An elephant never forgets, the saying goes. Or, at least, as my colleague and Fortune Editor in Chief Clifton Leaf explained a few weeks ago, it doesn’t experience nearly the same level of brain deterioration that humans do as it ages despite having way more neurons. But the massive creatures—which have lifespans that can reach up to 70 years (and in some cases, beyond)—have another advantage over mammals like us lowly humans: They seem to be strikingly resistant to cancer. And new research suggests that a certain “zombie gene” reactivated over the course of elephants’ evolutionary process may be the reason why.
The study published in the journal Cell Reports starts off by tackling what some might consider a common-sense hypothesis about cancer and the organisms that it affects: “Large-bodied organisms have more cells that can potentially turn cancerous than small-bodied organisms, imposing an increased risk of developing cancer. This expectation predicts a positive correlation between body size and cancer risk.”
Makes sense, right? Cancer is the uninhibited multiplication of cells. The larger a species, the more cells that can fall prey to this bioligical malfunction. But here’s the thing—”there is no correlation between body size and cancer risk across species (“Peto’s paradox”),” the researchers note.
So what’s going on here? Why are elephants, and a number of other mammals like bats and naked mole rats, seemingly resistant to cancer in a way that other humans aren’t?
Scientist Vincent J. Lynch of the University of Chicago, a lead author of the study, explained some of the nuances to the Los Angeles Times. A version of the “Leukemia Inhibiting Factor” (LIF) genes that can hit the biological brakes on rapidly-growing malignant cells in animals were both present and active in certain modern elephants, even though they’d been turned inactive over evolution’s course in multiple other animals. This LIF6 “zombie gene” as the authors dubbed it, once activated, went on to lead damaged, future-cancerous tissue to self destruct in a process called “apoptosis.”
The researchers had a slightly, uh, nerdier way of putting things: “These results suggest that refunctionalizing of a pro-apoptotic LIF pseudogene may have been permissive (although not sufficient) for the evolution of large body sizes in proboscideans.”
Whether or not such discoveries can eventually bolster human drug development is an open question. Fundamental differences in biology, as the researchers note, are millions of years in the making and can have unexpected effects. But our trunk-bearing cohabitants certainly offer plenty of food for thought in the life sciences.
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