ArticleBlood neoplasia2026
IMiD/CELMoD resistance in myeloma is associated with changes in lipid metabolism that may be targetable.
Article in Blood neoplasia, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
1 citing paper in PubMed.
- SETD2 is a novel and druggable dependency in IMiD/CELMoD resistant multiple myeloma models.Blood cancer journal · 2026Article
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Authors and funding
21 authors.
Funding
Abstract
Immunomodulatory drugs (IMiDs) are a cornerstone of multiple myeloma treatment, and newer cereblon E3 ligase modulatory drugs (CELMoDs) are in clinical trials. However, a major barrier to improving patient outcomes is the inevitable development of resistance to these agents. To explore the mechanisms underlying IMiD/CELMoD resistance and identify novel targets for treatment, human cell line models of acquired IMiD/CELMoD resistance were generated. A quantitative proteome analysis of these models identified common changes in lipid synthesis proteins, and glucose-labeling experiments confirmed altered lipid flux. Proteomic analysis of paired patient samples at diagnosis and relapse on IMiD suggested similar changes in lipid pathways. A genome-wide CRISPR screen performed in a human multiple myeloma cell line with acquired CELMoD resistance identified dependencies in the lipid pathway genes stearoyl-CoA desaturase and membrane-bound transcription factor peptidase, site 1. This study has led to novel insights into lipid pathway changes in the IMiD/CELMoD-resistant state, which may represent targetable cancer cell vulnerabilities.
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Registered trials
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