Evidence map›Paper›PMID 40475489›Full record

ArticlebioRxiv : the preprint server for biology2025

A signature-agnostic test for differences between tumor mutation spectra reveals carcinogen and ancestry effects.

Samuel F M Hart, Nicolas Alcala, Alison F Feder, Kelley Harris

Abstract readPreprint
In one paragraph

Article in bioRxiv : the preprint server for biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from 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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

4 authors.

Samuel F M HartDepartment of Genome Sciences, University of Washington, Seattle, USA.ORCID 0000-0002-5068-2199
Nicolas AlcalaComputational Cancer Genomics Team, International Agency for Research on Cancer (IARC/WHO), Genomic Epidemiology Branch, Lyon, France.ORCID 0000-0002-5961-5064
Alison F FederDepartment of Genome Sciences, University of Washington, Seattle, USA.ORCID 0000-0003-2915-089X
Kelley HarrisDepartment of Genome Sciences, University of Washington, Seattle, USA.ORCID 0000-0003-0302-2523

Funding

INTERDISCIPLINARY TRAINING IN GENOMIC SCIENCEST32HG000035 · NHGRI · UNIVERSITY OF WASHINGTON · PI Bruce Colston Trapnell · 1995 to 2026
$24.2M
Investigating the landscape and genetic architecture of germline mutagenesisR35GM133428 · NIGMS · UNIVERSITY OF WASHINGTON · PI Kelley Harris · 2019 to 2026
$2.8M
A phylodynamic time machine for solid tumorsDP2CA280623 · NCI · UNIVERSITY OF WASHINGTON · PI FEDER, ALISON F · 2022 to 2025
$2.3M
NCI NIH HHS DP2 CA280623NHGRI NIH HHS T32 HG000035NIGMS NIH HHS R35 GM133428
6 · The paper itself

Abstract

Mutational signatures contain valuable information about the mutational processes shaping cancer genomes. However, despite dozens of tools to identify signatures in cancer samples, there is not an established metric for statistically comparing mutational signature results and quantifying the overall significance of differences among complex mixtures of signatures. To close this methodological gap, we demonstrate that a signature-agnostic metric for measuring differences in mutation spectra - the aggregate mutation spectrum distance permutation method (AMSD) - can discover differences overlooked by signature analysis. First, we reanalyzed a study of carcinogen exposure in mice, identifying statistically significant shifts in mutation spectra caused by eleven of twenty tested carcinogens. Only three carcinogens were previously reported to induce distinct mutation signatures, suggesting that many carcinogens perturb mutagenesis by altering the composition of endogenous signatures rather than introducing unique signatures. Next, we used human tumor data to determine whether patient ancestry has a measurable impact on tumor mutation spectra, finding significant ancestry-associated differences across ten cancer types: for example, Africans have elevated SBS4 in lung adenocarcinomas, East Asians have elevated SBS16 in esophageal and liver cancers plus elevated SBS10a/b in uterine and colorectal cancers, and Europeans have elevated SBS17b in esophageal cancers plus elevated SBS2/13 in bladder cancers. These examples suggest that AMSD is a robust tool for detecting differences among tumor mutation spectra, complementing signature-based approaches and enabling the discovery of environmental and genetic influences on mutagenesis in large datasets.

Identifiers

PMID40475489
PMCPMC12139916

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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 OpenQuestion graph.