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A new study published today in Science shows that the mechanical beating of the heart prevents cancer cells from proliferating in mouse hearts. Researchers transplanted non-beating hearts and observed rapid cancer growth compared to native beating hearts. This finding may explain the rarity of cardiac tumors in mammals, including humans.
Substrate placeholder — needs reviewA study published today in Science reports that the beating of the heart stops cancers from growing in this organ in mice, according to @Nature. The research, led by clinician-scientist Serena Zacchigna at the University of Trieste, Italy, demonstrates how mechanical strain from heartbeats inhibits tumor formation.
Zacchigna and her team transplanted hearts onto the necks of genetically modified mice, where these external hearts did not beat but still received a blood supply and remained functional.
The team injected cancer cells into both the transplanted hearts on the necks 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. In contrast, about 20% of tissue in the native hearts was cancerous.
To further explore this, the researchers grew engineered heart tissue from rat cells in a dish. The cells in this engineered tissue beat only if exposed to calcium, which helps drive heartbeats in the body. The team then injected the heart tissue with lung cancer cells.
Cancer cells grew in number and took up more space in the static tissue than in the beating tissue. Additionally, cancer cells were distributed throughout the static tissue but clustered only in the outer layers of the beating tissue. This could explain the rarity of heart tumors in mammals, including people, @Nature reported.
Primary cardiac tumours have been identified in fewer than 1% of autopsies in people, while secondary cancers in the heart, where the primary tumour occurs in a different part of the body, have been found in up to 18% of autopsies. James Chong, a cardiologist and researcher at the University of Sydney, Australia, stated that until now there has not been a satisfactory explanation for why cardiac tumours are so uncommon.
Chong added that this latest study puts forward a compelling case that mechanical strain on the heart could be an explanation.
The findings build on observations that almost all organs and tissues in the body can develop tumours, but those affecting the heart are seldom observed. The study provides experimental evidence linking the heart's constant motion to cancer resistance. Zacchigna's team used genetically modified mice for the transplants, ensuring the external hearts maintained blood supply without beating.
This setup allowed direct comparison of cancer progression in beating versus non-beating cardiac environments. In the dish-based experiments, the reliance on calcium exposure to induce beating mimicked natural heart function, revealing how mechanical activity limits cancer cell invasion. Cancer cells in beating tissue remained confined, unlike in static conditions where they spread extensively.
Chong emphasized the study's implications for understanding cardiac oncology. He noted the long-standing puzzle of low tumor incidence in the heart despite its exposure to circulating cancer cells. The research highlights differences between primary and secondary cardiac cancers, with the latter being more common but still relatively rare compared to other organs.
Autopsy data underscores this disparity, with primary tumors under 1% and secondary up to 18%. By transplanting hearts to the neck, the team created a controlled model to isolate the beating mechanism's role. The rapid replacement of healthy cells in non-beating transplants contrasted sharply with the limited 20% cancerous tissue in native hearts.
Engineered tissues further confirmed that beating restricts cancer to outer layers, preventing deeper infiltration. This spatial distribution suggests mechanical forces create an inhospitable environment for tumor growth inside the heart muscle. The study, appearing in today's issue of Science, offers a mechanical explanation for a phenomenon observed across species.
Researchers injected lung cancer cells into the engineered tissues, observing greater proliferation in static conditions. Chong's comments provide expert context, affirming the study's contribution to resolving a key question in cardiology and oncology. The work involved interdisciplinary approaches, combining transplantation, tissue engineering, and cancer cell injection to yield these insights.
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