ArticleHaematologica2025
Acid ceramidase controls proteasome inhibitor resistance and is a novel therapeutic target for the treatment of relapsed/refractory multiple myeloma.
Article in Haematologica, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
3 citing papers in PubMed.
- Proteasome Dysregulation in Parkinson's Disease: Insights from Blood-Based Analyses.Molecular neurobiology · 2025Article
- The Involvement of Ceramide, Sphingosine-1-Phosphate and Ganglioside GM1 in Regulating Some Nervous System Functions.International journal of molecular sciences · 2025Review
- Unlocking acid ceramidase: a new weapon against proteasome chemoresistance in myeloma.Haematologica · 2025Article
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Authors and funding
16 authors.
Funding
Abstract
Multiple myeloma (MM) patients are often refractory to targeted therapies including proteasome inhibitors. Here, analysis of RNA sequencing data derived from 672 patients with newly diagnosed or relapsed/refractory disease identified the acid ceramidase, ASAH1, as a key regulator of resistance to proteasome inhibitors. Genetic or pharmacological blockade of ASAH1 remarkably restored sensitivity to proteasome inhibitors and protected mice from resistant MM progression in vivo. Mechanistically, ASAH1 depletion of ceramide promoted SET inhibition of PP2A phosphatase activity, thus facilitating increased expression and activity of the pro-survival proteins, MCL-1 and BCL-2. We corroborated these findings in human MM datasets, and in ex vivo patients' MM cells. These preclinical studies suggest that ASAH1 may be a potential therapeutic target for the treatment of relapsed/refractory MM.
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Registered trials
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