ArticleNeoplasia (New York, N.Y.)2007
Origin of androgen-insensitive poorly differentiated tumors in the transgenic adenocarcinoma of mouse prostate model.
Article in Neoplasia (New York, N.Y.), 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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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
41 citing papers in PubMed, 68 citations in OpenAlex.
- Jaboticaba peel extract limits castration-resistant prostate cancer aggressiveness by counteracting EMT through steroid hormone and TGF-β signaling modulation.Journal of molecular histology · 2026Article
- Mapping prostate cancer pathobiology: A review of genetically engineered mouse models (GEMMs).Gene · 2026Review
- Stathmin 1 expression in neuroendocrine and proliferating prostate cancer.Discover oncology · 2025Article
- Stathmin 1 Expression in Neuroendocrine and Proliferating Prostate Cancer.Research square · 2024Article
- The expression of PKM1 and PKM2 in developing, benign, and cancerous prostatic tissues.bioRxiv : the preprint server for biology · 2024Article
- The expression of PKM1 and PKM2 in developing, benign, and cancerous prostatic tissues.Frontiers in oncology · 2024Article
- The Role of Epigenetic Change in Therapy-Induced Neuroendocrine Prostate Cancer Lineage Plasticity.Frontiers in endocrinology · 2022Review
- Repurposing of the Antiepileptic Drug Levetiracetam to Restrain Neuroendocrine Prostate Cancer and Inhibit Mast Cell Support to Adenocarcinoma.Frontiers in immunology · 2021Article
- Shaping Chromatin States in Prostate Cancer by Pioneer Transcription Factors.Cancer research · 2020Review
- Prostate cancer susceptibility geneOncotarget · 2018Article
- Gene expression signatures associated with suppression of TRAMP prostate carcinogenesis by a kavalactone-rich Kava fraction.Molecular carcinogenesis · 2016Article
- Neuronal Trans-Differentiation in Prostate Cancer Cells.The Prostate · 2016Article
- Genetic deletion of osteopontin in TRAMP mice skews prostate carcinogenesis from adenocarcinoma to aggressive human-like neuroendocrine cancers.Oncotarget · 2016Article
- Analysis of TMEFF2 allografts and transgenic mouse models reveals roles in prostate regeneration and cancer.The Prostate · 2016Article
- Chemopreventive Effects of Korean Angelica versus Its Major Pyranocoumarins on Two Lineages of Transgenic Adenocarcinoma of Mouse Prostate Carcinogenesis.Cancer prevention research (Philadelphia, Pa.) · 2015Article
- Dietary supplement 4-methylumbelliferone: an effective chemopreventive and therapeutic agent for prostate cancer.Journal of the National Cancer Institute · 2015Article
- The steroid receptor coactivator-3 is required for developing neuroendocrine tumor in the mouse prostate.International journal of biological sciences · 2014Article
- Conversion of androgen receptor signaling from a growth suppressor in normal prostate epithelial cells to an oncogene in prostate cancer cells involves a gain of function in c-Myc regulation.International journal of biological sciences · 2014Article
- Iodine uptake and prostate cancer in the TRAMP mouse model.Molecular medicine (Cambridge, Mass.) · 2013Article
- Gene signatures distinguish stage-specific prostate cancer stem cells isolated from transgenic adenocarcinoma of the mouse prostate lesions and predict the malignancy of human tumors.Stem cells translational medicine · 2013Article
Corrections and comments
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Authors and funding
8 authors at 5 institutions in 1 country.
Funding
Abstract
Following castration, the transgenic adenocarcinoma of mouse prostate (TRAMP) model demonstrates rapid development of SV40-Tag-driven poorly differentiated tumors that express neuroendocrine cell markers. The cell population dynamics within the prostates of castrated TRAMP mice were characterized by analyzing the incorporation of 5-bromodeoxyuridine (BrdUrd) and the expression of SV40-Tag, synaptophysin, and androgen receptor (AR). Fourteen days postcastration, the remaining epithelial cells and adenocarcinoma cells were nonproliferative and lacked detectable SV40-Tag or synaptophysin expression. In contrast, morphologically distinct intraglandular foci were identified which expressed SV40-Tag, synaptophysin, and Ki67, but that lacked AR expression. These proliferative SV40-Tag and synaptophysin-expressing intraglandular foci were associated with the rare BrdUrd-retaining cells. These foci expanded rapidly in the postcastration prostate environment, in contrast to the AR- and SV40-Tag-expressing adenocarcinoma cells that lost SV40-Tag expression and underwent apoptosis after castration. Intraglandular foci of synaptophysin-expressing cells were also observed in the prostates of intact TRAMP mice at a comparable frequency; however, they did not progress to rapidly expanding tumors until much later in the life of the mice. This suggests that the foci of neuroendocrine-like cells that express SV40-Tag and synaptophysin, but lack AR, arise independent of androgen-deprivation and represent the source of the poorly differentiated tumors that are the lethal phenotype in the TRAMP model.
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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.