| ▲ | robwwilliams 5 days ago |
| Not a solid paper—-more like an abstract. I could not find any information on the strain or type of mice they studied. Data from one strain often fails to generalize to others. Trying to leap to human implications is beyond risky. |
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| ▲ | jr000 5 days ago | parent | next [-] |
| It says in the paper they used 21-week-old male C57BL/6 mice, as well as AC16 human immortalized cardiomyocytes |
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| ▲ | robwwilliams 4 days ago | parent [-] | | Ah, thanks. I looked but not carefully enough! C57BL/6 – the canonical inbred fully homozygous mouse that unfortunately is used as the “HeLa cell” of almost all experimental murine biomedical research. I understand the reason this happened, but there is no excuse in 2024 to use just one genome (and an inbred one at that) to test translational relevance. Consider this work a pilot worth testing in NZO, DBA, A, C3H and BALB strains and some F1 hybrids. Whatever the results they should have good generality to mice in general. |
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| ▲ | insane_dreamer 5 days ago | parent | prev [-] |
| If you're trying to prove a positive benefit, then leaping from mice to humans is risky. If you're concerned about possible negative effects of something, then mice is a good place to start. |
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| ▲ | robwwilliams 4 days ago | parent [-] | | Yes, you are right, but ideally a team should test several genetic backgrounds of mice. Almost all cancer treatments have some negative effects. It is crucial to know what genetic and exposure variables to avoid to maximize therapeutic benefits. Cadmium in some strains of mice is highly toxic to male testes. But if, as in the C57BL/6J strain, you have a “lucky” transporter mutation, then no problems at all. This kind of variability has been known since the turn A. Garrod in the early 1900s. And ignored by many. Here is the data on the cadmium example I just mentioned: https://genenetwork.org/show_trait?trait_id=13035&dataset=BX... |
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