substances
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Antibodies, Anti-Idiotypic
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Carrier Proteins
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Interleukin-6
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Membrane Proteins
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Myeloma Proteins
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Nucleoside Transport Proteins
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Nucleosides
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Receptors, Interleukin
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Receptors, Interleukin-6
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Receptors, Lymphocyte Homing