ArticleCancer research2011
Evolved tumor suppression: why are we so good at not getting cancer?
Article in Cancer research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 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
67 citing papers in PubMed, 132 citations in OpenAlex.
- Evolution of the MUC1 gene in eutherian mammals as an adaptation responsible for the increasing incidence of cancer in humans.Biochimica et biophysica acta. Reviews on cancer · 2026Review
- Aging-associated differences in mammary tumor-initiating populations and immune evasion pathways in breast cancer.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Of Barriers and Loops-How Evolution Limits Most Cancer Risks to Older Ages.Cancer discovery · 2026Review
- Dark Skin Evolution in Early Humans: Revisiting the Skin Cancer Hypothesis Through Migration-Related Mismatch.Molecular biology and evolution · 2026Review
- Oncogenic stress alters predator-prey interactions between a globally invasive and a native planaria species.iScience · 2025Article
- The Evolutionary Misfit: Evolution, Epigenetics, and the Rise of Non-Communicable Diseases.Epigenomes · 2025Review
- The evolution of cancer and ageing: a history of constraint.Nature reviews. Cancer · 2025Review
- Ecology of vertical tumor transmission in the freshwater cnidarian Hydra oligactis.Scientific reports · 2025Article
- Cancer Prevalence across Vertebrates.Cancer discovery · 2025Article
- The Elephant and the Spandrel.Evolution, medicine, and public health · 2025Article
- The evolutionary theory of cancer: challenges and potential solutions.Nature reviews. Cancer · 2024Review
- Approaches and methods to study wildlife cancer.The Journal of animal ecology · 2024Review
- The complex effects of modern oncogenic environments on the fitness, evolution and conservation of wildlife species.Evolutionary applications · 2024Article
- Merkel Cell Carcinoma: Integrating Epidemiology, Immunology, and Therapeutic Updates.American journal of clinical dermatology · 2024Review
- The molecular evolution of cancer associated genes in mammals.Scientific reports · 2024Article
- A Poisson distribution-based general model of cancer rates and a cancer risk-dependent theory of aging.Aging · 2023Article
- Cancer Prevalence Across Vertebrates.Research square · 2023Article
- The paradox of cooperation among selfish cancer cells.Evolutionary applications · 2023Review
- The Rise of Gastrointestinal Cancers as a Global Phenomenon: Unhealthy Behavior or Progress?International journal of environmental research and public health · 2023Review
- The sculpting of somatic mutational landscapes by evolutionary forces and their impacts on aging-related disease.Molecular oncology · 2022Review
7 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
Abstract
The law of natural selection can be used to understand cancer development at the level of species as well as at the level of cells and tissues. Through this perspective, I seek to explain: (i) Why the lack of sufficient selective pressure to prevent cancers in old age helps explain the exponential increase in cancer incidence in the elderly. (ii) Why the evolution of long-lived animals necessitated the acquisition of potent tumor suppressive mechanisms. (iii) How the requirement to prevent inappropriate somatic cell expansion and cancer has constrained developmental and tissue architectural modalities. (iv) How the evolution of well-adapted stem cells with complex niche requirements has conferred resistance to oncogenic mutations, as phenotype-altering genetic change is almost always disadvantageous within a well-adapted cell population. (v) How the impairment of stem cell fitness, as occurs in old age, can promote selection for adaptive mutations and cancer initiation. (vi) Why differential maintenance of stem cell fitness may explain how different vertebrate species with enormous differences in life span and body size similarly avoid cancer through reproductive years.
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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.