ReviewBiomedicines2026
The Diverse Roles of the MEF2 Transcription Factor Family in Tumor Progression and Emerging Therapeutic Opportunities.
Review in Biomedicines, 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
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Authors and funding
5 authors.
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Abstract
The myocyte enhancer factor 2 (MEF2) transcription factor family plays crucial roles in differentiation, lineage specification, stress responses, and tissue homeostasis. Recent investigations have shown that the dysregulation of MEF2A, MEF2B, MEF2C, and MEF2D is associated with tumorigenesis, tumor progression, and adverse clinicopathological features in several cancers. MEF2B has a particularly important role in B-cell malignancies, where recurrent mutations deregulate BCL6 and promote lymphoma progression. MEF2A, MEF2C, and MEF2D also regulate malignant phenotypes, including proliferation, migration, invasion, apoptosis, drug resistance, angiogenesis, inflammation, and immune evasion, by the mechanism of regulating cell-cycle regulators, apoptosis-related genes, EMT-related genes, and other transcriptional programs. This review summarizes the mechanisms by which MEF2 family members contribute to tumor initiation and progression, with added emphasis on
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