ReviewProceedings. Biological sciences1999
Lineage selection and the evolution of multistage carcinogenesis.
Review in Proceedings. Biological sciences, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 78 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
78 citing papers in PubMed, 222 citations in OpenAlex.
- Evolution of Senescence by Damage Accumulation That Accelerates With Age Throughout an Organism's Lifespan.Ecology and evolution · 2026Article
- When cells rebel: a comparative genomics investigation into marsupial cancer susceptibility.Molecular biology and evolution · 2026Article
- A Test of the Adaptive Lag Hypothesis of the Evolution of Cancer Suppression and Lifespan in Dog Breeds.Genes · 2026Article
- Do turtles get cancer?Bioscience · 2025Review
- Advancing cancer research via comparative oncology.Nature reviews. Cancer · 2025Review
- Shrinking to bird size with dinosaur-level cancer defences: Evolution of cancer suppression over macroevolutionary time.PLoS computational biology · 2025Article
- Towards a more robust comparative oncology: a Bayesian reanalysis of Peto's paradox and discussion of comparative cancer risk studies in vertebrates.Royal Society open science · 2025Article
- Peto's paradox's relevance is off the scale.Aging · 2025Article
- The Evolutionary Interplay of Somatic and Germline Mutation Rates.Annual review of biomedical data science · 2024Review
- A whale of a tale: whale cells evade the driving mechanism for hexavalent chromium-induced chromosome instability.Toxicological sciences : an official journal of the Society of Toxicology · 2024Article
- The effect of body size and inbreeding on cancer mortality in breeds of the domestic dog: a test of the multi-stage model of carcinogenesis.Royal Society open science · 2024Article
- Chance, ignorance, and the paradoxes of cancer: Richard Peto on developing preventative strategies under uncertainty.European journal of epidemiology · 2023Article
- Reuniting philosophy and science to advance cancer research.Biological reviews of the Cambridge Philosophical Society · 2023Article
- Modeling of senescent cell dynamics predicts a late-life decrease in cancer incidence.Evolutionary applications · 2023Article
- Modeling cancer's ecological and evolutionary dynamics.Medical oncology (Northwood, London, England) · 2023Article
- Is chimerism associated with cancer across the tree of life?PloS one · 2023Article
- Quantifying substantial carcinogenesis of genetic and environmental factors from measurement error in the number of stem cell divisions.BMC cancer · 2022Article
- Article
- Cancer suppression and the evolution of multiple retrogene copies of TP53 in elephants: A re-evaluation.Evolutionary applications · 2022Article
- Trade-off between reducing mutational accumulation and increasing commitment to differentiation determines tissue organization.Nature communications · 2022Article
18 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A wide array of proto-oncogenes and tumour suppressor genes are involved in the prevention of cancer. Each form of cancer requires mutations in a characteristic group of genes, but no single group controls all cancers. This lack of generality shows that the control of cancer is not an ancient, fixed property of cells. By contrast, it supports a dynamic evolutionary model, whereby genetic controls over unregulated cell growth are recruited independently through evolutionary time in different tissues within different taxa. The complexity of this genetic control can be predicted from a population genetic model of lineage selection driven by the detrimental fitness effects of cancer. Cancer occurs because the genetic control of cell growth is vulnerable to somatic mutations (or 'hits'), particularly in large, continuously dividing tissues. Thus, compared to small rodents, humans must have evolved more complex genetic controls over cell growth in at least some of their tissues because of their greater size and longevity; an expectation relevant to the application of mouse data to humans. Similarly, the 'two-hit' model so successfully applied to retinoblastoma, which originates in a small embryonic tissue, is unlikely to be generally applicable to other human cancers; instead, more complex scenarios are expected to dominate, with complexity depending upon a tissue's size and its pattern of proliferation.
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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.