ArticleHuman pathology2014
Prostate cancer with Paneth cell-like neuroendocrine differentiation has recognizable histomorphology and harbors AURKA gene amplification.
Article in Human pathology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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16 citing papers in PubMed, 33 citations in OpenAlex.
- AURKA inhibitor VIC-1911 induces mitotic defects and functional BRCAness, sensitizing prostate cancer to PARP inhibition.JCI insight · 2026Article
- Protein kinase D2-Aurora kinase A-ERK1/2 signalling axis drives neuroendocrine differentiation of epithelial ovarian cancer.Molecular and cellular biochemistry · 2025Article
- Endocrine Disrupting Chemicals Influence Hub Genes Associated with Aggressive Prostate Cancer.International journal of molecular sciences · 2023Article
- Downregulation of MMP1 functions in preventing perineural invasion of pancreatic cancer through blocking the NT-3/TrkC signaling pathway.Journal of clinical laboratory analysis · 2022Article
- Early mRNA Expression of Neuroendocrine Differentiation Signals Predicts Recurrence After Radical Prostatectomy: A Transcriptomic Analysis.World journal of oncology · 2021Article
- CXCL12/CXCR4 facilitates perineural invasion via induction of the Twist/S100A4 axis in salivary adenoid cystic carcinoma.Journal of cellular and molecular medicine · 2021Article
- CXCR5 induces perineural invasion of salivary adenoid cystic carcinoma by inhibiting microRNA-187.Aging · 2021Article
- Neuroendocrine differentiation in usual-type prostatic adenocarcinoma: Molecular characterization and clinical significance.The Prostate · 2020Article
- Article
- Extensive Paneth cell metaplasia in an ovarian Krukenberg tumor: report of an unusual case and literature review.Journal of surgical case reports · 2018Article
- Paneth Cell-Like Component in Prostate Cancer - Case Report.Acta clinica Croatica · 2018Article
- RIPK1-dependent cell death: a novel target of the Aurora kinase inhibitor Tozasertib (VX-680).Cell death & disease · 2018Article
- Histopathology of Prostate Cancer.Cold Spring Harbor perspectives in medicine · 2017Review
- Aurora Kinase A Is a Prognostic Marker in Colorectal Adenocarcinoma.Journal of pathology and translational medicine · 2017Article
- Neuroendocrine Tumors of the Prostate: Emerging Insights from Molecular Data and Updates to the 2016 World Health Organization Classification.Endocrine pathology · 2016Review
- Sarcosine Up-Regulates Expression of Genes Involved in Cell Cycle Progression of Metastatic Models of Prostate Cancer.PloS one · 2016Article
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Authors and funding
13 authors at 6 institutions in 2 countries.
Funding
Abstract
Aurora kinase A (AURKA) gene amplification has been documented in 67% of hormone-naive prostate cancer cases that progress to a highly aggressive variant of castrate-resistant disease, clinically referred to as "neuroendocrine" prostate cancer, "small cell" prostate carcinoma, or "anaplastic" prostate cancer. Therefore, AURKA amplification is a potential prognostic biomarker that may help to identify patients with prostate cancer who are at high risk for developing castrate-resistant disease with clinical features of small cell carcinoma. Furthermore, AURKA inhibitors are currently being tested in clinical trials. In a previous study, we found AURKA amplification in 6 cases of prostate cancer with Paneth cell-like cells. This morphologic pattern has been suggested to represent low-grade neuroendocrine differentiation (NED) with generally favorable prognosis. We sought to investigate the frequency of AURKA amplification and the histologic characteristics of prostate cancer with Paneth cell-like NED. Twenty-five cases from 172 prostatectomies were evaluated for the presence of 18 morphologic features and AURKA amplification. Most prostate cancers with Paneth cell-like NED had macronucleoli (92%), basophilic appearance (88%), perineural invasion (72%), and nuclear stratification (76%). The frequency of AURKA amplification was 45%, present throughout the examined tumor nodule including areas without Paneth cell-like cells. When histologically similar cases with and without AURKA amplification were compared, this gene alteration was associated with larger extent of Paneth cell-like NED identified at magnification ×20 (P = .015), higher percentage of Paneth cell-like NED throughout the tumor nodule (P = .033), ductal features (P = .02), and higher overall Gleason grade (P = .039). AURKA amplification was not associated with age, serum prostate specific antigen, or tumor stage. The high frequency of AURKA amplification (45%) in localized prostate cancer with Paneth cell-like NED and its potential prognostic significance warrant further investigation.
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