ArticleNature genetics2016
Identification of neutral tumor evolution across cancer types.
Article in Nature genetics, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 353 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
353 citing papers in PubMed.
- An enhanced genetic model of relapsed IGH-translocated multiple myeloma evolutionary dynamics.Blood cancer journal · 2020Trial
- Mosaic Accumulation of Somatic Genetic Variation and Estimates of Age in the Long-Lived Reef-Building Coral Acropora palmata.Molecular ecology · 2026Article
- Clonal selection of somatic mutations shapes NK cell memory.bioRxiv : the preprint server for biology · 2026Article
- A guide to understanding tumour evolution through the lens of population genetics.Nature reviews. Cancer · 2026Review
- The Evolution of Polyclonal Competition in Aging Hematopoiesis.Cancer discovery · 2026Article
- Fluctuating environment causes neoplastic transition and epithelial-mesenchymal plasticity in human cells.Research square · 2026Article
- Tumor evolution: signaling pathways, molecular mechanisms and therapeutic targets.Signal transduction and targeted therapy · 2026Review
- LeafRank: A phylodynamic framework for inferring relative fitness from single-cell phylogenies in chromosomally unstable tumors.bioRxiv : the preprint server for biology · 2026Article
- Tumor heterogeneity: development, mechanisms, and therapeutic implications.Signal transduction and targeted therapy · 2026Review
- Fluctuating DNA methylation sites encode colorectal tumour growth history.bioRxiv : the preprint server for biology · 2026Article
- Accurate detection of tumor clonality and ongoing expansion mode from genomic data.bioRxiv : the preprint server for biology · 2026Article
- A new cancer progression model: From synthetic tumors to real data and back.PLoS computational biology · 2026Article
- Spatial transcriptomics of cervical cancer reveals microenvironment shaped the malignant epithelial programs and ECM-associated immune niches.Cancer immunology, immunotherapy : CII · 2026Article
- Beyond Darwin: reactive heredity, burst-drift dynamics and eco‑evolutionary control of cancer.Molecular cancer · 2026Review
- Novel antibody cocktail therapy targeting extracellular tumor-specific mutations to treat EMT6 cell line-derived triple-negative breast cancer.Scientific reports · 2026Article
- Transcriptomic Plasticity Is a Hallmark of Metastatic Pancreatic Cancer.Cancer research · 2026Article
- Is cancer the result of uncontrolled cellular growth? a glance into the tumorigenic process.Cancer cell international · 2026Review
- Inferring cancer type-specific patterns of metastatic spread using Metient.Nature methods · 2026Article
- Competing subclones and fitness diversity shape tumor evolution across cancer types.Bioinformatics (Oxford, England) · 2026Article
- Article
293 more citing papers are in PubMed but not listed here.
Corrections and comments
- Commented on by
- Commented on by
- Commented on by
- Commented on by
Authors and funding
5 authors.
Funding
Abstract
Despite extraordinary efforts to profile cancer genomes, interpreting the vast amount of genomic data in the light of cancer evolution remains challenging. Here we demonstrate that neutral tumor evolution results in a power-law distribution of the mutant allele frequencies reported by next-generation sequencing of tumor bulk samples. We find that the neutral power law fits with high precision 323 of 904 cancers from 14 types and from different cohorts. In malignancies identified as evolving neutrally, all clonal selection seemingly occurred before the onset of cancer growth and not in later-arising subclones, resulting in numerous passenger mutations that are responsible for intratumoral heterogeneity. Reanalyzing cancer sequencing data within the neutral framework allowed the measurement, in each patient, of both the in vivo mutation rate and the order and timing of mutations. This result provides a new way to interpret existing cancer genomic data and to discriminate between functional and non-functional intratumoral heterogeneity.
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.