ReviewCellular and molecular life sciences : CMLS2017
Molecularly targeted therapies for p53-mutant cancers.
Review in Cellular and molecular life sciences : CMLS, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 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
46 citing papers in PubMed, 78 citations in OpenAlex.
- p53-R280S mutation confers lenvatinib resistance in hepatocellular carcinoma via Bcl-2-mediated anti-apoptotic signaling.Molecular and cellular biochemistry · 2026Article
- Identification of cancer mini-drivers by deciphering selective landscape in the cancer genome.Briefings in bioinformatics · 2026Article
- Translating genomic insights into therapy: an NGS-based mutation profiling study in breast cancer.Medical oncology (Northwood, London, England) · 2025Article
- Restoration of TP53 strategy via specific nanoparticles for ovarian cancer therapy.Journal of ovarian research · 2025Article
- Enhanced pharmacological activities of AKR1C3-activated prodrug AST-3424 in cancer cells with defective DNA repair.International journal of cancer · 2025Article
- The influence of a modified p53 C-terminal peptide by using a tumor-targeting sequence on cellular apoptosis and tumor treatment.Apoptosis : an international journal on programmed cell death · 2024Article
- Current and Emerging Diagnostic, Prognostic, and Predictive Biomarkers in Head and Neck Cancer.Biomedicines · 2024Review
- ExploringPharmaceuticals (Basel, Switzerland) · 2024Article
- The nuclear factor erythroid 2-related factor 2/p53 axis in breast cancer.Biochemia medica · 2023Review
- Review
- The Role of Genetic Mutations in Mitochondrial-Driven Cancer Growth in Selected Tumors: Breast and Gynecological Malignancies.Life (Basel, Switzerland) · 2023Review
- TP53 Alterations in Myelodysplastic Syndromes and Acute Myeloid Leukemia.Biomedicines · 2023Review
- Mechanisms of myeloid leukemogenesis: Current perspectives and therapeutic objectives.Blood reviews · 2023Review
- Review
- Transcription profiling of feline mammary carcinomas and derived cell lines reveals biomarkers and drug targets associated with metabolic and cell cycle pathways.Scientific reports · 2022Article
- Human RAD51 Protein Forms Amyloid-like AggregatesInternational journal of molecular sciences · 2022Article
- Clinical Profile and Survival Outcome of Endometrial Cancer with p53 Mutation.Indian journal of surgical oncology · 2022Article
- Activating transcription factor 3 mediates apoptotic functions through a p53-independent pathway in human papillomavirus 18 infected HeLa cells.Virus genes · 2022Article
- [Research Advances of EGFR-TP53 Co-mutation in Advanced Non-small Cell Lung Cancer].Zhongguo fei ai za zhi = Chinese journal of lung cancer · 2022Review
- Identification of potential target genes of breast cancer in response to Chidamide treatment.Frontiers in molecular biosciences · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
The tumor suppressor p53 is lost or mutated in approximately half of human cancers. Mutant p53 not only loses its anti-tumor transcriptional activity, but also often acquires oncogenic functions to promote tumor proliferation, invasion, and drug resistance. Traditional strategies have been taken to directly target p53 mutants through identifying small molecular compounds to deplete mutant p53, or to restore its tumor suppressive function. Accumulating evidence suggest that cancer cells with mutated p53 often exhibit specific functional dependencies on secondary genes or pathways to survive, providing alternative targets to indirectly treat p53-mutant cancers. Targeting these genes or pathways, critical for survival in the presence of p53 mutations, holds great promise for cancer treatment. In addition, mutant p53 often exhibits novel gain-of-functions to promote tumor growth and metastasis. Here, we review and discuss strategies targeting mutant p53, with focus on targeting the mutant p53 protein directly, and on the progress of identifying genes and pathways required in p53-mutant cells.
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.