ArticleNature genetics2020
Multi-cancer analysis of clonality and the timing of systemic spread in paired primary tumors and metastases.
Article in Nature genetics, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 206 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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
206 citing papers in PubMed, 354 citations in OpenAlex.
- Unlocking the therapeutic potential of immuno-radiotherapy: insights from preclinical and clinical research.Oncoimmunology · 2026Review
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- Clinical metastatic cancer from initiation to colonization: emerging challenges and breakthroughs.Oncogene · 2026Review
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- Genomic characterization of ER-positive primary tumors and corresponding relapses identifies potentially targetable alterations.NPJ breast cancer · 2026Article
- Molecular Residual Disease in Non-Small Cell Lung Cancer: Technology or Patient Outcomes?Journal of personalized medicine · 2026Review
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- MicroRNAs and Other Small RNAs in Liquid Biopsies as Biomarkers for Early Detection of Colorectal Cancer.International journal of molecular sciences · 2026Review
- Charting intratumor heterogeneity from bench to bedside.Nature cancer · 2026Review
- Tumor Plasticity and Microenvironmental Crosstalk as Drivers of Metastasis and Therapy Resistance.MedComm · 2026Review
- P95-HER2 promotes metastatic progression by biasing MRTFA dependent signaling.bioRxiv : the preprint server for biology · 2026Article
- Tumor heterogeneity: development, mechanisms, and therapeutic implications.Signal transduction and targeted therapy · 2026Review
- Breast cancer genomic subtype-specific copy number alterations in metastases.Scientific reports · 2026Article
- Mediator subunit MED4 enforces metastatic dormancy in breast cancer.Nature cell biology · 2026Article
- Formation of the pre-metastatic niche by COL9A1 + cancer-associated fibroblasts via SDC4 engagement promotes multi-organ metastasis in gastric cancer.Journal of gastroenterology · 2026Article
- Mutant KRAS peptide vaccine with dual checkpoint blockade in metastatic colorectal cancer: a phase I trial.Nature communications · 2026Article
- Bayesian inference of tissue-migration histories in metastatic cancer from cell-lineage tracing data.Cell genomics · 2026Article
- Geospatial genetic evolution and phenotypic plasticity in triple-negative breast cancer.Genome medicine · 2026Article
- Emerging landscape of oncogenic signaling pathways in cervical cancer.Discover oncology · 2026Review
- Convergence for Inactivation of TGFβ Signaling Is a Common Feature of Advanced Pancreatic Cancer.Cancer discovery · 2026Article
146 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 3 institutions in 2 countries.
Funding
Abstract
Metastasis is the primary cause of cancer-related deaths, but the natural history, clonal evolution and impact of treatment are poorly understood. We analyzed whole-exome sequencing (WES) data from 457 paired primary tumor and metastatic samples from 136 patients with breast, colorectal and lung cancer, including untreated (n = 99) and treated (n = 100) metastases. Treated metastases often harbored private 'driver' mutations, whereas untreated metastases did not, suggesting that treatment promotes clonal evolution. Polyclonal seeding was common in untreated lymph node metastases (n = 17 out of 29, 59%) and distant metastases (n = 20 out of 70, 29%), but less frequent in treated distant metastases (n = 9 out of 94, 10%). The low number of metastasis-private clonal mutations is consistent with early metastatic seeding, which we estimated occurred 2-4 years before diagnosis across these cancers. Furthermore, these data suggest that the natural course of metastasis is selectively relaxed relative to early tumorigenesis and that metastasis-private mutations are not drivers of cancer spread but instead associated with drug resistance.
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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.