ArticleThe American journal of pathology2002
Prostatic intraepithelial neoplasia in genetically engineered mice.
Article in The American journal of pathology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 98 papers.
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Who cites it
98 citing papers in PubMed.
- Article
- Targeting the histone reader ZMYND8 inhibits antiandrogen-induced neuroendocrine tumor transdifferentiation of prostate cancer.Nature cancer · 2025Article
- Integrative proteogenomic profiling of high-risk prostate cancer samples from Chinese patients indicates metabolic vulnerabilities and diagnostic biomarkers.Nature cancer · 2024Article
- CRISPR/Cas9 model of prostate cancer identifies Kmt2c deficiency as a metastatic driver by Odam/Cabs1 gene cluster expression.Nature communications · 2024Article
- Immune mechanisms shape the clonal landscape during early progression of prostate cancer.Developmental cell · 2023Article
- Hyperphosphorylated PTEN exerts oncogenic properties.Nature communications · 2023Article
- Conditional gene regulation models demonstrate a pro-proliferative role for growth hormone receptor in prostate cancer.The Prostate · 2023Article
- ARID1A loss induces polymorphonuclear myeloid-derived suppressor cell chemotaxis and promotes prostate cancer progression.Nature communications · 2022Article
- Celastrol recruits UBE3A to recognize and degrade the DNA binding domain of steroid receptors.Oncogene · 2022Article
- Article
- Leukemia inhibitory factor receptor homodimerization mediated by acetylation of extracellular lysine promotes prostate cancer progression through the PDPK1/AKT/GCN5 axis.Clinical and translational medicine · 2022Article
- Article
- Article
- Loss of Ceacam1 promotes prostate cancer progression in Pten haploinsufficient male mice.Metabolism: clinical and experimental · 2020Article
- Superior cancer preventive efficacy of low versus high dose of mTOR inhibitor in a mouse model of prostate cancer.Oncotarget · 2020Article
- Membrane metalloendopeptidase suppresses prostate carcinogenesis by attenuating effects of gastrin-releasing peptide on stem/progenitor cells.Oncogenesis · 2020Article
- Prostate epithelial-specific expression of activated PI3K drives stromal collagen production and accumulation.The Journal of pathology · 2020Article
- STAT5a/b Deficiency Delays, but does not Prevent, Prolactin-Driven Prostate Tumorigenesis in Mice.Cancers · 2019Article
- Relationship between ETS Transcription Factor ETV1 and TGF-β-regulated SMAD Proteins in Prostate Cancer.Scientific reports · 2019Article
- Genetically Engineered Mouse Models of Prostate Cancer in the Postgenomic Era.Cold Spring Harbor perspectives in medicine · 2019Review
38 more citing papers are in PubMed but not listed here.
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Authors and funding
7 authors.
Funding
Abstract
Several mouse models of human prostate cancer were studied to identify and characterize potential precursor lesions containing foci of atypical epithelial cells. These lesions exhibit a sequence of changes suggesting progressive evolution toward malignancy. Based on these observations, a grading system is proposed to classify prostatic intraepithelial neoplasia (PIN) in genetically engineered mice (GEM). Four grades of GEM PIN are proposed based on their architecture, differentiation pattern, and degree of cytological atypia. PIN I lesions have one or two layers of atypical cells. PIN II has two or more layers of atypical cells. PIN III has large, pleomorphic nuclei with prominent nucleoli and the cells tend to involve the entire lumen with expansion of the duct outlines. PIN IV lesions contain atypical cells that fill the lumen and bulge focally into, and frequently compromise, the fibromuscular sheath. Within the same cohorts, the lower grade PINs first appear earlier than the higher grades. Morphometric and immunohistochemical analyses confirm progressive change. Although the malignant potential of PIN IV in mice has not been proven, GEM PIN is similar to human PIN. This PIN classification system is a first step toward a systematic evaluation of the biological potential of these lesions in GEM.
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