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Copy number aberrations and SNVs define clonal relationships, revealing tumor-suppressor losses and oncogenic gains, and suggesting multidirectional dissemination with possible genomic stability in metastatic cells.",{"@graph":14,"@context":77},[15,34,56],{"@type":16,"itemListElement":17},"BreadcrumbList",[18,23,27,31],{"item":19,"name":20,"@type":21,"position":22},"https://docshare.wps.com","Home","ListItem",1,{"item":24,"name":25,"@type":21,"position":26},"https://docshare.wps.com/document/","Document",2,{"item":28,"name":29,"@type":21,"position":30},"https://docshare.wps.com/document/research-report/","Research & 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observed?",{"text":72,"@type":64},"Frequent monoallelic losses occurred in tumor suppressors such as PTEN, TP53, FOXO4, and STAG2, while gains were observed in oncogenes including MTOR, RAF1, and HRAS, along with an angiogenic growth factor (VEGFB).",{"name":74,"@type":61,"acceptedAnswer":75},"What spreading model do the clonal evolution results suggest?",{"text":76,"@type":64},"The clonal evolution shows a complex branching pattern consistent with multidirectional dissemination, suggesting possible bidirectional seeding between the primary tumor, circulation, and metastatic sites, with limitations for single-patient 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BMC Genomic Data (2026) 27:50 BMC Genomic Data  \n[https://doi.org/10.1186/s12863-026-01435-5](https://doi.org/10.1186/s12863-026-01435-5)  \nRESEARCH Open Access  \nSingle-cell genomic analysis of cancer cells from one treatment-naïve patient with metastatic prostate cancer  \nJuan Jovel1,2, Bernhard Polzer3, Jordan Patterson4, Hou Yong5, Catalina Vasquez6, Sandra O’keefe4, Desmond Pink6, Guibo Li5, Adrian Fairey7, Benjamin Adam8, Jeremy Teitelbaum9, Amir Salimi10, Stefan Kirsh 11, Barbara Alberter3, Lori Lowes12, Eric Carpenter13, Michael Kolinsky6, Zhongyi Zhu5, Qing Zhou5, Peter Venner6, Christopher Venner6, David Williams6, Alison Allan12, Paul C. Boutros 14, Christoph A. Klein3,11, Gane Wong4,13 and John D. Lewis6*  \nAbstract  \nBackground Prostate cancer is among the most prevalent malignancies in men and a leading cause of cancer mortality worldwide. While localized prostate cancer is often curable, progression to metastatic and castrationresistant disease either in lymph nodes or bone/bone marrow remains the major cause of death. Understanding the genomic events that drive metastasis—particularly in treatment-naïve patients—is critical to improving early detection and individualized therapy. Bulk tumor sequencing has revealed key mutational signatures but cannot resolve the cellular heterogeneity and clonal dynamics underlying metastatic spread. Single-cell genomic approaches now enable high-resolution dissection of tumor evolution, uncovering the diversity of cancer clones across disease sites.  \nResults We performed whole-genome and whole-exome sequencing on single cancer cells from a treatmentnaïve patient with metastatic prostate cancer, isolating cells from the primary tumor, circulating tumor cells (CTCs), disseminated tumor cells (DTCs) in bone marrow, and metastatic bone lesions. Copy number aberrations (CNAs) and single-nucleotide variants (SNVs) were characterized to define genomic heterogeneity and infer clonal relationships. Frequent monoallelic losses in tumor suppressors (PTEN, TP53, FOXO4, STAG2) and gains in oncogenes (MTOR, RAF1, HRAS) and an angiogenic growth factor (VEGFB), were observed. Metastatic cells displayed fewer genomic alterations than CTCs or DTCs. While this observation is consistent with the hypothesis that metastatic competence may be associated with relative genomic stability, normal cell contamination of the metastatic biopsy cannot be excluded, and this interpretation should be considered preliminary. Clonal evolution analysis revealed a complex branching pattern consistent with multidirectional dissemination, suggesting bidirectional seeding between the primary tumor, circulation, and metastatic sites as one possible model of spread, though alternative explanations including phylogenetic reconstruction artefacts cannot be excluded from a single-patient study.  \n*Correspondence: John D. Lewis [jdlewis@ualberta.ca](jdlewis@ualberta.ca)  \nFull list of author information is available at the end of the article  \n© The Author(s) 2026. Open Access This article is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License, which permits any non-commercial use, sharing, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if you modified the licensed material. You do not have permission under this licence to share adapted material derived from this article or parts of it. The images or other third party material in this article are included in the article’s Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licenc","cbCaiptJvrRbp4C5","https://ap.wps.com/l/cbCaiptJvrRbp4C5","pdf",2204424,13,"English","# Abstract\n## Background\n## Results\n## Conclusions\n# Keywords\n# Background","[{\"question\":\"What is the main goal of this study?\",\"answer\":\"To build a single-cell genomic map of metastatic prostate cancer in a treatment-naïve patient and to characterize genomic heterogeneity and clonal relationships across disease sites.\"},{\"question\":\"Which sample types were analyzed using single-cell sequencing?\",\"answer\":\"Single cancer cells were isolated from the primary tumor, circulating tumor cells (CTCs), disseminated tumor cells (DTCs) in bone marrow, and metastatic bone lesions.\"},{\"question\":\"What genomic alterations were commonly observed?\",\"answer\":\"Frequent monoallelic losses occurred in tumor suppressors such as PTEN, TP53, FOXO4, and STAG2, while gains were observed in oncogenes including MTOR, RAF1, and HRAS, along with an angiogenic growth factor (VEGFB).\"},{\"question\":\"What spreading model do the clonal evolution results suggest?\",\"answer\":\"The clonal evolution shows a complex branching pattern consistent with multidirectional dissemination, suggesting possible bidirectional seeding between the primary tumor, circulation, and metastatic sites, with limitations for single-patient inference.\"}]","Single-cell genomic analysis of cancer cells from one treatment-naïve patient with metastatic prostate cancer | PDF",1790083185,33]