ArticleEJHaem2025
Venetoclax in the Therapeutic Strategy for BPDCN Management.
Article in EJHaem, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
2 citing papers in PubMed.
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Corrections and comments
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Authors and funding
16 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Venetoclax, a B-cell lymphoma 2 (BCL-2) inhibitor, is a promising treatment for blastic plasmacytoid dendritic cell neoplasm (BPDCN) and is currently under evaluation in clinical trials. However, several case reports have reported relapses after prolonged treatment, and development of resistance. To date, no study has investigated resistance to venetoclax in BPDCN. Therefore, we sought to investigate the mechanisms that trigger resistance during treatment. Methods: We developed an in vitro model of chronic exposure of a BPDCN cell line to venetoclax that leads to resistance to the drug. We then characterized the resistant cell line using genomic and proteomic analyses and evaluated drug combinations to overcome the resistance. Results: We found an upregulation of BCL-xL, both at genomic and protein levels in the resistant BPDCN cell line. By combining venetoclax with a hypomethylating agent, we were able to overcome venetoclax resistance and induce resistant cell-line death. However, association with a proteasome inhibitor, known to be efficient against BPDCN, failed to restore sensitivity to venetoclax, probably due to modification of the NF-κB pathway observed by bulk-RNAseq analysis. Conclusions: Collectively, these data suggest that acquired venetoclax resistance in BPDCN is mediated by a modification of the balance of BCL-2 family proteins. Also, the mechanisms involved in resistance may also lead to resistance to other molecules among the drugs that might otherwise have been considered as alternative therapies. Clinical Trial Registration Including Trial Number: The authors have confirmed clinical trial registration is not needed for this submission.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.