ArticleNature communications2018
Whole genome sequencing puts forward hypotheses on metastasis evolution and therapy in colorectal cancer.
Article in Nature communications, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 98 papers, 1 of them a synthesis that pooled it.
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
98 citing papers in PubMed, 1 synthesis or guideline pooled it, 137 citations in OpenAlex.
- The Role of the Gut Microbiome in Clinical Outcomes of Colorectal Cancer: A Systematic Review (2020-2025).Oncology research · 2026Pooled it
- MiR-494-5p suppresses colorectal cancer metastasis by multi-level targeting of KAT2B, a novel mechanism disrupting KAT2B enhancer-promoter looping, and inhibiting c-JUN-driven pro-metastatic properties.Molecular cancer · 2026Article
- KAT2B-mediated epigenetic suppression of RAD51C enhances olaparib sensitivity in colorectal cancer.Cancer chemotherapy and pharmacology · 2026Article
- Linkage-aware inference of fitness from short-read time-series genomic data.bioRxiv : the preprint server for biology · 2026Article
- Linkage-aware inference of fitness from short-read time-series genomic data.Virus evolution · 2026Article
- Comparison of gene mutations of liver metastases to the primary tumor in colorectal cancer: lessons from a small cohort.Frontiers in oncology · 2026Article
- Utilization of whole exome sequencing to identify hereditary mutations in Palestinian families with hereditary cancers.Frontiers in genetics · 2026Article
- Transient receptor melastatin channel in colorectal cancer: pathophysiological mechanisms and a promising drug target.Cancer chemotherapy and pharmacology · 2025Review
- FOXP2/SOS1/AKT negative feedback loop inhibits cell proliferation in KRAS-mutant colorectal cancer.Apoptosis : an international journal on programmed cell death · 2025Article
- Targeting Voltage-Gated Potassium Channels in Breast Cancer: Mechanistic Insights into 4-Aminopyridine-Induced Cell Death.International journal of molecular sciences · 2025Article
- Epithelial-to-mesenchymal transition (EMT) and cancer metastasis: the status quo of methods and experimental models 2025.Molecular cancer · 2025Review
- Identification of Key lncRNAs Associated with Immune Infiltration and Prognosis in Gastric Cancer.Biochemical genetics · 2025Article
- Small intestinal neuroendocrine tumors lack early genomic drivers, acquire DNA repair defects and harbor hallmarks of low REST expression.Scientific reports · 2025Article
- Cytogenetic signatures favoring metastatic organotropism in colorectal cancer.Nature communications · 2025Article
- Molecular identification ofMolecular biology research communications · 2025Article
- The roles of PD-L1 in the various stages of tumor metastasis.Cancer metastasis reviews · 2024Review
- From Genomic Exploration to Personalized Treatment: Next-Generation Sequencing in Oncology.Current issues in molecular biology · 2024Review
- TMEM16 proteins: CaInternational journal of molecular medicine · 2024Review
- Identification of hub lncRNAs correlated with tetralogy of fallot based on weighted gene co-expression network analysis.Biochemistry and biophysics reports · 2024Article
- Molecular perspectives on systemic priming and concomitant immunity in colorectal carcinoma.Journal of the Egyptian National Cancer Institute · 2024Review
38 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
26 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Incomplete understanding of the metastatic process hinders personalized therapy. Here we report the most comprehensive whole-genome study of colorectal metastases vs. matched primary tumors. 65% of somatic mutations originate from a common progenitor, with 15% being tumor- and 19% metastasis-specific, implicating a higher mutation rate in metastases. Tumor- and metastasis-specific mutations harbor elevated levels of BRCAness. We confirm multistage progression with new components ARHGEF7/ARHGEF33. Recurrently mutated non-coding elements include ncRNAs RP11-594N15.3, AC010091, SNHG14, 3' UTRs of FOXP2, DACH2, TRPM3, XKR4, ANO5, CBL, CBLB, the latter four potentially dual protagonists in metastasis and efferocytosis-/PD-L1 mediated immunosuppression. Actionable metastasis-specific lesions include FAT1, FGF1, BRCA2, KDR, and AKT2-, AKT3-, and PDGFRA-3' UTRs. Metastasis specific mutations are enriched in PI3K-Akt signaling, cell adhesion, ECM and hepatic stellate activation genes, suggesting genetic programs for site-specific colonization. Our results put forward hypotheses on tumor and metastasis evolution, and evidence for metastasis-specific events relevant for personalized therapy.
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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 Socratic graph.