ReviewCancers2026
MDM4 at the Crossroads: Beyond p53 and MDM2.
Review in Cancers, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- p53 Pathway-Targeted Therapeutic Strategies in Glioblastoma: A CNS-Specific Framework Integrating Therapeutic Resistance, Molecular Stratification, CNS Pharmacology, and Clinical Translation.Drug design, development and therapy · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
Abstract
MDM4 (Murine Double Minute 4), also known as MDMX, is a crucial negative regulator of the tumor suppressor p53. MDM4 heterodimerizes with MDM2 to enhance MDM2-mediated ubiquitination and degradation of p53, thereby promoting tumorigenesis. Beyond its canonical role in inhibiting p53 activity, recent studies have revealed diverse p53-independent functions. MDM4 interacts with various proteins, including p73, E2F1, casein kinase 1α, PPARα, and TRIM21 to regulate cell cycle progression, β-catenin-mediated pre-leukemic progression, and ferroptosis independent of p53. In addition, MDM4 functions independently of both p53 and MDM2 by interacting with proteins, such as SMAD family members 3/4, retinoblastoma protein (pRB), p21, Nbs1 (also known as Nibrin), mTOR complex 1 (mTORC1), and the Polycomb Repressive Complexes (PRCs) complex, to control cell proliferation and survival, as well as protein degradation, double-strand break (DSB) repair, and replication fork progression. Intriguingly, multiple studies suggest that MDM4 exhibits oncogenic activity independent of p53; however, other reports highlight a potential tumor-suppressive role for MDM4 in the absence of p53. Thus, MDM4's functions extend well beyond the canonical p53-MDM2 axis. A deeper understanding of MDM4 biology may facilitate the development of novel targeted therapies for various cancers.
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.