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Arthur T Knackerbracket has processed the following story:
[...] The cells in the body can be thought of as tiny archery targets, each vulnerable to the deadly arrow of cancer. The more cells a given animal has and the longer it lives, the greater its odds of accumulating harmful cell mutations that can eventually lead to cancer. Or at least, this is what intuition suggests.
Nevertheless, many very large animals bearing huge cell populations, including elephants and whales, not only survive to old age, but have remarkably low rates of cancer. This biological enigma bears the name Peto’s paradox. In short, the paradox says that species size and longevity should be proportional to cancer incidence, yet the real-world data across species suggest this association does not hold.
In a new study appearing in the journal Nature, Carlo Maley, a researcher with the Biodesign Center for Biocomputing, Security and Society at Arizona State University, along with international colleagues, explore recent implications of Peto’s paradox and highlight what science is learning about cancer across the tree of life.
The researchers analyze the largest cross-species database of its kind—a pool of adult mammalian life from zoo records that includes 110,148 individuals spanning 191 species.
The aim is to assess species-specific cancer mortality rates across a wide assortment of mammals, re-examine the claims of Peto’s paradox in a rigorously quantitative way and explore possible cancer-suppression mechanisms relevant for fighting the disease in both humans and animals.
The study provides the most intensive evaluation of Peto’s paradox to date. The findings offer conclusive proof that cancer mortality risk is largely independent of both body mass and adult life expectancy across species.
The solution to the paradox lies in the fact that the evolution of greater size and longevity in species has been accompanied by the co-evolution of potent mechanisms of cancer resistance.
Journal Reference:
Orsolya Vincze, Fernando Colchero, Jean-Francois Lemaître, et al. Cancer risk across mammals [open], Nature (DOI: 10.1038/s41586-021-04224-5)
(Score: 3, Interesting) by hendrikboom on Monday December 27 2021, @01:35PM (5 children)
Is the arrival of omicron and its evident reproductive success analogous to the appearance of unbounded reproductive success of a cancer cell?
Will omicron cause a widespread immune reaction that ultimately dooms the "body" of covid-19 disease?
(Score: 2) by janrinok on Monday December 27 2021, @02:58PM (1 child)
It's a very good question but I have no insightful contribution to make in response to it.
(Score: 4, Funny) by nostyle on Monday December 27 2021, @03:17PM
Whenever that happens to me, I go for "funny".
(Score: 0) by Anonymous Coward on Monday December 27 2021, @11:12PM (2 children)
No, eventually there will be multiple strains with specific mutations so that strong immunity towards one enhances infectivity of the other. You can count on it.
(Score: 2) by hendrikboom on Tuesday December 28 2021, @11:48AM (1 child)
I can see how immunity to one could leave the other free to infect, but I do not see how it would enhance the other's infectivity.
(Score: 0) by Anonymous Coward on Tuesday December 28 2021, @03:46PM
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7573563/ [nih.gov]
(Score: 1, Informative) by Anonymous Coward on Monday December 27 2021, @11:08PM
One stem cell divides into two daughter cells. The first daughter cell stays behind as the new stem cell, the second divides and differentiates into a batch of whatever cell type is needed. In this way you can generate hundreds of cells per day for a century, while the stem cell has only divided a couple dozen times since conception.
https://pubmed.ncbi.nlm.nih.gov/25459141/ [nih.gov]
This explains many "paradoxes" at the same time. Unfortunately, some people do not like the implications this has for cancer research and treatment. Just look at the responses this paper got: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4446723/?report=classic [nih.gov]
It was INSANE.