Multiple Myeloma

Pathophysiology

Multiple myeloma is an incurable hematologic cancer of plasma cells characterized by increased monoclonal (M) protein levels due to proliferation of malignant clonal plasma cells.1-4 Plasma cells transform into malignant myeloma cells through the acquisition of genetic events, activation of key signaling pathways, and aberrant stromal and cellular signaling.5-12 The pathophysiology of multiple myeloma is characterized by promotion of immune dysregulation, malignant plasma cell survival, and aberrant stromal-cell support.5,13-17 Multiple myeloma is associated with regrowth of residual tumor and immune suppression.18,19 Malignant plasma cells are able to evade detection by the immune system through altering their phenotype and simultaneously inducing the production of immune-suppressing cytokines and other molecules.19

Landscape

In multiple myeloma, significant treatment advances have been made. Some areas of research focus on the high burden of both the disease and its treatments, identifying treatment strategies for specific populations (including transplant-ineligible patients and elderly, unfit, and high-risk patients), the role of salvage therapies, treatment-resistant disease, and clonal evolution.20-22 The current landscape continues to expand, and investigational therapies include cereblon E3 ligase modulators, antibodies targeting plasma cells, chimeric antigen receptor T cell therapy, bi-specific T-cell engager antibodies, and antibody-drug conjugates.21-23

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The safety and efficacy of the agents and/or uses under investigation have not been established. There is no guarantee that the agents will receive health authority approval or become commercially available in any country for the uses being investigated.

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In Our Pipeline

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Clinical trial information is sourced from ClinicalTrials.gov. Information is updated manually as clinical trials are published. The efficacy and safety of the agents and/or uses under investigation have not been established. There is no guarantee that the agents will receive health authority approval or become commercially available in any country for the uses being investigated.

References

  1. International Myeloma Working Group. Br J Haematol. 2003;121:749-757. PMID: 12780789
  2. Kyle RA, et al. Best Pract Res Clin Haematol. 2007;20:637-664. PMID: 18070711
  3. Harousseau J-L. Cancer Treat Rev. 2010;36(suppl 2):S33-S35. PMID: 20472187
  4. Dimopoulos MA, et al. Leukemia. 2009;23:2147-2152. PMID: 19626046
  5. Morgan GJ, et al. Nat Rev Cancer. 2012;12:335-348. PMID: 22495321
  6. Raab MS, et al. Lancet. 2009;374:324-339. PMID: 19541364
  7. Podar K, et al. Expert Opin Emerg Drugs. 2009;14:99-127. PMID: 19249983
  8. Gupta D, et al. Leukemia. 2001;15:1950-1961. PMID: 11753617
  9. Jourdan M, et al. Eur Cytokine Netw. 1999;10:65-70. PMID: 10210775
  10. Laubach J, et al. Ann Rev Med. 2011;62:249-264. PMID: 21090965
  11. Shaffer AL, et al. Clin Cancer Res. 2009;15:2954-2961. PMID: 19383829
  12. Leung-Hagesteijn C, et al. Cancer Cell. 2013;24:289-304. PMID: 24029229
  13. Zheng MM, et al. PLoS ONE. 2013;8:e58504. PMID: 23544044
  14. Bernal M, et al. Hum Immunol. 2009;70:854-857. PMID: 19580833
  15. Holien T, et al. Blood. 2012;120:2450-2453. PMID: 22806891
  16. Braga WM, et al. Clin Dev Immunol. 2012;2012:293479. PMID: 22489248
  17. Damiano JS, et al. Blood. 1999;93:1658-1667. PMID: 10029595
  18. Corradini P, et al. Blood. 2003;102:1927-1929. PMID: 12738666
  19. Cook G, et al. Blood Rev. 1999;13:151-162. PMID: 10527267
  20. Monterosso L, et al. J Patient Exp. 2018;5:6-15. PMID: 29582005
  21. Chim CS, et al. Leukemia. 2018;32:252-262. PMID: 29257139
  22. Minnema M, Gavriatopoulou M. Eur Oncol Haematol. 2018;14:96-104.
  23. Rasco DW, et al. Clin Cancer Res. 2019;25:90-98. PMID: 30201761