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Updated: Feb 14, 2026

An Organotypic High Throughput System for Characterization of Drug Sensitivity of Primary Multiple Myeloma Cells
Published on: July 15, 2015
Targeting MYC in multiple myeloma
K K Jovanović1, C Roche-Lestienne1,2, I M Ghobrial3
1IRCL, INSERM UMR-S1172, Univ. Lille, Lille, France.
Abstract:
Multiple myeloma (MM) is a plasma cell tumor marked by clonal evolution and preceded by a premalignant stage, which progresses via molecular pathway deregulation, including MYC activation. This activation relates to translocation or gain of the MYC locus and deregulation of upstream pathways such as IRF4, DIS3/LIN28B/let-7, or MAPK. Precision medicine is an approach to predict more accurately which treatment strategies for a particular disease will work in which groups of patients, in contrast to a "one-size-fits-all" approach. The knowledge of mechanisms responsible for MYC deregulation in MM enables identification of vulnerabilities and therapeutic targets in MYC-driven tumors. MYC can be targeted directly or indirectly, by interacting with several of its functions in cancer. Several such therapeutic strategies are evaluated in clinical trials in MM. In this review, we describe the mechanism of MYC activation in MM, the role of MYC in cancer progression, and the therapeutic options to targeting MYC.
Insights
Multiple myeloma involves MYC gene activation, a key driver of cancer progression. Targeting MYC offers precision medicine strategies for treating this plasma cell tumor.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Multiple myeloma (MM) is a plasma cell malignancy characterized by clonal evolution.
- MYC activation, often via genetic alterations, is a critical step in MM progression.
- Understanding MYC deregulation is crucial for developing targeted therapies.
Purpose of the Study:
- To review the mechanisms of MYC activation in multiple myeloma.
- To elucidate the role of MYC in MM pathogenesis and cancer progression.
- To discuss current and emerging therapeutic strategies targeting MYC in MM.
Main Methods:
- Literature review of molecular mechanisms and genetic alterations.
- Analysis of pathways regulating MYC expression (e.g., IRF4, MAPK).
- Examination of preclinical and clinical data on MYC-targeted therapies.
Main Results:
- MYC activation in MM results from genetic events like translocations or locus gain.
- Deregulation involves upstream pathways including IRF4 and DIS3/LIN28B/let-7.
- MYC plays a significant role in the clonal evolution and progression of MM.
- Targeting MYC directly or indirectly presents therapeutic vulnerabilities.
Conclusions:
- MYC activation is a pivotal event in multiple myeloma development and progression.
- Targeting MYC offers a promising avenue for precision medicine in MM.
- Further clinical evaluation of MYC-directed therapies is warranted for MM patients.
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