Animal Study Details ⁤Fat’s⁣ Role

The study, published in‍ Nature Communications, was led by Héctor Peinado, head of the Micro-Environmental Group and ⁤CNIO Metastasis. The research utilized animal⁢ models of triple-negative breast cancer, a particularly aggressive form of the disease, that‍ develop metastasis in the lungs.

For metastasis to occur, cancer cells must ⁤detach from the primary tumor,⁢ travel through the bloodstream, ⁢and successfully colonize a new organ. In some⁤ instances, the primary tumor sends signals that modify the target organ, creating ⁤a “pre-metastatic niche” conducive to tumor cell growth.

Fatty Diet ⁣Facilitates Niche Creation

The⁤ CNIO group’s research indicates that mice with diet-induced obesity exhibit changes that facilitate the formation of this pre-metastatic niche in the lungs. Specifically, the study found increased platelet activation⁣ and blood coagulation, along with the ‍activation of fibronectin, a protein that connects lung tissue cells.

Platelet Shell Hypothesis

It is well-established that obesity promotes blood coagulation, a process involving platelets. Marta Hergueta, a researcher at CNIO and the study’s first author, observed that tumor cells traveling through the bloodstream in animals fed a high-fat diet were⁤ surrounded by more platelets compared ⁣to those in mice with a⁣ normal diet. ‍One hypothesis ⁢is that platelets may shield⁣ cancer ⁢cells from⁤ the body’s immune defenses. “Platelets would form a‍ shell ⁤around tumor cells, preventing the ⁣immune system from recognizing and eliminating⁢ them,” Peinado explained.

fibronectin’s Role

Along with platelet activity, the researchers found that a high-fat diet increased the expression of fibronectin in lung tissue. Fibronectin helps construct the tissue⁣ connecting lung cells, ⁢which facilitates ⁤the creation of the pre-metastatic niche. It also enhances the interaction between tumor cells and platelets. “We⁢ have seen that the interaction of the tumor cell both with the lung endothelium and with the platelet ⁤is regulated by fibronectin,” Peinado said.

Combined Effects Increase Metastasis

The combination of increased platelet activation and elevated fibronectin expression due to a high-fat diet⁢ leads to a greater number of potential metastases and⁢ accelerates ‍their progression.

Potential Implications for Other Cancers

While the study focused on triple-negative breast ‍cancer, Peinado believes that “this mechanism could be extrapolated to other tumor types and other organs.”

Clinical ⁢Research unit Investigates human Implications

The Breast Cancer Clinical Research unit at CNIO, led ⁢by Miguel Ángel Quintela, is investigating the implications of these findings for human patients.

Initial Findings in Human Samples

An analysis of ⁣blood samples from triple-negative breast cancer patients, taken before⁣ surgery and after chemotherapy, did not confirm that obesity was an additional risk factor for⁢ metastasis. However, the study did find that patients with increased blood coagulation had a higher risk of relapse within five years.

Identifying Risk Factors

These ‍findings “could help identify additional risk factors in patients with breast ⁤cancer in treatment, ⁤contributing to a better clinical management of the disease,” Peinado ⁢said.

Dietary ⁣Intervention‍ Shows Promise in Animal Models

The research team also explored potential clinical applications by modifying the diet of animal models. When the high-fat diet‍ was ⁢removed and the mice lost weight, platelet behavior and coagulation returned to normal levels, resulting in a reduction in metastases.

Future Directions

“I believe that these results, united to clinical studies of other groups, present a future in ‍which⁢ dietary intervention or diet changes, together⁢ with ⁤the control of ⁢platelet activity, can increase the efficiency of certain antitumor treatments,” Peinado ‍said. “They will not constitute a treatment in themselves, but they can complement them.”