ArticleMolecular biology and evolution2022
Attribution of Cancer Origins to Endogenous, Exogenous, and Preventable Mutational Processes.
Article in Molecular biology and evolution, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 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.
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Who cites it
23 citing papers in PubMed, 40 citations in OpenAlex.
- Empowering Inference of Epistasis on the Basis of Mutual Exclusivity, Co-Occurrence, Functional Antagonism and Synergy in ERK-Pathway Oncogenes.International journal of cancer · 2026Article
- A comparative mutation-selection reanalysis of colon and rectal adenocarcinoma highlights PIK3CA variants and BRAF V600E.Journal of translational medicine · 2026Article
- An investigative network analysis mapping global cancer epidemiology.Theory in biosciences = Theorie in den Biowissenschaften · 2026Article
- Accelerating discovery of cancer causes for prevention in the era of rising early-onset cancers.Cell · 2026Review
- Germline Predisposition to Oncogenic Alkylating Damage in Colorectal Cancer.Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology · 2026Article
- Biomimetic hydrogel for the construction of patient-derived bladder cancer organoids with aggressive growth.iScience · 2026Article
- Mutational landscape of normal breast tissues adjacent to invasive breast cancer.Cell reports. Medicine · 2026Article
- Evaluating the prognostic value of mutational signatures in small-cell lung cancer through reference-based signature assignment and continuous activity analysis.Frontiers in genetics · 2026Article
- Article
- EarlybioRxiv : the preprint server for biology · 2025Article
- DiffInvex identifies evolutionary shifts in driver gene repertoires during tumorigenesis and chemotherapy.Nature communications · 2025Article
- Glioma mutational signatures associated with haloalkane exposure are enriched in firefighters.Cancer · 2025Article
- A comprehensive comparison of tools for fitting mutational signatures.Nature communications · 2024Article
- Rare Drivers at Low Prevalence with High Cancer Effects in T-Cell and B-Cell Pediatric Acute Lymphoblastic Leukemia.International journal of molecular sciences · 2024Article
- Article
- Pairwise and higher-order epistatic effects among somatic cancer mutations across oncogenesis.Mathematical biosciences · 2023Article
- Low mutation rate in epaulette sharks is consistent with a slow rate of evolution in sharks.Nature communications · 2023Article
- Treatment of evolving cancers will require dynamic decision support.Annals of oncology : official journal of the European Society for Medical Oncology · 2023Review
- New insights into the biology and development of lung cancer in never smokers-implications for early detection and treatment.Journal of translational medicine · 2023Review
- Mutation bias and the predictability of evolution.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2023Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Mutational processes in tumors create distinctive patterns of mutations, composed of neutral "passenger" mutations and oncogenic drivers that have quantifiable effects on the proliferation and survival of cancer cell lineages. Increases in proliferation and survival are mediated by natural selection, which can be quantified by comparing the frequency at which we detect substitutions to the frequency at which we expect to detect substitutions assuming neutrality. Most of the variants detectable with whole-exome sequencing in tumors are neutral or nearly neutral in effect, and thus the processes generating the majority of mutations may not be the primary sources of the tumorigenic mutations. Across 24 cancer types, we identify the contributions of mutational processes to each oncogenic variant and quantify the degree to which each process contributes to tumorigenesis. We demonstrate that the origination of variants driving melanomas and lung cancers is predominantly attributable to the preventable, exogenous mutational processes associated with ultraviolet light and tobacco exposure, respectively, whereas the origination of selected variants in gliomas and prostate adenocarcinomas is largely attributable to endogenous processes associated with aging. Preventable mutations associated with pathogen exposure and apolipoprotein B mRNA-editing enzyme activity account for a large proportion of the cancer effect within head-and-neck, bladder, cervical, and breast cancers. These attributions complement epidemiological approaches-revealing the burden of cancer driven by single-nucleotide variants caused by either endogenous or exogenous, nonpreventable, or preventable processes, and crucially inform public health strategies.
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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.