ReviewCellular & molecular biology letters2025
Bypassing the guardian: regulated cell death pathways in p53-mutant cancers.
Review in Cellular & molecular biology letters, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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.
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Who cites it
7 citing papers in PubMed.
- Beyond apoptosis: nanomedicine enabled reprogramming of tumor cell death for next-generation radiosensitization.Journal of nanobiotechnology · 2026Review
- Functional variants in ATF4 and PMAIP1 reveal mitochondrial apoptosis dependencies driving pancreatic cancer progression.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Pyroptosis- and Necroptosis-Related Signaling in Salicylate UV Absorber-Induced Toxicity: Implications for Sustainable Chemistry and Human Health.International journal of molecular sciences · 2026Article
- Transcriptomic and multi-layer variant analysis identifies STAT3 and HIF1A as central regulators of regulated cell death pathways in lung squamous cell carcinoma.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Bioactive glass nanoparticles induce intrinsic p53-dependent apoptosis and promote genomic instability via ROS overproduction and mitochondrial depolarization in triple-negative breast cancer cells.Scientific reports · 2026Article
- Bioengineering Strategies to Address Key Bottlenecks in Ferroptosis-Based Cancer Therapy: A Critical Review.International journal of nanomedicine · 2026Review
- Dual RNA Polymerase I Inhibition with CX-5461 and BMH-21 Synergizes in Breast Cancer by Activating p53-Dependent Stress.bioRxiv : the preprint server for biology · 2025Article
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
Abstract
Approximately half of all cancers bear mutations in the tumor suppressor p53. Despite decades of research studying p53 function, treatment of p53-mutant cancers remains challenging owing to the effects of p53 mutations on many complex and interrelated signaling networks that promote tumor metastasis and chemoresistance. Mutations in p53 promote tumor survival by dysregulating cellular homeostasis and preventing activation of regulated cell death (RCD) pathways, which normally promote organismal health by eliminating dysregulated cells. Activation of RCD is a hallmark of effective cancer therapies, and p53-mutant cancers may be particularly susceptible to activation of certain RCD pathways. In this review, we discuss four RCD pathways that are the targets of emerging cancer therapeutics to treat p53-mutant cancers. These RCD pathways include E2F1-dependent apoptosis, necroptosis, mitochondrial permeability transition-driven necrosis, and ferroptosis. We discuss mechanisms of RCD activation, effects of p53 mutation on RCD activation, and current pharmaceutical strategies for RCD activation in p53-mutant cancers.
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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.