ReviewPharmacological reports : PR2026
DUSP6/MKP3 as an emerging therapeutic target in glioblastoma.
Review in Pharmacological reports : PR, 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
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The role of MKP family dual-specificity phosphatases (DUSPs) in oncogenesis, together with their potential as therapeutic targets in precision oncology, is now well established. These enzymes dephosphorylate both phosphotyrosine and phosphothreonine residues on extracellular signal-regulated kinase ERK1/2, thereby attenuating mitogen-activated protein kinase (MAPK) signalling. DUSP6/MKP3 acts as a context-dependent regulator with tumour-suppressive or tumour-promoting roles across cancers. Glioblastoma (GBM), an aggressive primary brain tumour with dismal clinical outcomes, has shown limited response to both oncogene-targeted and immunotherapeutic approaches. DUSP6/MKP3 is frequently overexpressed in GBM and contributes to tumour growth, invasive behaviour, and treatment resistance. Computational analyses identify DUSP family genes, including DUSP6/MKP3, as recurrently dysregulated within GBM driver networks, supporting a central role in gliomagenesis. Here, we discuss DUSP6/MKP3 in glioblastoma, integrating transcriptional and cell-based evidence to define its molecular mechanisms and clinical relevance.
Identifiers
42909790What OpenQuestion holds
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.