Abstract

Multiple myeloma is an invariably fatal cancer of plasma cells. Despite tremendous advances in treatment, this malignancy remains incurable in most individuals. We postulate that strategies aimed at prevention have the potential to be more effective in preventing myeloma-related death than additional pharmaceutical strategies aimed at treating advanced disease. Here, we present a rationale for the development of prevention therapy and highlight potential target areas of study.

Highlights

  • Monoclonal Gammopathy of Undetermined Significance (MGUS) Itself Is Not a Benign ConditionPre-malignant condition has been termed to be of “undetermined significance” in pre-malignant condition has been termed to be of “undetermined significance” in terms of the transition to MM, it does not mean that it is not clinically important

  • Compared with other solid tumor cancers that have been subject to multiple, large screening and Compared with other solid tumor cancers that have been subject to multiple, large screening prevention trials, there have yet been no efforts to try and prevent the development of multiple and prevention trials, there have yet been no efforts to try and prevent the development of multiple myeloma

  • We previously reviewed the literature linking obesity with the progression of multiple myeloma [55] and much attention has been given to understanding the mechanism that link these two pathologies

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Summary

MGUS Itself Is Not a Benign Condition

Pre-malignant condition has been termed to be of “undetermined significance” in pre-malignant condition has been termed to be of “undetermined significance” in terms of the transition to MM, it does not mean that it is not clinically important. Associated pathologies include sensorimotor neuropathy [15], renal Falconi syndrome [16] and and glomerulonephritis [17,18], POEMS [19], capillary leak syndrome [20], ocular disease [21,22], glomerulonephritis [17,18], POEMS [19], capillary leak syndrome [20], ocular disease [21,22], and and crystal storing histiocytosis [23,24,25], among others. There may be value in defining intervention strategies to reduce monoclonal antibody populations, beyond preventing the MGUS to MM transition.

Factors Associated with the MGUS to MM Transition
Race as a Risk Factor in MM
Uniquely Dysregulated Genes in Plasma Cells of MGUS
Antigenic Stimulation
Obesity and Inflammation
Immune Dysregulation
Use of Mathematical Models in Studying Prevention
Obesity Intervention
Metformin
Vitamin Deficiency
Sleep Disturbance and Intermittent Hypoxia
Additional Modifiers of the Inflammatory Response
Conclusions

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