Evidence map›Paper›PMID 36433937›Full record

ArticleNature communications2022

Evaluating cancer etiology and risk with a mathematical model of tumor evolution.

Sophie Pénisson, Amaury Lambert, Cristian Tomasetti

Abstract read
In one paragraph

Article in Nature communications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing 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

5 citing papers in PubMed.

  1. Article
  2. Review
  3. An investigative network analysis mapping global cancer epidemiology.Theory in biosciences = Theorie in den Biowissenschaften · 2026
    Article
  4. Article
  5. 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

3 authors.

Sophie PénissonCenter for Cancer Prevention and Early Detection, City of Hope, Duarte, CA, 91010, USA.ORCID 0000-0002-6268-3842
Amaury LambertSMILE Group, Center for Interdisciplinary Research in Biology, Collège de France, 75231, Paris, Cedex 05, France.
Cristian TomasettiCenter for Cancer Prevention and Early Detection, City of Hope, Duarte, CA, 91010, USA. ctomasetti@coh.org.ORCID 0000-0003-3277-4804

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Recent evidence arising from DNA sequencing of healthy human tissues has clearly indicated that our organs accumulate a relevant number of somatic mutations due to normal endogenous mutational processes, in addition to those caused by environmental factors. A deeper understanding of the evolution of this endogenous mutational load is critical for understanding what causes cancer. Here we present a mathematical model of tumor evolution that is able to predict the expected number of endogenous somatic mutations present in various tissue types of a patient at a given age. These predictions are then compared to those observed in patients. We also obtain an improved fitting of the variation in cancer incidence across cancer types, showing that the endogenous mutational processes can explain 4/5 of the variation in cancer risk. Overall, these results offer key insights into cancer etiology, by providing further evidence for the major role these endogenous processes play in cancer.

Indexed as

NeoplasmsBase SequenceHumansModels, TheoreticalMutationSequence Analysis, DNA

Identifiers

PMID36433937
PMCPMC9700699

What OpenQuestion holds

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Registered trials

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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.