ReviewCell communication and signaling : CCS2024
Targeting mutant p53: a key player in breast cancer pathogenesis and beyond.
Review in Cell communication and signaling : CCS, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 1 of them a synthesis that pooled it.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
24 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Somatic mutations in Middle East and North Africa breast cancer patients: a systematic review.The oncologist · 2025Pooled it
- Fast-Food Component-Induced Epigenetic Modifications Modulate Immunotherapy in Metastatic Breast Cancer.ACS omega · 2026Article
- Current Study of Alpha-Mangostin in Breast Cancer Therapy: Antioxidant Mechanisms and Redox Modulation from In Silico to In Vivo Studies.Antioxidants (Basel, Switzerland) · 2026Review
- Antitumor Effects ofMolecules (Basel, Switzerland) · 2026Article
- Molecular profiling of breast cancer pleural effusions using cytology specimens: Impact of sample source and cytological features on next-generation sequencing performance.Cancer cytopathology · 2026Article
- Ferroptosis-related gene EPAS1 suppresses breast cancer progression by inhibiting M2 macrophage polarization.Discover oncology · 2026Article
- Fundamentals and emerging frontiers in p53-targeted drug development.Biochemistry and biophysics reports · 2026Review
- TP53 mutations in triple-negative breast cancer cells confer sensitivity to ASCT2 inhibition via arginine uptake.Cell death & disease · 2026Article
- Integrated Transcriptomic Analysis Identifies a Six-Gene Prognostic Signature, RNA Editing Derived Neoantigens, and miRNA Regulatory Networks in Renal Cell Carcinoma.Iranian journal of medical sciences · 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
- Mutant p53 and TP53 mutations in esophageal squamous cell carcinoma: consistency and diagnostic significance.Frontiers in genetics · 2026Article
- Review
- Identification of Somatic and Germline Mutations Influencing Treatment Outcomes and Disease Susceptibility in Tunisian Triple-Negative Breast Cancer Using Next-Generation Sequencing.British journal of biomedical science · 2026Article
- CAF-derived exosomes: orchestrators of dysregulated signaling pathways in breast cancer progression.Naunyn-Schmiedeberg's archives of pharmacology · 2026Review
- Interplay of Interleukin-1Oncology research · 2026Article
- Decoding the relationships among miRNA, HPV infection, and tumor suppressor gene expression in breast cancer patients.Scientific reports · 2025Article
- Chemotherapy-induced cardiotoxicity in breast cancer: mechanisms, diagnostic advances, and emerging protective strategies.American journal of physiology. Heart and circulatory physiology · 2025Review
- Integrating proteomics and bioinformatics for the identification of breast cancer biomarkers interacting with telomeric G-quadruplex.Cancer cell international · 2025Article
- Integrative systems biology and in-vitro analysis of cryptolepine's therapeutic role in breast cancer.Discover oncology · 2025Article
- Radiogenomic Landscape of Metastatic Endocrine-Positive Breast Cancer Resistant to Aromatase Inhibitors.Cancers · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
Abstract
The p53 mutation is the most common genetic mutation associated with human neoplasia. TP53 missense mutations, which frequently arise early in breast cancer, are present in over thirty percent of breast tumors. In breast cancer, p53 mutations are linked to a more aggressive course of the disease and worse overall survival rates. TP53 mutations are mostly seen in triple-negative breast cancer, a very diverse kind of the disease. The majority of TP53 mutations originate in the replacement of individual amino acids within the p53 protein's core domain, giving rise to a variety of variations referred to as "mutant p53s." In addition to gaining carcinogenic qualities through gain-of-function pathways, these mutants lose the typical tumor-suppressive features of p53 to variable degrees. The gain-of-function impact of stabilized mutant p53 causes tumor-specific dependency and resistance to therapy. P53 is a prospective target for cancer therapy because of its tumor-suppressive qualities and the numerous alterations that it experiences in tumors. Phenotypic abnormalities in breast cancer, notably poorly differentiated basal-like tumors are frequently linked to high-grade tumors. By comparing data from cell and animal models with clinical outcomes in breast cancer, this study investigates the molecular mechanisms that convert gene alterations into the pathogenic consequences of mutant p53's tumorigenic activity. The study delves into current and novel treatment approaches aimed at targeting p53 mutations, taking into account the similarities and differences in p53 regulatory mechanisms between mutant and wild-type forms, as well.
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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.