ArticleNature genetics2015
A Big Bang model of human colorectal tumor growth.
Article in Nature genetics, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 635 papers.
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
635 citing papers in PubMed.
- A single-cell lens into the co-evolution of genotypes and phenotypes in cancer.Nature reviews. Cancer · 2026Review
- Article
- Modeling human tumor evolution in mice.STAR protocols · 2026Review
- Differences between mitotically old and young endometrial tumors.The Journal of pathology · 2026Article
- Phylogenetic and phylodynamic approaches to understanding the evolution of non-small cell lung cancer using single-cell sequencing.Oncogene · 2026Article
- Chromosomal instability in cancer: sources, consequences and new therapeutic opportunities.Signal transduction and targeted therapy · 2026Review
- Review
- A guide to understanding tumour evolution through the lens of population genetics.Nature reviews. Cancer · 2026Review
- Spatiotemporal lineage tracing reveals the dynamic spatial architecture of tumor growth and metastasis.Nature genetics · 2026Article
- Article
- Charting intratumor heterogeneity from bench to bedside.Nature cancer · 2026Review
- Tumor evolution: signaling pathways, molecular mechanisms and therapeutic targets.Signal transduction and targeted therapy · 2026Review
- Multi-modal data integration reveals functionally credible predictive biomarkers in ovarian cancer.Genome medicine · 2026Article
- Fluctuating DNA methylation sites encode colorectal tumour growth history.bioRxiv : the preprint server for biology · 2026Article
- Mutational landscape in the precancerous stages of sporadic colorectal cancer.Oncology letters · 2026Article
- Pathophysiology of colitis-associated colorectal cancer.Nature reviews. Gastroenterology & hepatology · 2026Review
- Guarding epithelial integrity: origins of adaptive immunity and cancer immunosurveillance over time and space.Journal for immunotherapy of cancer · 2026Review
- Article
- A new cancer progression model: From synthetic tumors to real data and back.PLoS computational biology · 2026Article
- Convergence for Inactivation of TGFβ Signaling Is a Common Feature of Advanced Pancreatic Cancer.Cancer discovery · 2026Article
575 more citing papers are in PubMed but not listed here.
Corrections and comments
- Commented on by
- Commented on by
Authors and funding
11 authors.
Funding
Abstract
What happens in early, still undetectable human malignancies is unknown because direct observations are impractical. Here we present and validate a 'Big Bang' model, whereby tumors grow predominantly as a single expansion producing numerous intermixed subclones that are not subject to stringent selection and where both public (clonal) and most detectable private (subclonal) alterations arise early during growth. Genomic profiling of 349 individual glands from 15 colorectal tumors showed an absence of selective sweeps, uniformly high intratumoral heterogeneity (ITH) and subclone mixing in distant regions, as postulated by our model. We also verified the prediction that most detectable ITH originates from early private alterations and not from later clonal expansions, thus exposing the profile of the primordial tumor. Moreover, some tumors appear 'born to be bad', with subclone mixing indicative of early malignant potential. This new model provides a quantitative framework to interpret tumor growth dynamics and the origins of ITH, with important clinical implications.
Indexed as
Identifiers
What OpenQuestion holds
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.