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Novel anti-B-cell maturation antigen antibody-drug conjugate (GSK2857916) selectively induces killing of multiple myeloma.

Blood·2014
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Daratumumab granted breakthrough drug status.

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A phase 2 trial of lenalidomide, bortezomib, and dexamethasone in patients with relapsed and relapsed/refractory myeloma.

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Heterogeneity of genomic evolution and mutational profiles in multiple myeloma.

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International Myeloma Working Group consensus statement for the management, treatment, and supportive care of patients with myeloma not eligible for standard autologous stem-cell transplantation.

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Updated: Mar 14, 2026

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Vision Statement for Multiple Myeloma: Future Directions.

Kenneth C Anderson1

  • 1Jerome Lipper Multiple Myeloma Center, Dana-Farber Cancer Institute, Harvard Medical School, Boston, USA. kenneth_anderson@dfci.harvard.edu.

Cancer Treatment and Research
|October 4, 2016
PubMed
Summary
This summary is machine-generated.

Novel therapies targeting multiple myeloma vulnerabilities are urgently needed. Targeting protein degradation, immune response, and DNA damage early could transform myeloma into a chronic, curable disease.

Keywords:
Immune therapiesMultiple myelomaProtein degradationTargetted therapies

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Area of Science:

  • Hematology
  • Oncology
  • Immunology

Background:

  • Significant advancements in multiple myeloma management have been achieved with novel agents like immunomodulatory drugs and proteasome inhibitors.
  • Despite progress, there remains an urgent need for new therapeutic strategies to further improve patient outcomes.

Purpose of the Study:

  • To identify and discuss three key vulnerabilities in multiple myeloma for novel therapeutic targeting.
  • To explore the potential of early intervention in smouldering multiple myeloma to alter disease trajectory.

Main Methods:

  • Review of current therapeutic landscape and identification of emerging targets in multiple myeloma.
  • Analysis of biological pathways including protein degradation (ubiquitin-proteasome and aggresome), autologous immunity, and DNA damage response in myeloma cells.

Main Results:

  • Three critical vulnerabilities identified: 1) protein degradation pathways, 2) restoration of antimyeloma immunity, and 3) targeting aberrant biology from DNA damage.
  • Early application of therapies targeting these vulnerabilities, particularly in smouldering multiple myeloma, shows promise.

Conclusions:

  • Targeting these specific vulnerabilities offers a promising avenue for novel multiple myeloma therapies.
  • Early therapeutic intervention has the potential to significantly alter the natural history of multiple myeloma, potentially leading to a chronic and curable disease state.