ArticlePloS one2012
Inactivation and inducible oncogenic mutation of p53 in gene targeted pigs.
Article in PloS one, 2012. 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, 76 citations in OpenAlex.
- Article
- The Vietnamese swine as a translational model of invasive ductal carcinoma of the breast.Animal models and experimental medicine · 2025Article
- Tissue-engineered patient-derived osteosarcoma models dissecting tumour-bone interactions.Cancer metastasis reviews · 2024Review
- Pigs: Large Animal Preclinical Cancer Models.World journal of oncology · 2024Review
- Swine models for translational oncological research: an evolving landscape and regulatory considerations.Mammalian genome : official journal of the International Mammalian Genome Society · 2022Review
- In vitro genome editing activity of Cas9 in somatic cells after random and transposon-based genomic Cas9 integration.PloS one · 2022Article
- Use of Translational, Genetically Modified Porcine Models to Ultimately Improve Intestinal Disease Treatment.Frontiers in veterinary science · 2022Review
- Efficient Generation of P53 Biallelic Mutations in Diannan Miniature Pigs Using RNA-Guided Base Editing.Life (Basel, Switzerland) · 2021Article
- Porcine pancreatic ductal epithelial cells transformed with KRASScientific reports · 2021Article
- The CRISPR/Cas9 Minipig-A Transgenic Minipig to Produce Specific Mutations in Designated Tissues.Cancers · 2021Article
- Allelic Expression Imbalance Analysis IdentifiedCancers · 2021Article
- Cas9-expressing chickens and pigs as resources for genome editing in livestock.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Beyond tradition and convention: benefits of non-traditional model organisms in cancer research.Cancer metastasis reviews · 2021Review
- Porcine model elucidates function of p53 isoform in carcinogenesis and reveals novel circTP53 RNA.Oncogene · 2021Article
- The Missing Link: Cre Pigs for Cancer Research.Frontiers in oncology · 2021Article
- Perspective: Humanized Pig Models of Bladder Cancer.Frontiers in molecular biosciences · 2021Article
- A collection of bacterial isolates from the pig intestine reveals functional and taxonomic diversity.Nature communications · 2020Article
- Review
- Gain-of-Function Mutations in p53 in Cancer Invasiveness and Metastasis.International journal of molecular sciences · 2020Review
- Genetically Engineered Pigs to Study Cancer.International journal of molecular sciences · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mutation of the tumor suppressor p53 plays a major role in human carcinogenesis. Here we describe gene-targeted porcine mesenchymal stem cells (MSCs) and live pigs carrying a latent TP53(R167H) mutant allele, orthologous to oncogenic human mutant TP53(R175H) and mouse Trp53(R172H), that can be activated by Cre recombination. MSCs carrying the latent TP53(R167H) mutant allele were analyzed in vitro. Homozygous cells were p53 deficient, and on continued culture exhibited more rapid proliferation, anchorage independent growth, and resistance to the apoptosis-inducing chemotherapeutic drug doxorubicin, all characteristic of cellular transformation. Cre mediated recombination activated the latent TP53(R167H) allele as predicted, and in homozygous cells expressed mutant p53-R167H protein at a level ten-fold greater than wild-type MSCs, consistent with the elevated levels found in human cancer cells. Gene targeted MSCs were used for nuclear transfer and fifteen viable piglets were produced carrying the latent TP53(R167H) mutant allele in heterozygous form. These animals will allow study of p53 deficiency and expression of mutant p53-R167H to model human germline, or spontaneous somatic p53 mutation. This work represents the first inactivation and mutation of the gatekeeper tumor suppressor gene TP53 in a non-rodent mammal.
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.