ReviewActa biochimica et biophysica Sinica2014
Tumor suppressor p53 and its gain-of-function mutants in cancer.
Review in Acta biochimica et biophysica Sinica, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 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
70 citing papers in PubMed, 1 synthesis or guideline pooled it, 133 citations in OpenAlex.
- Clinical significance of miRNA‑1 and its potential target gene network in lung squamous cell carcinoma.Molecular medicine reports · 2019Pooled it
- Tumoral Metabolism at the Intersection of Oncogene Signaling, Epigenetics and Immunology: Emerging Therapeutic Strategies in Cancer.Current issues in molecular biology · 2026Review
- APOBEC3B-driven mutations negatively regulated by P53 promote tumor progression and immunosuppressive microenvironment in prostate cancer.Molecular and cellular biochemistry · 2026Article
- Construction and verification of a prognostic model for cervical cancer based on genes associated with the p53 regulatory pathway.Translational cancer research · 2025Article
- Frankincense oil nanoemulsion induces selective cytotoxicity and over ROS-mediated oxidative stress and apoptotic DNA damage in Hep-G2 hepatic cancer cells.Scientific reports · 2025Article
- SET8 is a novel negative regulator of TGF-β signaling in a methylation-independent manner.Scientific reports · 2023Article
- p53 Dysregulation in Breast Cancer: Insights on Mutations in theInternational journal of molecular sciences · 2023Article
- TP53 somatic mutations in Asian breast cancer are associated with subtype-specific effects.Breast cancer research : BCR · 2023Article
- Different impacts of TP53 mutations on cell cycle-related gene expression among cancer types.Scientific reports · 2023Article
- Reactivation of mutant p53 in esophageal squamous cell carcinoma by isothiocyanate inhibits tumor growth.Frontiers in pharmacology · 2023Article
- Review
- Article
- Alterations in p53 Influence hTERT, VEGF and MMPs Expression in Oral Cancer Patients.Asian Pacific journal of cancer prevention : APJCP · 2022Article
- Review
- The two-faced role of ATF2 on cisplatin response in gastric cancer depends on p53 context.Cell & bioscience · 2022Article
- Liquid biopsies to occult brain metastasis.Molecular cancer · 2022Review
- Association between extract of Euphorbia szovitsii and expression level of microRNAs in MDA-MB-231 cell line.Molecular biology reports · 2022Article
- Article
- Aberrant calcium signalling downstream of mutations in TP53 and the PI3K/AKT pathway genes promotes disease progression and therapy resistance in triple negative breast cancer.Cancer drug resistance (Alhambra, Calif.) · 2022Review
- Expert consensus on the clinical application of recombinant adenovirus human p53 for head and neck cancers.International journal of oral science · 2021Article
10 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
Abstract
Tumor suppressor p53 plays a pivotal role in tumor suppression. p53 is the most frequently mutated gene in cancer. As a transcription factor, p53 mainly exerts its role in tumor suppression through transcriptional regulation of its downstream target genes. Thus, p53 and its target genes form a complex p53 signaling pathway to regulate a wide variety of biological processes to prevent tumorigenesis. Recent studies have revealed that in addition to apoptosis, cell cycle arrest and senescence, p53's functions in the regulation of energy metabolism and anti-oxidant defense contribute significantly to its role in tumor suppression. Studies further show that many tumor-associated mutant p53 proteins not only lose tumor suppressive functions of wild-type p53, but also gain new oncogenic activities that are independent of wild-type p53, including promoting tumor cell proliferation, survival, metabolic changes, angiogenesis, and metastasis, which are defined as mutant p53 gain-of-function. The frequent loss of wild-type p53 function and the gain-of-function of mutant p53 in human tumors make p53 an extremely attractive target for cancer therapy. Different strategies and many small-molecule drugs are being developed for the p53-based tumor therapy. Here, we review the mechanisms of p53 in tumor suppression and gain-of-function mutant p53 in tumor development, as well as the recent advances in the development of the p53-based tumor therapy.
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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.