ReviewJournal of cellular and molecular medicine2025
Therapeutic Strategies Targeting Anti-CD47 Therapies in Glioblastoma Multiforme: Lead or Dead End?
Review in Journal of cellular and molecular medicine, 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
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
2 citing papers in PubMed.
- CD47-mediated efferocytosis in diseases: A comprehensive review.Molecular biology reports · 2026Review
- Therapeutic Strategies Targeting Anti-CD47 Therapies in Glioblastoma Multiforme: Lead or Dead End?Journal of cellular and molecular medicine · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glioblastoma multiforme (GBM) remains the most aggressive primary brain tumour in adults, characterised by marked cellular heterogeneity, stem-like subpopulations, and profound resistance to standard therapies. The failure of conventional approaches underscores the need for novel immunotherapeutic strategies that can effectively overcome tumour immune evasion. Multiple therapeutic strategies have been explored to disrupt CD47 signalling in GBM, including monoclonal antibodies, soluble SIRPα fusion proteins, recombinant or peptide fragments derived from TSP-1, dual CD47/CD36 inhibitors, and antisense oligonucleotides. Overall, anti-CD47 therapy represents a promising but incomplete strategy in GBM treatment. Its success will likely depend on multimodal approaches integrating surgical, cytotoxic and immune-modulatory interventions that also target glioma stem-like populations. Rational combinations that address both immune suppression and tumour heterogeneity could transform CD47 inhibition from a transient lead into a viable therapeutic path for this intractable malignancy.
Indexed as
Identifiers
What 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.