ArticleNeoplasia (New York, N.Y.)2015
Specific TP53 Mutants Overrepresented in Ovarian Cancer Impact CNV, TP53 Activity, Responses to Nutlin-3a, and Cell Survival.
Article in Neoplasia (New York, N.Y.), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 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
40 citing papers in PubMed, 52 citations in OpenAlex.
- Detection of mutant cancer-derived circRNAs in extracellular vesicles by rolling circle amplification.Molecular therapy. Nucleic acids · 2026Article
- Atranorin suppresses the LUCAT1/STAT3 axis to induce ferroptotic cell death in ovarian cancer.Molecular biology reports · 2026Article
- The Enigmatic Tumor Suppressor p53 Biomolecule: Its Role and Prognostic and Predictive Values in Cancer Therapy and Precision Medicine.Biomolecules · 2026Review
- New cell lines expanding the diversity of Ewing sarcoma models.International journal of cancer · 2026Article
- Arginine Deprivation Induces Quiescence and Confers Vulnerability to Ferroptosis in Colorectal Cancer.Cancer research · 2025Article
- Article
- Proteasome Inhibitor MG-132 and PKC-ι-Specific Inhibitor ICA-1S Degrade Mutant p53 and Induce Apoptosis in Ovarian Cancer Cell Lines.International journal of molecular sciences · 2025Article
- Characterization of p53 p.T253I as a pathogenic mutation underlying Li-Fraumeni Syndrome.PloS one · 2025Article
- HOXA9 versus HOXB9; particular focus on their controversial role in tumor pathogenesis.Journal of applied genetics · 2024Review
- Functional evaluation of germline TP53 variants identified in Brazilian families at-risk for Li-Fraumeni syndrome.Scientific reports · 2024Article
- Predictive value of miR-582-5p for onset of sepsis-induced acute kidney injury and its functional role during disease development.Central-European journal of immunology · 2024Article
- Rescue of p53 functions by in vitro-transcribed mRNA impedes the growth of high-grade serous ovarian cancer.Cancer communications (London, England) · 2024Article
- ATAD2 is a driver and a therapeutic target in ovarian cancer that functions by upregulating CENPE.Cell death & disease · 2023Article
- Article
- ReducedCells · 2022Article
- Genome interpretation using in silico predictors of variant impact.Human genetics · 2022Review
- Article
- TGFBI Production by Macrophages Contributes to an Immunosuppressive Microenvironment in Ovarian Cancer.Cancer research · 2021Article
- The Synthetic Curcumin Analog HO-3867 Rescues Suppression of PLAC1 Expression in Ovarian Cancer Cells.Pharmaceuticals (Basel, Switzerland) · 2021Article
- Can Glycosylation Mask the Detection of MHC Expressing p53 Peptides by T Cell Receptors?Biomolecules · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Evolutionary Action analyses of The Cancer Gene Atlas data sets show that many specific p53 missense and gain-of-function mutations are selectively overrepresented and functional in high-grade serous ovarian cancer (HGSC). As homozygous alleles, p53 mutants are differentially associated with specific loss of heterozygosity (R273; chromosome 17); copy number variation (R175H; chromosome 9); and up-stream, cancer-related regulatory pathways. The expression of immune-related cytokines was selectively related to p53 status, showing for the first time that specific p53 mutants impact, and are related to, the immune subtype of ovarian cancer. Although the majority (31%) of HGSCs exhibit loss of heterozygosity, a significant number (24%) maintain a wild-type (WT) allele and represent another HGSC subtype that is not well defined. Using human and mouse cell lines, we show that specific p53 mutants differentially alter endogenous WT p53 activity; target gene expression; and responses to nutlin-3a, a small molecular that activates WT p53 leading to apoptosis, providing "proof of principle" that ovarian cancer cells expressing WT and mutant alleles represent a distinct ovarian cancer subtype. We also show that siRNA knock down of endogenous p53 in cells expressing homozygous mutant alleles causes apoptosis, whereas cells expressing WT p53 (or are heterozygous for WT and mutant p53 alleles) are highly resistant. Therefore, despite different gene regulatory pathways associated with specific p53 mutants, silencing mutant p53 might be a suitable, powerful, global strategy for blocking ovarian cancer growth in those tumors that rely on mutant p53 functions for survival. Knowing p53 mutational status in HGSC should permit new strategies tailored to control this disease.
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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.