Circulating tumor cell heterogeneity in neuroendocrine prostate cancer by single cell copy number analysis
Abstract Neuroendocrine prostate cancer is an aggressive variant of prostate cancer that may arise de novo or develop from pre-existing prostate adenocarcinoma as a mechanism of treatment resistance. The combined loss of tumor suppressors RB1, TP53, and PTEN are frequent in NEPC but also present in...
| Main Authors: | , , , , , , , , , , , , , , , |
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| Format: | Article |
| Language: | English |
| Published: |
Nature Portfolio
2021-08-01
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| Series: | npj Precision Oncology |
| Online Access: | https://doi.org/10.1038/s41698-021-00211-1 |
| _version_ | 1797641661229039616 |
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| author | Vincenza Conteduca Sheng-Yu Ku Luisa Fernandez Angel Dago-Rodriquez Jerry Lee Adam Jendrisak Megan Slade Cole Gilbertson Jyothi Manohar Michael Sigouros Yipeng Wang Ryan Dittamore Rick Wenstrup Juan Miguel Mosquera Joseph D. Schonhoft Himisha Beltran |
| author_facet | Vincenza Conteduca Sheng-Yu Ku Luisa Fernandez Angel Dago-Rodriquez Jerry Lee Adam Jendrisak Megan Slade Cole Gilbertson Jyothi Manohar Michael Sigouros Yipeng Wang Ryan Dittamore Rick Wenstrup Juan Miguel Mosquera Joseph D. Schonhoft Himisha Beltran |
| author_sort | Vincenza Conteduca |
| collection | DOAJ |
| description | Abstract Neuroendocrine prostate cancer is an aggressive variant of prostate cancer that may arise de novo or develop from pre-existing prostate adenocarcinoma as a mechanism of treatment resistance. The combined loss of tumor suppressors RB1, TP53, and PTEN are frequent in NEPC but also present in a subset of prostate adenocarcinomas. Most clinical and preclinical studies support a trans-differentiation process, whereby NEPC arises clonally from a prostate adenocarcinoma precursor during the course of treatment resistance. Here we highlight a case of NEPC with significant intra-patient heterogeneity observed across metastases. We further demonstrate how single-cell genomic analysis of circulating tumor cells combined with a phenotypic evaluation of cellular diversity can be considered as a window into tumor heterogeneity in patients with advanced prostate cancer. |
| first_indexed | 2024-03-11T13:48:54Z |
| format | Article |
| id | doaj.art-192f8c4983314673aa85a47274caaba0 |
| institution | Directory Open Access Journal |
| issn | 2397-768X |
| language | English |
| last_indexed | 2024-03-11T13:48:54Z |
| publishDate | 2021-08-01 |
| publisher | Nature Portfolio |
| record_format | Article |
| series | npj Precision Oncology |
| spelling | doaj.art-192f8c4983314673aa85a47274caaba02023-11-02T09:26:55ZengNature Portfolionpj Precision Oncology2397-768X2021-08-01511810.1038/s41698-021-00211-1Circulating tumor cell heterogeneity in neuroendocrine prostate cancer by single cell copy number analysisVincenza Conteduca0Sheng-Yu Ku1Luisa Fernandez2Angel Dago-Rodriquez3Jerry Lee4Adam Jendrisak5Megan Slade6Cole Gilbertson7Jyothi Manohar8Michael Sigouros9Yipeng Wang10Ryan Dittamore11Rick Wenstrup12Juan Miguel Mosquera13Joseph D. Schonhoft14Himisha Beltran15Dana Farber Cancer Institute and Harvard Medical SchoolDana Farber Cancer Institute and Harvard Medical SchoolEpic Sciences, Inc.Epic Sciences, Inc.Epic Sciences, Inc.Epic Sciences, Inc.Epic Sciences, Inc.Epic Sciences, Inc.Weill Cornell MedicineWeill Cornell MedicineEpic Sciences, Inc.Epic Sciences, Inc.Epic Sciences, Inc.Weill Cornell MedicineEpic Sciences, Inc.Dana Farber Cancer Institute and Harvard Medical SchoolAbstract Neuroendocrine prostate cancer is an aggressive variant of prostate cancer that may arise de novo or develop from pre-existing prostate adenocarcinoma as a mechanism of treatment resistance. The combined loss of tumor suppressors RB1, TP53, and PTEN are frequent in NEPC but also present in a subset of prostate adenocarcinomas. Most clinical and preclinical studies support a trans-differentiation process, whereby NEPC arises clonally from a prostate adenocarcinoma precursor during the course of treatment resistance. Here we highlight a case of NEPC with significant intra-patient heterogeneity observed across metastases. We further demonstrate how single-cell genomic analysis of circulating tumor cells combined with a phenotypic evaluation of cellular diversity can be considered as a window into tumor heterogeneity in patients with advanced prostate cancer.https://doi.org/10.1038/s41698-021-00211-1 |
| spellingShingle | Vincenza Conteduca Sheng-Yu Ku Luisa Fernandez Angel Dago-Rodriquez Jerry Lee Adam Jendrisak Megan Slade Cole Gilbertson Jyothi Manohar Michael Sigouros Yipeng Wang Ryan Dittamore Rick Wenstrup Juan Miguel Mosquera Joseph D. Schonhoft Himisha Beltran Circulating tumor cell heterogeneity in neuroendocrine prostate cancer by single cell copy number analysis npj Precision Oncology |
| title | Circulating tumor cell heterogeneity in neuroendocrine prostate cancer by single cell copy number analysis |
| title_full | Circulating tumor cell heterogeneity in neuroendocrine prostate cancer by single cell copy number analysis |
| title_fullStr | Circulating tumor cell heterogeneity in neuroendocrine prostate cancer by single cell copy number analysis |
| title_full_unstemmed | Circulating tumor cell heterogeneity in neuroendocrine prostate cancer by single cell copy number analysis |
| title_short | Circulating tumor cell heterogeneity in neuroendocrine prostate cancer by single cell copy number analysis |
| title_sort | circulating tumor cell heterogeneity in neuroendocrine prostate cancer by single cell copy number analysis |
| url | https://doi.org/10.1038/s41698-021-00211-1 |
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