ArticleScientific reports2016
Evolutionary constraints over microsatellite abundance in larger mammals as a potential mechanism against carcinogenic burden.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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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.
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Who cites it
4 citing papers in PubMed.
- A High-Quality Blue Whale Genome, Segmental Duplications, and Historical Demography.Molecular biology and evolution · 2024Article
- Global abundance of short tandem repeats is non-random in rodents and primates.BMC genomic data · 2022Article
- All's well that ends well: why large species have short telomeres.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2018Article
- Importance of metabolic rate to the relationship between the number of genes in a functional category and body size in Peto's paradox for cancer.Royal Society open science · 2016Article
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Larger organisms tend to live longer, have more potentially carcinogenic cells, and undergo more cell divisions. While one might intuitively expect cancer incidence to scale with body size, this assertion does not hold over the range of different mammals. Explaining this lack of correlation, so-called 'Peto's paradox' can likely increase our understanding of how cancer defense mechanisms are shaped by natural selection. Here, we study the occurrence of microsatellite in mammal genomes and observe that animals with expanded body size restrain the number of microsatellite. To take into account of higher mutation rate in the microsatellite region compared to that of genome, limiting the abundance of somatic mutations might explain how larger organisms could overcome the burden of cancer. These observations may serve as the basis to better understand how evolution has modeled protective mechanisms against cancer development.
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