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available at http://www.ncbi.nlm.nih.gov/pubmed/30232014 Editorial Comment: The authors used a pan-stem cell, pan-cancer approach to investigate the relationship between epithelial cancers and normal stem cell associated expression networks. They show that a number of epithelial cancers become enriched for a human epithelial adult stem cell signature during progression to an advanced, aggressive state. The human adult stem cell signature provided prognostic information and was associated with genomic alterations that influence cancer aggressiveness and lineage differentiation. In this analysis the authors simplified the nomenclature for histologically defined neuroendocrine cancers and defined all epithelial derived neuroendocrine cancer subtypes as small cell neuroendocrine to prevent confusion when alternating between tissue types. Using multiple gene expression data sets composed of clinical samples, they found that aggressive small cell neuroendocrine cancers derived from different tissues have higher adult stem cell signature scores than nonsmall cell neuroendocrine phenotypes. Furthermore, they provide evidence that small cell neuroendocrine cancers share a core set of methylation regulated genes that are linked to their adult stem cell associated expression programs. The pan-cancer analysis establishes an adult stem cell based transcriptional and epigenomic foundation for identifying additional therapeutic targets for the treatment of aggressive epithelial malignancies from multiple tissue types. Anthony Atala, MD Suggested Reading Galleggiante V, Rutigliano M, Sallustio F et al: CTR2 identifies a population of cancer cells with stem cell-like features in patients with clear cell renal cell carcinoma. J Urol 2014; 192: 1831. Re: Diverse AR-V7 Cistromes in Castration-Resistant Prostate Cancer are Governed by HoxB13 Z. Chen, D. Wu, J. M. Thomas-Ahner, C. Lu, P. Zhao, Q. Zhang, C. Geraghty, P. S. Yan, W. Hankey, B. Sunkel, X. Cheng, E. S. Antonarakis, Q. E. Wang, Z. Liu, T. H. Huang, V. X. Jin, S. K. Clinton, J. Luo, J. Huang and Q. Wang Department of Pathology and Duke Cancer Institute, Duke University School of Medicine, Durham, North Carolina, Departments of Cancer Biology and Genetics, Internal Medicine and Radiology, Ohio State University College of Medicine, Columbus, Ohio, Department of Urology, Johns Hopkins University School of Medicine, Baltimore, Maryland, Department of Oncology, St. Jude Children’s Research Hospital, Memphis, Tennessee, Department of Molecular Medicine, University of Texas Health Science Center at San Antonio, San Antonio, Texas, and State Key Laboratory of Molecular Oncology, Peking Union Medical College, Chinese Academy of Medical Sciences, Beijing, China Proc Natl Acad Sci U S A 2018; 115: 6810e6815. doi: 10.1073/pnas.1718811115 Abstract available at http://www.ncbi.nlm.nih.gov/pubmed/29844167available at http://www.ncbi.nlm.nih.gov/pubmed/29844167 Editorial Comment: Mechanisms underlying androgen receptor splice variant 7 oncogenic function at the genomic level remain poorly defined. These authors found that androgen receptor splice variant 7 cistromes are cell context dependent in castration resistant prostate cancer cells and tissues, 446 URO-SCIENCE Copyright © 2019 American Urological Association Education and Research, Inc. Unauthorized reproduction of this article is prohibited.