ReviewDiscover oncology2026
Unrevealing the dual role of paired box and sex determining region Y related high mobility group box in glioblastoma.
Review in Discover oncology, 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
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
This narrative review summarises glioblastoma (GBM), a very frequent invasive kind of brain tumour in the elderly that is extremely aggressive, resistant to treatment, and has a bad prognosis because of its substantial genetic and cellular heterogeneity. With a median survival of about 15 months, GBM is still an incurable cancer. This review takes full 3 months for collect all relevant knowledge about PAX and SOX gene families, which have crucial roles in the biology of GBM, as shown by recent developments in molecular pathology. Depending on certain gene expression patterns, members of these transcription factor families have been shown to have both oncogenic and tumor suppressive properties. They are important regulators of brain development, stem cell maintenance, and tumor progression. While PAX6 functions as a tumor suppressor, preventing growth and angiogenesis, PAX3, PAX5, and PAX8 are increased in GBM, encouraging proliferation, stemness, and survival. Similarly, SOX7 and SOX11 act as suppressors, and their downregulation is associated with malignancy and a bad prognosis, while SOX2, SOX3, SOX4, and SOX9 increase tumor aggressiveness and resistance to treatment. Glioma cell migration, growth, and death inhibition are further fueled through the complex interactions between canonical and non-canonical WNT signaling that modulate PAX and SOX pathways. These results highlight how crucial thorough molecular profiling is for improved categorization, prognostication, and the creation of focused treatment plans in GBM. The discovery of the dual functions of the PAX and SOX genes in GBM highlights their potential as therapeutic targets and biomarkers, opening up new possibilities for more individualised and accurate treatment approaches.
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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.