ArticleOncogene1999
Mutant p53 gain of function: differential effects of different p53 mutants on resistance of cultured cells to chemotherapy.
Article in Oncogene, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 191 papers, 1 of them a synthesis that pooled it.
What it found
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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.
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
191 citing papers in PubMed, 1 synthesis or guideline pooled it, 440 citations in OpenAlex.
- P53 abnormalities and outcomes in colorectal cancer: a systematic review.British journal of cancer · 2005Pooled it
- Trial
- Alterations in p53 predict response to preoperative high dose chemotherapy in patients with gastric cancer.Molecular pathology : MP · 2003Trial
- A phase I/II trial of rAd/p53 (SCH 58500) gene replacement in recurrent ovarian cancer.Cancer gene therapy · 2002Trial
- Fulfilling multiple roles in PROTAC design: The emerging potential of oligonucleotides.European journal of medicinal chemistry · 2026Review
- Targeting mutant p53 in cancer: from mechanistic insights to therapeutic strategies.Cellular & molecular biology letters · 2026Review
- Carbon-11 Isotopic Radiolabeling of CP31398 and Development of a Fluorine-18 Derivative to Target Protein p53 with PET Imaging.ACS omega · 2026Article
- Prognostic impact of TP53 mutations in diffuse large B-cell lymphoma.Annals of hematology · 2026Article
- Decoding the functional impact of the cancer genome through protein-protein interactions.Nature reviews. Cancer · 2025Review
- Genome-wide CRISPR screens identify novel regulators of wild-type and mutant p53 stability.Molecular systems biology · 2024Article
- Dysregulation of cellular membrane homeostasis as a crucial modulator of cancer risk.The FEBS journal · 2024Review
- Molecular Evidence of Breast Cancer Cell Proliferation Inhibition by a Combination of Selected Qatari Medicinal Plants Crude Extracts.Nutrients · 2023Article
- Targeting Oncogenic Mutant p53 and BCL-2 for Small Cell Lung Cancer Treatment.International journal of molecular sciences · 2023Article
- Pectolinarigenin inhibits bladder urothelial carcinoma cell proliferation by regulating DNA damage/autophagy pathways.Cell death discovery · 2023Article
- TP53 mutations predict poor response to immunotherapy in patients with metastatic solid tumors.Cancer medicine · 2023Article
- Cellular and Genetic Background of Osteosarcoma.Current issues in molecular biology · 2023Review
- Characteristics of endoplasmic reticulum stress in colorectal cancer for predicting prognosis and developing treatment options.Cancer medicine · 2023Article
- Auranofin Synergizes with the PARP Inhibitor Olaparib to Induce ROS-Mediated Cell Death in Mutant p53 Cancers.Antioxidants (Basel, Switzerland) · 2023Article
- BAG2 drives chemoresistance of breast cancer by exacerbating mutant p53 aggregate.Theranostics · 2023Article
- Revisiting a challenging p53 binding site: a diversity-optimized HEFLib reveals diverse binding modes in T-p53C-Y220C.RSC medicinal chemistry · 2022Article
131 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 2 institutions in 2 countries.
Funding
Abstract
Many tumors overexpress mutant forms of p53. A growing number of studies suggest that the nature of a p53 mutation in a cell can impact upon cellular properties, clinical responses to therapy and prognosis of a tumor. To explore the cellular basis of these observations, experiments were designed to compare the properties of cells with and without p53 mutations within the same cell population. To that end, various tumor-derived human p53 mutants were introduced into p53-null H1299 lung adenocarcinoma cells. Clonogenic survival assays revealed that cells overexpressing the p53His175 mutant, but not the p53His273 mutant, recover preferentially from etoposide treatment. Moreover, p53His175 as well as p53His179 reduced substantially the rate of etoposide-induced apoptosis, whereas p53His273 and p53Trp248 had a much milder protective effect. In contrast, p53His175 and p53His273 exerted very similar effects on the cellular response to cisplatin; both conferred increased resistance to low concentrations of the drug (2.5 microg/ml), but did not protect at all against high concentrations (10 microg/ml). Hence particular p53 mutants may confer upon tumor cells a selective survival advantage during chemotherapy. These findings define a new type of mutant p53 selective gain of function, which may compromise the efficacy of cancer chemotherapy.
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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.