ArticleNature communications2023
Copy number architectures define treatment-mediated selection of lethal prostate cancer clones.
Article in Nature communications, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
9 citing papers in PubMed, 10 citations in OpenAlex.
- Recurrent intra-tumour heterogeneity is a hallmark of metastatic prostate cancer.Nature communications · 2026Article
- Convergent evolution of complex structural variants drives therapy resistance in metastatic prostate cancer.Genome biology · 2026Article
- Divergent Clonal Evolution and Early Dissemination Promote Genetic Heterogeneity of Metastases in Castration-Resistant Prostate Cancer.Cancer research · 2025Article
- Uncovering phenotypic heterogeneity through research autopsy in lethal prostate cancer.The Journal of clinical investigation · 2025Article
- Patterns of intra- and intertumor phenotypic heterogeneity in lethal prostate cancer.The Journal of clinical investigation · 2025Article
- Precision Targeting in Metastatic Prostate Cancer: Molecular Insights to Therapeutic Frontiers.Biomolecules · 2025Review
- Chromosomal instability as a driver of cancer progression.Nature reviews. Genetics · 2025Review
- Treatment-induced stemness and lineage plasticity in driving prostate cancer therapy resistance.Cancer heterogeneity and plasticity · 2024Article
- Copy number architectures define treatment-mediated selection of lethal prostate cancer clones.Nature communications · 2023Article
Corrections and comments
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Authors and funding
24 authors at 20 institutions in 2 countries.
Funding
Abstract
Despite initial responses to hormone treatment, metastatic prostate cancer invariably evolves to a lethal state. To characterize the intra-patient evolutionary relationships of metastases that evade treatment, we perform genome-wide copy number profiling and bespoke approaches targeting the androgen receptor (AR) on 167 metastatic regions from 11 organs harvested post-mortem from 10 men who died from prostate cancer. We identify diverse and patient-unique alterations clustering around the AR in metastases from every patient with evidence of independent acquisition of related genomic changes within an individual and, in some patients, the co-existence of AR-neutral clones. Using the genomic boundaries of pan-autosome copy number changes, we confirm a common clone of origin across metastases and diagnostic biopsies, and identified in individual patients, clusters of metastases occupied by dominant clones with diverged autosomal copy number alterations. These autosome-defined clusters are characterized by cluster-specific AR gene architectures, and in two index cases are topologically more congruent than by chance (p-values 3.07 × 10
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.