ArticleCancer letters2022
Structural or functional defects of PTEN in urothelial cells lacking P53 drive basal/squamous-subtype muscle-invasive bladder cancer.
Article in Cancer letters, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 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
8 citing papers in PubMed, 8 citations in OpenAlex.
- Targeted therapies for urothelial carcinoma: From FGFR inhibitors to next‑generation antibody-drug conjugates (Review).International journal of oncology · 2026Review
- SWI/SNF-associated molecular subtypes reshape tumor microenvironmental features and inform precision therapeutic strategies in bladder cancer.Frontiers in cellular and infection microbiology · 2026Article
- Tumor dormancy and relapse: understanding the molecular mechanisms of cancer recurrence.Military Medical Research · 2025Review
- Histological and immunohistochemical approaches to molecular subtyping in muscle-invasive bladder cancer.Frontiers in oncology · 2025Review
- Preclinical models of bladder cancer: BBN and beyond.Nature reviews. Urology · 2024Review
- Lysine Methyltransferase 9 (KMT9) Is an Actionable Target in Muscle-Invasive Bladder Cancer.Cancers · 2024Article
- Development and validation of a disulfidptosis and M2 TAM-related classifier for bladder cancer to explore tumor subtypes, immune landscape and drug treatment.Journal of cancer research and clinical oncology · 2023Article
- The mechanism and clinical application of DNA damage repair inhibitors combined with immune checkpoint inhibitors in the treatment of urologic cancer.Frontiers in cell and developmental biology · 2023Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Muscle-invasive bladder cancer (MIBC) exhibits strong inter- and intra-tumor heterogeneity that affects biological behaviors, therapeutic responses, and prognoses. Mutations that activate RTK-RAS-PI3K and inactivate P19-P53-P21 coexist in 60-70% of MIBC. By time-controlled ablation of Tp53 and Pten, singly or combined, in adult mouse urothelium, we found that Tp53 loss alone produced no abnormality. While Pten loss elicited hyperplasia, it synergized with Tp53 loss to trigger 100% penetrant MIBC that exhibited basal/squamous features that resembled its human counterpart. Furthermore, PTEN was inactivated in human MIBC cell lines and specimens primarily by hyperphosphorylation of the C-terminus. Mutated or tailless PTEN incapable of C-terminal phosphorylation demonstrated increased inhibition of proliferation and invasion than full-length PTEN in cultured MIBC cells. In xenograft and transgenic mice, tailless PTEN, but not full-length PTEN, prevented further growth in established tumors. Collectively, deficiencies of both PTEN and P53 drive basal/squamous subtype MIBC. PTEN is inactivated by C-terminal hyperphosphorylation, and this modification may serve as a biomarker for subtyping MIBC and predicting tumor progression. Tailless PTEN is a potential molecular therapeutic for tumors, such as bladder cancer (BC), that can be readily accessed.
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Registered trials
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