ReviewCancer cell international2022
Transition of amyloid/mutant p53 from tumor suppressor to an oncogene and therapeutic approaches to ameliorate metastasis and cancer stemness.
Review in Cancer cell international, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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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.
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Who cites it
13 citing papers in PubMed, 20 citations in OpenAlex.
- Inhalable Mucoadhesive Redox-Triggered Nanotherapeutics for p53-Mediated Lung Cancer Therapy and Metastasis Suppression.Advanced healthcare materials · 2026Article
- mTOR signaling networks: mechanistic insights and translational frontiers in disease therapeutics.Signal transduction and targeted therapy · 2025Review
- Multi-omics analysis reveals cancer stemness function and establishes a predictive model for thyroid cancer prognosis and immunotherapy.Discover oncology · 2025Article
- Amyloids in bladder cancer hijack cancer-related proteins and are positive correlated to tumor stage.Scientific reports · 2025Article
- Curcumin: A Potential Weapon in the Prevention and Treatment of Head and Neck Cancer.ACS pharmacology & translational science · 2024Review
- Cell plasticity modulation by flavonoids in resistant breast carcinoma targeting the nuclear factor kappa B signaling.Cancer metastasis reviews · 2024Review
- CHEK2 germline variants identified in familial nonmedullary thyroid cancer lead to impaired protein structure and function.The Journal of biological chemistry · 2024Article
- DNp73 enhances tumor progression and immune evasion in multiple myeloma by targeting the MYC and MYCN pathways.Frontiers in immunology · 2024Article
- Amyloids and brain cancer: molecular linkages and crossovers.Bioscience reports · 2023Review
- Multifaceted role of mTOR (mammalian target of rapamycin) signaling pathway in human health and disease.Signal transduction and targeted therapy · 2023Review
- p53 amyloid pathology is correlated with higher cancer grade irrespective of the mutant or wild-type form.Journal of cell science · 2023Article
- P53/MDM2 Complex-Based Targeted Strategies in Colon Adenocarcinoma.Acta medica academica · 2023Article
- Potential enhancement of post-stroke angiogenic response by targeting the oligomeric aggregation of p53 protein.Frontiers in cellular neuroscience · 2023Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
The tumor suppressor p53 when undergoes amyloid formation confers several gain-of-function (GOF) activities that affect molecular pathways crucial for tumorigenesis and progression like some of the p53 mutants. Even after successful cancer treatment, metastasis and recurrence can result in poor survival rates. The major cause of recurrence is mainly the remnant cancer cells with stem cell-like properties, which are resistant to any chemotherapy treatment. Several studies have demonstrated the role of p53 mutants in exacerbating cancer stemness properties and epithelial-mesenchymal transition in these remnant cancer cells. Analyzing the amyloid/mutant p53-mediated signaling pathways that trigger metastasis, relapse or chemoresistance may be helpful for the development of novel or improved individualized treatment plans. In this review, we discuss the changes in the metabolic pathways such as mevalonate pathway and different signaling pathways such as TGF-β, PI3K/AKT/mTOR, NF-κB and Wnt due to p53 amyloid formation, or mutation. In addition to this, we have discussed the role of the regulatory microRNAs and lncRNAs linked with the mutant or amyloid p53 in human malignancies. Such changes promote tumor spread, potential recurrence, and stemness. Importantly, this review discusses the cancer therapies that target either mutant or amyloid p53, restore wild-type functions, and exploit the synthetic lethal interactions with mutant p53.
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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.