ReviewFrontiers in oncology2015
The Contrived Mutant p53 Oncogene - Beyond Loss of Functions.
Review in Frontiers in oncology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 24 papers.
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
24 citing papers in PubMed, 42 citations in OpenAlex.
- A set cover algorithm identifies minimal circulating tumour DNA sequencing targets for colorectal cancer detection.Scientific reports · 2025Article
- Role of Amide Proton Transfer Weighted MRI in Predicting MGMTp Methylation Status, p53-Status, Ki-67 Index, IDH-Status, and ATRX Expression in WHO Grade 4 High Grade Glioma.Tomography (Ann Arbor, Mich.) · 2025Article
- Therapeutic potential of combating cancer by restoring wild-type p53 through mRNA nanodelivery.Nanomedicine : nanotechnology, biology, and medicine · 2024Review
- Repeated Lineage Switches in an Elderly Case of Refractory B-Cell Acute Lymphoblastic Leukemia WithFrontiers in oncology · 2022Article
- Review
- Suppression of HSF1 activity by wildtype p53 creates a driving force for p53 loss-of-heterozygosity.Nature communications · 2021Article
- Oligomerization of Mutant p53 R273H is not Required for Gain-of-Function Chromatin Associated Activities.Frontiers in cell and developmental biology · 2021Article
- STAT3 and p53: Dual Target for Cancer Therapy.Biomedicines · 2020Review
- Li-Fraumeni syndrome heterogeneity.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2020Review
- Therapeutic potential of ReACp53 targeting mutant p53 protein in CRPC.Prostate cancer and prostatic diseases · 2020Article
- Fam83F induces p53 stabilisation and promotes its activity.Cell death and differentiation · 2019Article
- Article
- Understanding p53 functions through p53 antibodies.Journal of molecular cell biology · 2019Review
- Regulators of Oncogenic Mutant TP53 Gain of Function.Cancers · 2018Review
- Patterns of mutations in TP53 mutated AML.Best practice & research. Clinical haematology · 2018Review
- Epidermal Tissue Adapts to Restrain Progenitors Carrying Clonal p53 Mutations.Cell stem cell · 2018Article
- Mutant p53 blocks SESN1/AMPK/PGC-1α/UCP2 axis increasing mitochondrial OBritish journal of cancer · 2018Article
- Natural products targeting the p53-MDM2 pathway and mutant p53: Recent advances and implications in cancer medicine.Genes & diseases · 2018Review
- Wild-type p53 oligomerizes more efficiently than p53 hot-spot mutants and overcomes mutant p53 gain-of-function via a "dominant-positive" mechanism.Oncotarget · 2018Article
- Complexes formed by mutant p53 and their roles in breast cancer.Breast cancer (Dove Medical Press) · 2018Review
Corrections and comments
- Erratum issued
Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mutations in p53 are almost synonymous with cancer - be it susceptibility to the disease or response to treatment - and therefore, are a critical determinant of overall survival. As most of these mutations occur in the DNA-binding domain of p53, many of the clinical correlations with mutant p53 have been initially relegated to the loss of its transcription-dependent activities as a tumor suppressor. However, significant efforts over the last two decades have led to the vast knowledge on the potential functions of the mutated p53 protein, which have been attributed to the physical presence of the mutant protein rather than the loss of its wild-type (WT) functions. Beyond the inhibitory effects of mutant p53 on the remaining WT protein that leads to the dominant-negative effect in the heterozygous state, mutant p53's presence has also been significantly attributed to novel gain-of-functions that lead to addiction of cancer cells to its presence for survival, as well as for their ability to invade and metastasize, elevating it to a contrived oncogene that drives the cancer cells forward. This review will summarize the functional consequences of the presence of mutant p53 protein on cellular and organismal physiology.
Indexed as
Identifiers
What OpenQuestion holds
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.