Why Don’t Bats Get Cancer? Scientists Uncover Genetic Defenses and Robust Immune Systems Behind Their Resistance

In a groundbreaking study recently published in Nature Communications, researchers from the University of Rochester have unveiled remarkable biological mechanisms that enable certain long-lived bat species to resist cancer, despite possessing cellular features that would typically predispose mammals to malignancies. This investigative work sheds new light on how these mammals achieve life spans equating to the human equivalent of nearly two centuries without succumbing to cancer, illuminating pathways that could inspire revolutionary therapeutic approaches for human oncology and aging.

Bats represent a unique model for cancer resistance, living up to 35 years—equivalent to around 180 human years—and yet they enjoy remarkably low incidences of tumor formation. The research team, led by Dr. Vera Gorbunova and Dr. Andrei Seluanov, focused on four common bat species, including the “little brown” bat ubiquitous across upstate New York. These bats harbor an enhanced tumor-suppressor gene profile that is unusually robust compared to humans, particularly regarding their p53 gene, a critical regulator in preventing cancer formation.

Unlike humans, in which mutations to the p53 gene occur in approximately half of all cancers and severely diminish its protective function, the little brown bat contains two functional copies of p53. This duplication translates into significantly elevated p53 activity, which empowers an advanced apoptotic response—programmed cell death—that selectively eliminates potentially malignant cells before they can develop into tumors. This controlled apoptotic activity is finely balanced, preventing excessive cell death that would otherwise be detrimental to tissue health.

.adsslot_wx1QUXzP0H{width:728px !important;height:90px !important;}
@media(max-width:1199px){ .adsslot_wx1QUXzP0H{width:468px !important;height:60px !important;}
}
@media(max-width:767px){ .adsslot_wx1QUXzP0H{width:320px !important;height:50px !important;}
}

ADVERTISEMENT

In parallel with heightened p53 expression, bats possess constitutively active telomerase, an enzyme responsible for maintaining chromosome integrity during cell division. Telomerase activity in humans is typically repressed in most somatic cells, leading to cellular senescence and tissue aging. However, bats maintain higher telomerase activity, which promotes prolonged cellular proliferation and robust tissue regeneration capabilities throughout their lifespan. This characteristic likely plays a vital role in their remarkable longevity and resistance to age-related functional decline.

The interplay of elevated p53 activity and active telomerase forms a biological safeguard: while telomerase allows cells to replicate over an extended period, high p53 function simultaneously monitors and suppresses any aberrant, cancerous proliferation. This dynamic equilibrium prevents unchecked cellular growth—a hallmark of cancer—while promoting tissue renewal, representing a sophisticated cellular maintenance system unseen in most mammals.

Moreover, bats exhibit an extraordinarily efficient immune system, acting as a formidable defense against both pathogens and cancer cells alike. Their immune surveillance not only counters viral and bacterial infections but also identifies and eradicates cells exhibiting abnormal, pre-cancerous changes. This immunological prowess curbs chronic inflammation, a common aging-associated contributor to cancer risk in humans, enabling bats to maintain systemic homeostasis even as they age.

The researchers emphasize that, intriguingly, bats’ cancer resistance is not due to a cellular barrier preventing mutation or transformation per se. In fact, bat cells require only two mutational “hits” to become cancerous, distinguishing them from humans, whose cells generally require a greater number of such events over time. It is the combination of their enhanced tumor suppressive mechanisms, immune efficiency, and telomerase activity that successfully bars progression to malignancy despite this genetic susceptibility.

This study carries potent implications for human medicine, especially in oncology and gerontology. Since increased p53 activity appears to be a principal anti-cancer mechanism in bats, modulating or mimicking this pathway in humans could potentiate novel cancer therapeutics. Existing pharmaceuticals targeting p53 are already in development, and this new evidence provides robust justification for their continued refinement. Moreover, safely enhancing telomerase activity in human tissues might mitigate aging processes and support regenerative therapies, although this remains a cautious and complex challenge to balance against cancer risk.

Beyond cancer resistance, the intricate bat biological system underscores a masterful orchestration between genome maintenance, immune regulation, and apoptosis. Bats’ ability to control low-level inflammation is also critical, preventing the tissue damage and systemic dysfunction associated with age-related diseases in humans. Such findings invite further exploration into inflammatory pathways, epigenetic regulation, and longevity genes that bats may uniquely employ.

Drs. Gorbunova and Seluanov, who have extensive research backgrounds studying other exceptionally long-lived mammals like naked mole rats and bowhead whales, underscore that bats represent an additional frontier in understanding mammalian longevity and disease resistance. Their ongoing studies also incorporate cohorts of long-lived humans to uncover conserved genetic and epigenetic factors that promote healthy aging across species.

The National Institute on Aging’s support of this project highlights the broad interest and potential impact of these findings. By further dissecting the molecular and cellular underpinnings of bats’ resilience, scientists anticipate transformational advances in biomedical sciences that may one day extend healthy human lifespan and drastically reduce cancer incidence.

This study invites a paradigm shift, moving away from viewing cancer purely as a consequence of accumulated mutations, toward a holistic appreciation of complex, evolved defense systems. Bats’ “superpower” lies not in impermeability to mutations but in biological checks and balances that manage cellular integrity over time, a bioengineering marvel ripe for translation into human health solutions.

Altogether, these revelations underscore the promise that comparative biology holds for unraveling the mysteries of longevity and disease resistance. Through deepening our knowledge of these unique mammals, humanity gains critical insight into pathways that might be harnessed or mimicked, ultimately rejuvenating medical approaches and recasting aging as a modifiable state rather than an immutable fate.

Subject of Research: Animals
Article Title: Limited cell-autonomous anticancer mechanisms in long-lived bats
News Publication Date: 3-May-2025
Web References:

https://www.nature.com/articles/s41467-025-59403-z
http://dx.doi.org/10.1038/s41467-025-59403-z
https://pmc.ncbi.nlm.nih.gov/articles/PMC9856662/

References: Gorbunova, V., Seluanov, A., et al. “Limited cell-autonomous anticancer mechanisms in long-lived bats.” Nature Communications, 2025. DOI: 10.1038/s41467-025-59403-z

Keywords: Bat longevity, cancer resistance, p53 tumor suppressor, telomerase activity, apoptosis, immune system, aging, regenerative biology, comparative oncology, inflammation, cellular senescence, tumor suppression

Tags: bats cancer resistance mechanismsbiology of aging in mammalscancer research breakthroughsevolutionary adaptations in batshuman oncology inspiration from batsimmune systems in batslong-lived bat species geneticslow cancer incidence in batsp53 gene duplication in batstherapeutic approaches from bat biologytumor-suppressor gene profileUniversity of Rochester bat study