ArticleOncogene2025
PTEN loss drives p53 LOH and immune evasion in a novel urothelial organoid model harboring p53 missense mutations.
Article in Oncogene, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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.
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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
1 citing paper in PubMed.
- Regulation of Keratin Chemical Modifications: Potential Molecular Mechanisms in Proliferative Diseases.International journal of molecular sciences · 2026Review
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Authors and funding
18 authors.
Funding
Abstract
Despite missense mutation accounts for over 60% of p53 alterations while homozygous deletion (HOM) for only 5% or less in advanced bladder cancer cases, most of the previously reported mouse models are deficient of p53. Accordingly, few studies have addressed the mechanisms of missense mutation occurrence and its functional advantage over HOM in bladder cancer development. Organoids derived from Krt5-expressing mouse urothelium (K5-mUrorganoid) demonstrated the crucial role of Pten loss in driving loss of wild-type allele of Trp53 (Trp53
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