ArticleProceedings of the National Academy of Sciences of the United States of America2010
Cis lethal genetic interactions attenuate and alter p53 tumorigenesis.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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.
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Who cites it
7 citing papers in PubMed, 8 citations in OpenAlex.
- Advances in next-generation sequencing and emerging technologies for hematologic malignancies.Haematologica · 2024Review
- Analysis of 1276 Haplotype-Resolved Genomes Allows Characterization of Cis- and Trans-Abundant Genes.Methods in molecular biology (Clifton, N.J.) · 2023Article
- Gain-of-function mutations in RPA1 cause a syndrome with short telomeres and somatic genetic rescue.Blood · 2022Article
- Article
- A comprehensively molecular haplotype-resolved genome of a European individual.Genome research · 2011Article
- Increased RPA1 gene dosage affects genomic stability potentially contributing to 17p13.3 duplication syndrome.PLoS genetics · 2011Article
- Genes essential for cell viability that are linked to tumor suppressor genes play a role in cancer susceptibility.Cell cycle (Georgetown, Tex.) · 2010Article
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 4 institutions in 1 country.
Funding
Abstract
Rpa1, an essential gene involved in DNA replication and genome maintenance, is syntenic and linked to Trp53 in mice and humans. To study the genetic interaction between Rpa1 and Trp53 in tumorigenesis, we generated compound Rpa1(L230P/+); Trp53(+/-) mutant mice with the mutant alleles in either trans or cis configuration. We demonstrate that the Rpa1(L230P) missense mutation significantly alters the tumor phenotype and spectrum of Trp53 mutant mice by modifying the genetic mechanisms underlying tumorigenesis. Importantly, when the Rpa1(L230P) and Trp53 mutant alleles are in cis, the tumor phenotype is attenuated and altered and loss of heterozygosity (LOH) at the Trp53 wild-type locus is selected against, whereas in the trans configuration, Rpa1(L230P) enhances the Trp53(+/-) tumor phenotype even though Rpa1(L230P) is ultimately lost by LOH. These studies indicate that polymorphic genetic variants in cell essential genes can genetically affect closely linked tumor suppressor loci via allelic phasing, which can result in profound phenotypic variations in tumorigenesis.
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Registered trials
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