ArticleScientific reports2019
Maintenance of the bladder cancer precursor urothelial hyperplasia requires FOXA1 and persistent expression of oncogenic HRAS.
Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 15 citations in OpenAlex.
- Prophylactic role of artemisinin in modulating FGFR3, HRAS, and TP53 to prevent early-stage urothelial carcinoma in BBN-induced mouse models.BMC biotechnology · 2025Article
- Epicatechin attenuates the stemness of liver cancer stem cells and tumorigenesis through DNA methylation-mediated inactivation of GINS1/HRAS.Journal of translational medicine · 2025Article
- KDM6A Loss Triggers an Epigenetic Switch That Disrupts Urothelial Differentiation and Drives Cell Proliferation in Bladder Cancer.Cancer research · 2023Article
- Article
- Cancer incidence and surveillance strategies in individuals with RASopathies.American journal of medical genetics. Part C, Seminars in medical genetics · 2022Review
- Novel Mouse Models of Bladder Cancer Identify a Prognostic Signature Associated with Risk of Disease Progression.Cancer research · 2021Article
- KDM6A-ARHGDIB axis blocks metastasis of bladder cancer by inhibiting Rac1.Molecular cancer · 2021Article
- Article
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
Tumorigenesis requires accumulation of genetic and epigenetic alterations, some of which drive tumor initiation. "Oncogene addiction" describes the phenomenon that (1) well-established cancers are dependent on one mutated oncogene or pathway for the maintenance of a malignant phenotype and that (2) withdrawal of the single oncogenic event leads to growth arrest and/or cancer regression. While oncogene addiction has been experimentally validated in advanced tumor models, its role in tumor precursors has not been investigated. We utilized the requirement of Forkhead box A1 (Foxa1) for transcriptional activation of the Upk2-promoter to temporally control the expression of Upk2-HRAS* oncogene, an inducer of urothelial hyperplasia in transgenic mice. Inducible homozygous knockout of Foxa1 in Upk2-HRAS*/UBC-Cre
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Registered trials
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