Naked mole-rats can live for more than 37 years, roughly ten times longer than a typical mouse, and they almost never develop cancer. For decades, biologists have wanted to know why. Now a team at the University of Rochester believes it has found at least part of the answer, and they have proven it works in another species.
In a study published in Nature, the researchers engineered mice to carry a naked mole-rat gene called nmrHas2, which drives production of an unusually large sugar molecule known as high-molecular-mass hyaluronan (HMM-HA). The modified mice lived about 4.4% longer than unmodified controls, aged with fewer health problems, and showed a striking reduction in spontaneous cancers. It was the first time a longevity-linked gene from one rodent species had produced measurable anti-aging and anti-cancer benefits when transferred into another.
“It took us 10 years from the discovery of HMM-HA in the naked mole-rat to showing that it improves health in mice,” Vera Gorbunova, a biology professor at Rochester who co-led the study, told the university’s news service. “Our next goal is to transfer this benefit to humans.”
A sugar molecule with unusual power
Hyaluronan is not exotic. It already exists in human skin, joints, and connective tissue, and it is a common ingredient in cosmetic fillers. But the version found in naked mole-rats is different. Their bodies produce hyaluronan molecules roughly five times larger than those found in mice or humans, and they produce far more of it. That oversized molecule turns out to be central to the animal’s remarkable cancer resistance.
The Rochester group first identified this connection in a 2013 Nature paper. They showed that when they removed HMM-HA from naked mole-rat cells, either by silencing the HAS2 gene or by overexpressing an enzyme that breaks hyaluronan down, those cells became vulnerable to malignant transformation. The molecule was not just correlated with cancer resistance; it was mechanistically required for it.
Even earlier, in 2009, the same team had published findings in the Proceedings of the National Academy of Sciences showing that naked mole-rat cells exhibit an unusually aggressive form of contact inhibition, the process by which normal cells stop dividing when they bump into their neighbors. The researchers called it “early contact inhibition,” and it provided one of the first biological clues to the animal’s near-immunity to tumors. The later work revealed that HMM-HA was the molecule triggering that protective brake.
What the modified mice showed
For the 2023 experiment, the team created transgenic mice that overexpress the naked mole-rat version of the Has2 gene throughout their bodies. These animals were then tracked across their entire lifespans alongside unmodified control mice.
The results went beyond cancer. The nmrHas2 mice maintained healthier body weight as they aged, stayed more physically active, and showed less organ deterioration at necropsy. Researchers describe this distinction as improved “healthspan,” meaning the animals did not just live slightly longer but spent more of their lives in good condition. Inflammation, a hallmark of aging across mammalian species, was lower in the modified animals.
On the cancer front, the transgenic mice developed significantly fewer spontaneous tumors than controls. While the headline framing of “never got cancer” overstates the finding slightly (the study reports reduced incidence, not complete elimination), the protection was robust enough to be statistically significant across the cohort.
The underlying data are publicly available. RNA-seq records from multiple tissues, ages, and genotypes have been deposited in the NCBI Gene Expression Omnibus under accession GSE234563, allowing independent labs to scrutinize and attempt to replicate the analysis.
Why a 4.4% lifespan gain matters more than it sounds
A 4.4% increase in median lifespan may seem modest, especially compared with caloric restriction, which can extend rodent lifespans by 30% or more. But context matters. This result came from a single genetic change, not a comprehensive lifestyle intervention. And the lifespan extension was accompanied by broad improvements in health, which is arguably more important than raw survival time.
The finding also carries conceptual weight. Most longevity genes studied in mice are mouse genes that have been tweaked. Here, a gene was borrowed wholesale from a different species and still produced benefits, suggesting that the HMM-HA mechanism is not unique to naked mole-rat biology but taps into conserved pathways that other mammals can exploit.
That said, the study has clear boundaries. The researchers did not test whether the protection holds against environmentally induced or more aggressive cancers. Brain tissue and neurological outcomes were not assessed in the published data. And whether the benefits persist across generations, or come with trade-offs that only emerge over longer timescales, remains unknown.
The distance from mice to humans
Translating a transgenic mouse experiment into a human therapy is a process measured in decades, not years. The Rochester team has not proposed a clinical timeline, and for good reason. Engineering humans to overexpress a foreign gene is not currently feasible as a medical intervention, and the ethical questions surrounding heritable genetic modifications for longevity are substantial.
The more realistic near-term path, as Gorbunova and co-author Andrei Seluanov have suggested, involves finding pharmacological ways to boost HMM-HA levels without genetic engineering. If a drug or small molecule could safely increase high-molecular-mass hyaluronan production in human tissues, it might deliver some of the same protective effects seen in the mice. As of mid-2026, no such compound has entered clinical trials for this purpose, but the genetic proof of concept gives drug developers a specific molecular target to pursue.
There are also basic biological questions that need answers first. Human cancer develops over decades of exposure to environmental carcinogens, chronic inflammation, and accumulated mutations, a complexity that short-lived laboratory mice cannot fully replicate. Whether elevated HMM-HA would remain protective under those conditions is genuinely unknown.
What comparative biology keeps revealing about aging
The naked mole-rat experiment belongs to a growing body of research that treats unusual animals as natural laboratories. Bowhead whales, which can live more than 200 years, have yielded insights into DNA repair. Certain bat species, despite high metabolic rates, show negligible senescence. Greenland sharks may survive for centuries. Each of these organisms has evolved solutions to problems, like cancer and cellular decay, that humans have spent billions of dollars trying to solve through medicine.
What makes the Rochester work distinctive is that it moved beyond observation. Rather than simply cataloging what makes naked mole-rats special, the team extracted a specific gene, inserted it into a different mammal, and measured what happened. The result was not a cure for aging, but it was something arguably more valuable at this stage: a clean demonstration that a longevity mechanism from one species can function in another.
For researchers working on the biology of aging, that principle opens a door. For everyone else, it is a reminder that some of the most promising leads in medicine are not being invented in labs. They are being discovered in animals that figured out the problem a long time ago.
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*This article was researched with the help of AI, with human editors creating the final content.
