ReviewTheranostics2023
Role of p53 in breast cancer progression: An insight into p53 targeted therapy.
Review in Theranostics, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 142 papers, 1 of them a synthesis 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
142 citing papers in PubMed, 1 synthesis or guideline pooled it, 193 citations in OpenAlex.
- Somatic mutations in Middle East and North Africa breast cancer patients: a systematic review.The oncologist · 2025Pooled it
- Covalent Targeting and Thermostabilization of Oncogenic R280K and R273H Mutants p53 by Small Molecule RVJB59.ChemMedChem · 2026Article
- TFAP2B and FOXC1 are associated with biologically and clinically distinct differentiation states in triple-negative breast cancer.Scientific reports · 2026Article
- Jujube Peel Pigment-Loaded Thermosensitive Hydrogel with In Vitro Pro-Apoptotic and Antibacterial Activities.Gels (Basel, Switzerland) · 2026Article
- Structure-based identification of small-molecule stabilizers targeting mutant TP53 (Y220C) in breast cancer: a pharmacophore modeling, molecular docking and dynamics study.Journal, genetic engineering & biotechnology · 2026Article
- Associations of neighborhood deprivation with breast cancer tumor genomics, targeted treatment use, and survival.Breast cancer research and treatment · 2026Observational
- Food-Derived Natural Compounds as Molecular Targets in Cancer Prevention.Pharmaceutics · 2026Review
- TRIM Protein Superfamily in Breast Cancer: Yin and Yang.Biochemical genetics · 2026Review
- FBXL5 depletion as a novel strategy against osteosarcoma: Evidence for MEK/ERK inhibition and enhanced therapeutic sensitivity.Oncology letters · 2026Article
- Antitumor Effects ofMolecules (Basel, Switzerland) · 2026Article
- MicroRNA Expression Links Transportation Environmental Burden to Late-Stage Triple-Negative Breast Cancer.Genes · 2026Article
- Multi-omic Profiling of Recurrence Risk Across Breast Cancer Subtypes.medRxiv : the preprint server for health sciences · 2026Article
- SIVA1 Knockdown Drives Aggressive Phenotypes in Triple-Negative Breast Cancer Cells while Enhancing Paclitaxel Efficacy.ACS omega · 2026Article
- Tetrahedral framework nucleic acids: Nanokeys unlocking a new era of precision biomedicine.Journal of advanced research · 2026Review
- Unraveling the intricate molecular mechanisms of sex hormones' roles in breast cancer pathogenesis: A review.Medicine · 2026Review
- TP53-META, a meta-analysis tool for comparative transcriptomics of TP53 dependency: examples from target silencing and liver fibrosis.BMC bioinformatics · 2026Article
- Geospatial genetic evolution and phenotypic plasticity in triple-negative breast cancer.Genome medicine · 2026Article
- Development of a LiDia-SEQ™ platform compatible breast cancer panel and testing with metastatic breast cancer patient samples: A rapid, sample-to-result, fully integrated next-generation sequencing (NGS)-based platform, LiDia-SEQ, for use at the point-of-need.The journal of liquid biopsy · 2026Article
- A natural coumarin, benjaminin, suppresses proliferation and migration and induces apoptosis in MCF-7 breast cancer cells.Scientific reports · 2026Article
- Postpartum breast cancer: evidence for a distinct phenotype.Journal of the National Cancer Institute · 2026Article
82 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
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The transcription factor p53 is an important regulator of a multitude of cellular processes. In the presence of genotoxic stress, p53 is activated to facilitate DNA repair, cell cycle arrest, and apoptosis. In breast cancer, the tumor suppressive activities of p53 are frequently inactivated by either the overexpression of its negative regulator MDM2, or mutation which is present in 30-35% of all breast cancer cases. Notably, the frequency of p53 mutation is highly subtype dependent in breast cancers, with majority of hormone receptor-positive or luminal subtypes retaining the wild-type p53 status while hormone receptor-negative patients predominantly carry p53 mutations with gain-of-function oncogenic activities that contribute to poorer prognosis. Thus, a two-pronged strategy of targeting wild-type and mutant p53 in different subtypes of breast cancer can have clinical relevance. The development of p53-based therapies has rapidly progressed in recent years, and include unique small molecule chemical inhibitors, stapled peptides, PROTACs, as well as several genetic-based approaches using vectors and engineered antibodies. In this review, we highlight the therapeutic strategies that are in pre-clinical and clinical development to overcome p53 inactivation in both wild-type and mutant p53-bearing breast tumors, and discuss their efficacies and limitations in pre-clinical and clinical settings.
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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.