ArticleDifferentiation; research in biological diversity2009
Simultaneous haploinsufficiency of Pten and Trp53 tumor suppressor genes accelerates tumorigenesis in a mouse model of prostate cancer.
Article in Differentiation; research in biological diversity, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 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
25 citing papers in PubMed, 38 citations in OpenAlex.
- Mapping prostate cancer pathobiology: A review of genetically engineered mouse models (GEMMs).Gene · 2026Review
- Article
- Immunological facets of prostate cancer and the potential of immune checkpoint inhibition in disease management.Theranostics · 2024Review
- In Vivo Models for Prostate Cancer Research.Cancers · 2022Review
- Double heterozygosity for TP53 and BRCA1 mutations: clinical implications in populations with founder mutations.Breast cancer research and treatment · 2021Article
- Loss of Ceacam1 promotes prostate cancer progression in Pten haploinsufficient male mice.Metabolism: clinical and experimental · 2020Article
- Silencing of PTEN inhibits the oxidative stress damage and hippocampal cell apoptosis induced by Sevoflurane through activating MEK1/ERK signaling pathway in infant rats.Cell cycle (Georgetown, Tex.) · 2020Article
- Genetically Engineered Mouse Models of Prostate Cancer in the Postgenomic Era.Cold Spring Harbor perspectives in medicine · 2019Review
- Clinical implications of PTEN loss in prostate cancer.Nature reviews. Urology · 2018Review
- Efficient Generation of Somatic Cell Nuclear Transfer-Competent Porcine Cells with Mutated Alleles at Multiple Target Loci by Using CRISPR/Cas9 Combined with Targeted Toxin-Based Selection System.International journal of molecular sciences · 2017Article
- Combined Loss of EAF2 and p53 Induces Prostate Carcinogenesis in Male Mice.Endocrinology · 2017Article
- Transdifferentiation as a Mechanism of Treatment Resistance in a Mouse Model of Castration-Resistant Prostate Cancer.Cancer discovery · 2017Article
- E3 ubiquitin ligase isolated by differential display regulates cervical cancer growthExperimental and therapeutic medicine · 2016Article
- Mouse Models in Prostate Cancer Translational Research: From Xenograft to PDX.BioMed research international · 2016Review
- Drug discovery in prostate cancer mouse models.Expert opinion on drug discovery · 2015Review
- Androgen receptor (AR) differential roles in hormone-related tumors including prostate, bladder, kidney, lung, breast and liver.Oncogene · 2014Review
- Diverse mechanisms of AKT pathway activation in human malignancy.Current cancer drug targets · 2013Review
- Loss of survivin in the prostate epithelium impedes carcinogenesis in a mouse model of prostate adenocarcinoma.PloS one · 2013Article
- Androgen hormone action in prostatic carcinogenesis: stromal androgen receptors mediate prostate cancer progression, malignant transformation and metastasis.Carcinogenesis · 2012Article
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 7 institutions in 2 countries.
Funding
Abstract
Tumor suppressor gene PTEN is important in the initiation and progression of human prostate carcinoma, whereas the role of TP53 remains controversial. Since Pten/Trp53 double conditional knockout mice show earlier onset and fast progression of prostate cancer when compared to Pten knockout mice, we asked whether heterozygosity of these two tumor suppressor genes was sufficient to accelerate prostatic tumorigenesis. To answer this question we examined prostatic lesion progression of Pten/Trp53 double heterozygous mice and a series of controls such as Pten heterozygous, Pten conditional knockout, Trp53 heterozygous and Trp53 knockout mice. Tissue recombination of adult prostatic epithelium coupled with embryonic rat seminal vesicle mesenchyme was used as a tool to stimulate prostatic epithelial proliferation. In our study, high-grade prostatic intraepithelial neoplasia (PIN) was found with high frequency at 8 weeks post-tissue recombination transplantation. PIN lesions in Pten/Trp53 double heterozygous mice were more severe than those seen in Pten heterozygous alone. Furthermore, morphologic features attributable to Pten or Trp53 loss appeared to be enhanced in double heterozygous tissues. LOH analysis of Pten and Trp53 in genomic DNA collected from high-grade PIN lesions in Pten heterozygous and Pten/Trp53 double heterozygous mice showed an intact wild-type allele for both genes in all samples examined. In conclusion, simultaneous heterozygosity of Pten and Trp53 accelerates prostatic tumorigenesis in this mouse model of prostate cancer independently of loss of heterozygosity of either gene.
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.