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Multiregion sampling of de novo metastatic prostate cancer reveals complex polyclonality and augments clinical genotyping

Evan W. Warner, Kim Van der Eecken, Andrew J. Murtha, Edmond M. Kwan, Cameron Herberts, Joonatan Sipola, Sarah W. S. Ng, Xinyi E. Chen, Nicolette M. Fonseca, Elie Ritch, et al.
(2024) NATURE CANCER. 5(1). p.5-7
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Abstract
De novo metastatic prostate cancer is highly aggressive, but the paucity of routinely collected tissue has hindered genomic stratification and precision oncology. Here, we leveraged a rare study of surgical intervention in 43 de novo metastatic prostate cancers to assess somatic genotypes across 607 synchronous primary and metastatic tissue regions plus circulating tumor DNA. Intra-prostate heterogeneity was pervasive and impacted clinically relevant genes, resulting in discordant genotypes between select primary restricted regions and synchronous metastases. Additional complexity was driven by polyclonal metastatic seeding from phylogenetically related primary populations. When simulating clinical practice relying on a single tissue region, genomic heterogeneity plus variable tumor fraction across samples caused inaccurate genotyping of dominant disease; however, pooling extracted DNA from multiple biopsy cores before sequencing can rescue misassigned somatic genotypes. Our results define the relationship between synchronous treatment-sensitive primary and metastatic lesions in men with de novo metastatic prostate cancer and provide a framework for implementing genomics-guided patient management. Warner et al. analyze tumor tissue and ctDNA from patients with de novo metastatic castrate-sensitive prostate cancer and find high intratumoral heterogeneity, suggesting that genomic profiling of multiple samples per patient is needed for accurate outcome prediction.

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MLA
Warner, Evan W., et al. “Multiregion Sampling of de Novo Metastatic Prostate Cancer Reveals Complex Polyclonality and Augments Clinical Genotyping.” NATURE CANCER, vol. 5, no. 1, 2024, pp. 5–7, doi:10.1038/s43018-023-00692-y.
APA
Warner, E. W., Van der Eecken, K., Murtha, A. J., Kwan, E. M., Herberts, C., Sipola, J., … Wyatt, A. W. (2024). Multiregion sampling of de novo metastatic prostate cancer reveals complex polyclonality and augments clinical genotyping. NATURE CANCER, 5(1), 5–7. https://doi.org/10.1038/s43018-023-00692-y
Chicago author-date
Warner, Evan W., Kim Van der Eecken, Andrew J. Murtha, Edmond M. Kwan, Cameron Herberts, Joonatan Sipola, Sarah W. S. Ng, et al. 2024. “Multiregion Sampling of de Novo Metastatic Prostate Cancer Reveals Complex Polyclonality and Augments Clinical Genotyping.” NATURE CANCER 5 (1): 5–7. https://doi.org/10.1038/s43018-023-00692-y.
Chicago author-date (all authors)
Warner, Evan W., Kim Van der Eecken, Andrew J. Murtha, Edmond M. Kwan, Cameron Herberts, Joonatan Sipola, Sarah W. S. Ng, Xinyi E. Chen, Nicolette M. Fonseca, Elie Ritch, Elena Schonlau, Cecily Q. Bernales, Grainne Donnellan, Asli D. Munzur, Karan Parekh, Kevin Beja, Amanda Wong, Sofie Verbeken, Nicolaas Lumen, Jo Van Dorpe, Bram De Laere, Matti Annala, Gillian Vandekerkhove, Piet Ost, and Alexander W. Wyatt. 2024. “Multiregion Sampling of de Novo Metastatic Prostate Cancer Reveals Complex Polyclonality and Augments Clinical Genotyping.” NATURE CANCER 5 (1): 5–7. doi:10.1038/s43018-023-00692-y.
Vancouver
1.
Warner EW, Van der Eecken K, Murtha AJ, Kwan EM, Herberts C, Sipola J, et al. Multiregion sampling of de novo metastatic prostate cancer reveals complex polyclonality and augments clinical genotyping. NATURE CANCER. 2024;5(1):5–7.
IEEE
[1]
E. W. Warner et al., “Multiregion sampling of de novo metastatic prostate cancer reveals complex polyclonality and augments clinical genotyping,” NATURE CANCER, vol. 5, no. 1, pp. 5–7, 2024.
@article{01HS88HFW1BNFV5YFEVYD2ZFM2,
  abstract     = {{De novo metastatic prostate cancer is highly aggressive, but the paucity of routinely collected tissue has hindered genomic stratification and precision oncology. Here, we leveraged a rare study of surgical intervention in 43 de novo metastatic prostate cancers to assess somatic genotypes across 607 synchronous primary and metastatic tissue regions plus circulating tumor DNA. Intra-prostate heterogeneity was pervasive and impacted clinically relevant genes, resulting in discordant genotypes between select primary restricted regions and synchronous metastases. Additional complexity was driven by polyclonal metastatic seeding from phylogenetically related primary populations. When simulating clinical practice relying on a single tissue region, genomic heterogeneity plus variable tumor fraction across samples caused inaccurate genotyping of dominant disease; however, pooling extracted DNA from multiple biopsy cores before sequencing can rescue misassigned somatic genotypes. Our results define the relationship between synchronous treatment-sensitive primary and metastatic lesions in men with de novo metastatic prostate cancer and provide a framework for implementing genomics-guided patient management.

Warner et al. analyze tumor tissue and ctDNA from patients with de novo metastatic castrate-sensitive prostate cancer and find high intratumoral heterogeneity, suggesting that genomic profiling of multiple samples per patient is needed for accurate outcome prediction.}},
  author       = {{Warner, Evan W. and Van der Eecken, Kim and  Murtha, Andrew J. and  Kwan, Edmond M. and  Herberts, Cameron and  Sipola, Joonatan and  Ng, Sarah W. S. and  Chen, Xinyi E. and  Fonseca, Nicolette M. and  Ritch, Elie and  Schonlau, Elena and  Bernales, Cecily Q. and  Donnellan, Grainne and  Munzur, Asli D. and  Parekh, Karan and  Beja, Kevin and  Wong, Amanda and Verbeken, Sofie and Lumen, Nicolaas and Van Dorpe, Jo and De Laere, Bram and  Annala, Matti and  Vandekerkhove, Gillian and Ost, Piet and  Wyatt, Alexander W.}},
  issn         = {{2662-1347}},
  journal      = {{NATURE CANCER}},
  language     = {{eng}},
  number       = {{1}},
  pages        = {{5--7}},
  title        = {{Multiregion sampling of de novo metastatic prostate cancer reveals complex polyclonality and augments clinical genotyping}},
  url          = {{http://doi.org/10.1038/s43018-023-00692-y}},
  volume       = {{5}},
  year         = {{2024}},
}
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