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The beating of the heart stops cancers from growing in this organ in mice, reports a study published today in Science1. This could explain why tumours affecting the heart are so rare in all mammals, including in people.

Almost all organs and tissues in the body can develop tumours, but those that affect the heart are seldom observed. In people, primary tumours have been identified in fewer than 1% of autopsies, while secondary cancers, in which the primary tumour occurs in a different part of the body, have been found in up to 18% of autopsies.

Until now, there has not been a satisfactory explanation for why cardiac tumours are so uncommon, says James Chong, a cardiologist and researcher at the University of Sydney, Australia. This latest study puts forward a compelling case that mechanical strain on the heart could be an explanation, he says.

Serena Zacchigna, a clinician scientist at the University of Trieste, Italy, and her team transplanted hearts onto the necks of genetically modified mice. These external hearts did not beat but did still receive a blood supply and were functional.

The team then injected cancer cells into the transplanted hearts on the necks of mice and the ‘native’ hearts in the animals. Within two weeks, the cancer cells multiplied and replaced most of the healthy cells in the transplanted hearts. By contrast, about 20% of tissue in the native hearts was cancerous.

Engineered hearts

The team also grew engineered heart tissue from rat cells in a dish. The cells only beat if the researchers exposed the tissue to calcium — ions of which help to drive the beating of the heart inside the body.

The team then injected the heart tissue with lung cancer cells. It found that the number of cancer cells grew more and took up more space in the static tissue than they did in the beating tissue. Furthermore, the team found that cancer cells were distributed throughout the static tissue, but that they only clustered in the outer layers of the beating tissue.

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doi: https://doi.org/10.1038/d41586-026-01296-z

References

- Ciucci, G. et al. Science 392, eads9412 (2026).

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- Suzuki, R. et al. J. Thorac. Cardiovasc. Surg. 133, 1051–1058 (2007).

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