ArticleCancer cell2018
Clinical Sequencing Defines the Genomic Landscape of Metastatic Colorectal Cancer.
Article in Cancer cell, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 580 papers, 3 of them syntheses that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
580 citing papers in PubMed, 3 syntheses or guidelines pooled it, 842 citations in OpenAlex.
- A meta-analysis identifies driver genes and characterizes the molecular epidemiology of colorectal cancer.Scientific reports · 2026Pooled it
- Targeted therapy in advancedBMJ (Clinical research ed.) · 2025Pooled it
- Systematic literature review of the epidemiology of neurotrophic tyrosine receptor kinase positive solid tumor sites.Future oncology (London, England) · 2025Pooled it
- The BEVATOMOX phase II trial: raltitrexed/oxaliplatin/bevacizumab vs mFOLFOX6/bevacizumab in 2nd-line metastatic colorectal cancer.The oncologist · 2026Trial
- Efficacy and Safety of Adagrasib plus Cetuximab in Patients with KRASG12C-Mutated Metastatic Colorectal Cancer.Cancer discovery · 2024Trial
- Upregulation of LTF promotes left-sided colorectal cancer development via activating PI3K/AKT pathway.Cell adhesion & migration · 2026Article
- Reframing cancer therapy through tumor plasticity.Nature cancer · 2026Review
- Single-cell epigenomics of colorectal cancer.Experimental & molecular medicine · 2026Review
- Article
- Integrated clinicogenomic analysis reveals the evolution and metastatic tropisms of advanced colorectal cancer.Cancer cell · 2026Article
- Age-stratified mutation patterns in early-onset colorectal cancer reveal distinct molecular features and therapeutic implications.ESMO gastrointestinal oncology · 2026Article
- Colonoscope-derived mucus as a novel high-fidelity reservoir for KRAS-mutated precancerous colorectal neoplasia detection.Translational oncology · 2026Article
- Review
- Advances in Bispecific Antibodies and Antibody-Drug Conjugates for Colorectal Cancer Treatment.Antibodies (Basel, Switzerland) · 2026Review
- Clonal evolution from primary to locally recurrent rectal cancer reveals recurrence-acquired potentially actionable alterations in treatment-naïve tumors.Journal of gastroenterology · 2026Article
- Selenium Nanoparticles Selectively Target KRAS G13D to Inhibit Colorectal Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Review
- Genomic landscape and clinical characteristics of ERBB2/HER2-mutated colorectal cancers.The oncologist · 2026Article
- Analysis of cancer mutations introduced into theeLife · 2026Article
- Next-Generation Sequencing in Colorectal Cancer: Real-World Molecular Profiling and Clinical Correlations.International journal of molecular sciences · 2026Article
520 more citing papers are in PubMed but not listed here.
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Authors and funding
29 authors at 1 institution in 1 country.
Funding
Abstract
Metastatic colorectal cancers (mCRCs) are clinically heterogeneous, but the genomic basis of this variability remains poorly understood. We performed prospective targeted sequencing of 1,134 CRCs. We identified splice alterations in intronic regions of APC and large in-frame deletions in CTNNB1, increasing oncogenic WNT pathway alterations to 96% of CRCs. Right-sided primary site in microsatellite stable mCRC was associated with shorter survival, older age at diagnosis, increased mutations, and enrichment of oncogenic alterations in KRAS, BRAF, PIK3CA, AKT1, RNF43, and SMAD4 compared with left-sided primaries. Left-sided tumors frequently had no identifiable genetic alteration in mitogenic signaling, but exhibited higher mitogenic ligand expression. Our results suggest different pathways to tumorigenesis in right- and left-sided microsatellite stable CRC that may underlie clinical differences.
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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.