ArticleOncogene2003
Resistance to DNA-damaging agents is discordant from experimental metastatic capacity in MEF ras-transformants-expressing gain of function MTp53.
Article in Oncogene, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 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.
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.
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Who cites it
10 citing papers in PubMed, 23 citations in OpenAlex.
- Multi-omics characterization and machine learning of lung adenocarcinoma molecular subtypes to guide precise chemotherapy and immunotherapy.Frontiers in immunology · 2024Article
- Therapeutic targeting of p53: all mutants are equal, but some mutants are more equal than others.Nature reviews. Clinical oncology · 2018Review
- Article
- The Contrived Mutant p53 Oncogene - Beyond Loss of Functions.Frontiers in oncology · 2015Review
- RUNX Family Participates in the Regulation of p53-Dependent DNA Damage Response.International journal of genomics · 2013Review
- Gain-of-Function Activity of Mutant p53 in Lung Cancer through Up-Regulation of Receptor Protein Tyrosine Kinase Axl.Genes & cancer · 2012Article
- Mutant p53: one name, many proteins.Genes & development · 2012Review
- p53 mutants induce transcription of NF-κB2 in H1299 cells through CBP and STAT binding on the NF-κB2 promoter and gain of function activity.Archives of biochemistry and biophysics · 2012Article
- Tumor senescence and radioresistant tumor-initiating cells (TICs): let sleeping dogs lie!Breast cancer research : BCR · 2010Article
- Impaired p53 binding to importin: a novel mechanism of cytoplasmic sequestration identified in oxaliplatin-resistant cells.Oncogene · 2009Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Tumor cells can acquire aggressive phenotypes secondary to the loss of expression of the wild-type p53 (WTp53) protein or by the gain of function for selected mutant p53 (MTp53) proteins. However, it is unclear as to whether the development of aggressive phenotypes is inter-related. Herein we report the radiosensitivity, chemosensitivity, and in vivo growth characteristics of isogenic p53(-/-) MEF ras-transformants that variably express an MTp53 protein. Initial experiments revealed significant clonal heterogeneity with respect to cellular sensitivity to DNA-damaging agents (i.e. ionizing radiation, ultraviolet radiation, cis-platinum, and methotrexate) within subclones of a pre-existing p53(-/-) MEF cell population. Moreover, this differential sensitivity was also observed within subclones of p53(-/-) MEF cells transformed with an activated ras allele, suggesting that secondary genetic events and clonal selection, but not cellular transformation per se, may drive the resistance patterns for certain null-p53 tumors. In contrast, uniform resistance was observed following the additional transfection of an MTp53 allele (MTp53pro193) into p53(-/-) MEF transformants and p53(-/-) DP-16 Friend erythroleukemia cells, consistent with a gain of MTp53 function for this allele. Relative tumor growth rate and experimental metastatic ability was not enhanced by MTp53pro193 expression. Our results support the concept that gain of MTp53pro193 function leads to the selection of dominant clones, which may exhibit cellular resistance following cancer therapy.
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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.