“Animal models are limited in their ability to mimic the extremely complex process of human carcinogenesis, physiology and progression,” McMaster University scientists Isabella Mak, Nathan Evaniew, and Michelle Ghert, wrote in 2014. “Therefore the safety and efficacy identified in animal studies is generally not translated to human trials.”
While the systems that regulate gene activity are generally the same in mice and humans, there are key biological differences in other areas that prevent successful results from applying to humans. Transcription factor binding sites, where information is passed on, differ for between 41 and 89 percent of the genes that our species share. Moreover, unlike humans, mice used in studies are often highly inbred. The mouse immune system is also drastically different compared to a human’s. Laboratory rodents are also often overfed and sedentary. Thus, the positive effects of some drugs might result from improving factors associated with an unhealthy lifestyle rather than the drug counteracting the disease, itself.
All that complexity, and just think, it was randomly generated too. But only for humans, apparently.
A prime example of an outdated practice is how mice are “randomly” selected.
“You stick your hand in a cage, and pull out a rat,” Ian Roberts, a professor of epidemiology at the London School of Hygiene and Tropical Medicine, told The Scientist. “The rats that are the most vigorous are hardest to catch, so when you pull out 10 rats, they’re the sluggish ones, the tired ones, they’re not the same as the ones still in the cage, and they’re the control. More.
Maybe that’s one of the reasons replication often fails?
A friend recommends, as a guide to the problem and possible improvements, Systems Biology of Tumor Physiology.
See also: Replication as key science reform
Should science papers be anonymous? The problem with safeguards that don’t work is not just that they don’t work. Rather, they can work against the aims of the process.
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