ReviewMedicinal research reviews2026
Decoding WDR5-Mediated Interactions in Gliomas: Implications for Targeted Therapy.
Review in Medicinal research reviews, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
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Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Gliomas are aggressive and treatment-resistant tumors of the central nervous system, characterized by molecular heterogeneity, diffuse infiltration, rapid progression, and persistent poor prognosis despite multimodal therapy. Emerging evidence highlights the role of complex genetic changes (such as IDH1 and H3F3A mutations) and epigenetic interactions in reshaping chromatin structure and activity in gliomas, increasing their reliance on epigenetic regulators for their growth and resistance. The nuclear scaffolding protein WD repeat domain 5 (WDR5), is a core component of the MLL/SET1 (WRAD) methyltransferase complex, which has been recently validated as a molecular target for cancer. WDR5 implication in H3K4 trimethylation (H3K4me3)-mediated gene regulation sustains transcriptional programs linked to proliferation, ribosome biogenesis, stemness, and MYC-driven oncogenic activity. In gliomas, WDR5 expression is increased, promoting proliferation and migration, as well as maintaining the glioma stem cell population, contributing to tumor progression. Targeting of WDR5 through specific WIN-site and WBM-site inhibitors or PROTAC degraders has been shown to impair WRAD assembly, reduce H3K4me3 levels, weaken MYC-associated transcription, and suppress tumor growth. In this review, we highlight the significant role of WDR5 in gliomas as part of a tumor-specific epigenetic vulnerability network, providing a critical update on the major WDR5-targeted inhibitors and degraders for future therapeutic applications.
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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.