Evidence map›Paper›PMID 41331092›Full record

ReviewExperimental & molecular medicine2026

Somatic mutations and clonal evolution in normal tissues and cancer development.

Kenichi Yoshida

Abstract readReview
In one paragraph

Review in Experimental & molecular medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. Article
  2. Article
  3. What sets the mutation rate of a cell type in an animal species?bioRxiv : the preprint server for biology · 2025
    Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

1 author.

Kenichi YoshidaDivision of Cancer Evolution, National Cancer Center Research Institute, Tokyo, Japan. keyoshi2@ncc.go.jp.ORCID http://orcid.org/0000-0003-4612-2778

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Understanding the early stages of carcinogenesis requires detailed insight into the abnormalities present in normal cells before cancer onset. In the past, it was difficult to analyze genomic abnormalities in small clones in normal tissues. However, recent technological advances in genomic analysis have shed light on the process of accumulation of somatic mutations in normal cells, which is driven by factors such as aging and environmental influences. Even in normal tissues, clones that have acquired driver mutations-either directly contributing to carcinogenesis or adapting to specific pathological or genetic backgrounds-are frequently selected, leading to clonal expansion. Normal cells undergo clonal evolution into cancer cells over several decades, with the initial acquisition of a driver mutation occurring in early life. Here this review presents recent findings concerning the accumulation of somatic mutations in normal cells, acquisition of driver mutations and clonal evolution toward cancer.

Indexed as

CarcinogenesisCell Transformation, NeoplasticClonal EvolutionMutationNeoplasmsAnimalsHumans

Identifiers

PMID41331092
PMCPMC13144676

What OpenQuestion holds

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LicenceCC BY
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Registered trials

None linked

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.