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. 2020 Oct 1;105(10):2358-2367.
doi: 10.3324/haematol.2020.247015.

Multiple myeloma: the (r)evolution of current therapy and a glance into future

Affiliations

Multiple myeloma: the (r)evolution of current therapy and a glance into future

Annamaria Gulla et al. Haematologica. .

Abstract

Over the past 20 years, the regulatory approval of several novel agents to treat multiple myeloma (MM) has prolonged median patient survival from 3 to 8-10 years. Increased understanding of MM biology has translated to advances in diagnosis, prognosis, and response assessment, as well as informed the development of targeted and immune agents. Here we provide an overview of the recent progress in MM, and highlight research areas of greatest promise to further improve patient outcome in the future.

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Figures

Figure 1.
Figure 1.
Overview of the different anti-multiple myeloma (MM) strategies discussed in the review. Purple: strategies designed to directly target MM cell vulnerabilities; we can distinguish those exploiting “lineage dependencies” or “clonal dependencies”. (Center) Strategy targeting “epigenetic modifications” that may broadly affect both lineage and clonal vulnerabilities. (Bottom, yellow) Strategies aiming to disrupt MM-bone marrow microenvironment (BMM) interplay and restore host immunosurveillance. Purple double pointed arrows: MM-related approaches; yellow double pointed arrows: BMM-related approaches. These highlight the fact that one specific treatment, even in case of target therapy, may also affect multiple cellular components/interactions thus amplifying the therapeutic effects. OB: osteoblast; OC: osteoclasts; BMEC: bone marrow endothelial cells; ECM: extracellular matrix; BMSC: bone marrow stromal cells; DC: dendritic cell; pDC: plasmacytoid DC; MDSC: myeloid derived suppressor cells; Treg: regulatory T cell.
Graphical Abstract
Graphical Abstract

References

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