7 de Julho de 2025

 
 

EARA News Digest 2025 - Week 28


Welcome to your Monday morning update, from EARA, on the latest news in biomedical science, policy and openness on animal research. 

This week: EARA responds to Amazon Prime movieFruit flies reveal how immune cells may fuel cancer growthStudy in mice sheds light on prostate cancer development.

EARA responds to Amazon Prime movie 

EARA responded to the Spanish movie “Infiltrada en el Búnker” with a statement released both in English and Spanish.  

The movie, released last week on Amazon Prime, uses documentary footage, fictional scenes and undercover film to condemn animal use in scientific research. Re-enacted by actors, it is centred around the secret filming by a whistleblower named ‘Carlota’ and blurs the line between real and dramatic footage.  

“Infiltrada en el Búnker” features convicted felons portrayed only as brave activists, highlighting its dishonest narrative, and concludes with a criminally minded campaign targeting MBR Acres which has done a lot of work in openness and transparency in dogs used in research

Vivotecnia’s story is well-known, and the movie adds nothing new except for a conspiracy theory. EARA issued an immediate statement  condemning Vivotecnia’s animal welfare failures in April 2021 after undercover footage was released. Abuses were further met with a swift response from Spanish authorities and the Spanish scientific community, resulting in fines, structural changes and increased surveillance. 

Despite the film’s dramatised perspective and claims of court actions, no judicial finding of systemic malpractice beyond the documented incidents has been upheld in Spanish or European courts.  Although it also claims research facilities are inaccessible, it is widely known that 170 institutions are part of the Spanish Transparency Agreement and committed to openness, and this includes public visits to animal facilities. 

 

 

Fruit flies reveal how immune cells may fuel cancer growth  

A Japanese study conducted on fruit flies found that immune cells attacking cancer cells release signals that can actually cause tumours to grow more aggressively. 

Researchers at Nagoya University found that immune cells, when absorbing dying cancer cells, release signals that make the remaining cancer cells grow faster. This process, known as phagocytosis, normally helps the body clear damaged or infected cells. But in this case, it also triggered the release of inflammatory proteins, which then activated growth signals in the surviving cancer cells.  

"We used genetically modified fruit flies to study cancer because their immune system is similar to ours, and they offer a powerful model system for research in the laboratory," said Eri Hirooka, a Ph.D. student at Nagoya University and lead author. 

To better understand this process, the team used genetic tools to switch specific genes on and off and change the levels of certain proteins in the fruit flies. By turning off genes needed for phagocytosis, the researchers reduced the ability of macrophages to absorb dying cancer cells. As a result, tumour growth was reduced. The researchers linked this effect to a protein called Upd3, which is similar to IL-6, a protein found in human cancer.  

Shizue Ohsawa, senior author of the study, said: "Because the molecular pathways between fruit flies and humans are evolutionarily preserved, understanding these mechanisms could explain why some cancers with high cell death rates can still grow aggressively and lead to improved treatments."  

The study, published in the journal Current Biology, suggests that boosting the immune system’s ability to clear cancer cells may not always have the expected benefit, providing new insights on future therapies. 

 

 

Study in mice sheds light on prostate cancer development  

Researchers in Belgium have shown that inflammation plays a central role in the early development of prostate cancer. 

In this study from the Université Libre de Bruxelles (ULB), an EARA member, the team used genetically altered mice predisposed to develop prostate cancer to show how cell mutations can trigger a process called cell reprogramming, which leads to inflammation and tumour formation  

This inflammation was not evenly distributed throughout the prostate but affected specific regions differently, with the more inflamed areas exhibiting features similar to aggressive forms of human prostate cancer. 

Crucially, anti-inflammatory medication (rapamycin) prevented both cell reprogramming and tumour formation. This suggests that targeting inflammation at the earliest stages of tumour development could be a promising strategy for preventing prostate cancer, particularly in high-risk individuals.  

Chen Jiang, first author of the study published in Nature Cancer stated: "It is exciting to see that the cellular reprogramming identified in the mouse model correlates with more aggressive prostate cancers in men, suggesting that the reprogramming markers we identified could serve as a predictive biomarker for aggressive prostate cancer." 

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