ReviewNature reviews. Clinical oncology2018
Therapeutic targeting of p53: all mutants are equal, but some mutants are more equal than others.
Review in Nature reviews. Clinical oncology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT04869475 (Arsenic Trioxide in Refractory Solid Tumors With Rescuable p53 Mutation), which is not on this map. Cited by 305 papers, 2 of them syntheses that pooled it.
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.
Arsenic Trioxide in Refractory Solid Tumors With Rescuable p53 Mutation
Who cites it
305 citing papers in PubMed, 2 syntheses or guidelines pooled it.
- Targeting p53 pathways: mechanisms, structures, and advances in therapy.Signal transduction and targeted therapy · 2023Pooled it
- An Updated View of the Roles of p53 in Embryonic Stem Cells.Stem cells (Dayton, Ohio) · 2022Pooled it
- Preclinical Characterization of CLSP-1025, a First-in-Class, Mutation-Specific T-Cell Engager Targeting a Neoantigen Derived from a Common p53 Mutation.Clinical cancer research : an official journal of the American Association for Cancer Research · 2026Article
- Impact of differentTranslational lung cancer research · 2026Article
- Mutant p53Molecular oncology · 2026Article
- Special Issue "p53-Oncogene, Tumor Suppressor Gene, Guardian of the Genome and the Cell".International journal of molecular sciences · 2026Article
- Article
- p53 hotspot mutants attenuate CTL-mediated tumor cell killing through a novel ALKBH5-YTHDF3-PD-L1 pathway.Oncogene · 2026Article
- Structural basis for T-cell receptor recognition of p53Acta crystallographica. Section D, Structural biology · 2026Article
- SLC25A45 as a prognostic biomarker promotes malignant progression via mutant p53 in hepatocellular carcinoma.Journal of gastrointestinal oncology · 2026Article
- KRAS in Colorectal Cancer: Tumorigenesis, Surgical Implications and Evolving Treatment Target.Current oncology (Toronto, Ont.) · 2026Review
- Article
- p53 mutation-associated prognosis across cancer types underlines hematological malignancy as an applicable cancer type to p53-rescue therapy.Fundamental research · 2026Article
- TP53 mutation is associated with improved disease control in patients with advanced RAS wild-type colorectal adenocarcinoma treated with cetuximab and pembrolizumab.International journal of cancer · 2026Article
- Selective Elimination of TP53 Mutant Cells by Transcript-Activated Chromatin Shredding.bioRxiv : the preprint server for biology · 2026Article
- p53: from understanding its structure to advances in therapeutic targeting.Signal transduction and targeted therapy · 2026Review
- Primary pulmonary adenoid cystic carcinoma presenting with ground-glass opacity nodules coexisting with male breast adenoid cystic carcinoma: A case report.Radiology case reports · 2026Article
- p53 regulates glucose metabolic reprogramming in MASLD-related hepatocellular carcinoma via modulating mitochondrial pyruvate carriers.Hepatology international · 2026Article
- Prognostic value of systemic inflammation indices in patients with metastatic colorectal cancer treated with TAS-102: a single-center retrospective real-world study.Translational cancer research · 2026Article
- Targeting mutant p53 in cancer: from mechanistic insights to therapeutic strategies.Cellular & molecular biology letters · 2026Review
245 more citing papers are in PubMed but not listed here.
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
TP53, which encodes the tumour-suppressor protein p53, is the most frequently mutated gene across all cancer types. The presence of mutant p53 predisposes to cancer development, promotes the survival of cancer cells, and is associated with ineffective therapeutic responses and unfavourable prognoses. Despite these effects, no drug that abrogates the oncogenic functions of mutant p53 has yet been approved for the treatment of cancer. Current investigational therapeutic strategies are mostly aimed at restoring the wild-type activity of mutant p53, based on the assumption that all p53 mutants are functionally equal. Our increasing knowledge of mutant forms of p53, however, supports the antithetical hypothesis that not all p53 mutants have equivalent cellular effects; hence, a judicious approach to therapeutic targeting of mutant p53 is required. In this Review, we propose a categorization of the major classes of p53 mutants based on their functionality in tumour suppression and response to therapy. The emerging picture is that the mutations across TP53 form a 'rainbow of mutants', with varying degrees of functionality and different pathobiological consequences, necessitating the use of diverse therapeutic strategies to selectively target specific classes of mutation. The utility of this knowledge of TP53 mutations in developing selective therapeutic options, and in facilitating clinical decision-making is discussed.
Indexed as
Identifiers
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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.