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Experimental Therapy Targets Cancer’s Bodyguards, Turning Foe to Friend to Eliminate Tumors

Researchers at Mount Sinai have developed a novel immunotherapy strategy that targets the tumor microenvironment (TME) to overcome immune suppression in metastatic cancers. Addressing the protective role of tumor-associated macrophages (TAMs), which often shield malignancies and facilitate growth, the team engineered chimeric antigen receptor (CAR) T-cells to specifically recognize and target these stromal cells. Functioning as a “Trojan horse,” these modified T-cells not only engage macrophages but also release immune-activating molecules that reprogram the TME, converting immunosuppressive macrophages into anti-tumor effectors. In preclinical models of metastatic lung and ovarian cancer, this approach yielded significant therapeutic efficacy, resulting in extended survival and the complete eradication of tumors in some subjects. By transforming the tumor’s protective infrastructure into a mechanism of its destruction, this strategy offers a promising, potentially pan-cancer modality for treating solid tumors resistant to conventional immunotherapies.


Scientists at the Icahn School of Medicine at Mount Sinai have developed an experimental immunotherapy that takes an unconventional approach to metastatic cancer: instead of going after cancer cells directly, it targets the cells that protect them.

T he study, published in the January 22 online issue of Cancer Cell, a Cell Press Journal [DOI 10.1016/j.ccell.2025.12.021], was conducted in aggressive preclinical models of metastatic ovarian and lung cancer. It points to a new strategy for treating advanced-stage solid tumors.

In a strategy modeled after the famed Trojan horse, the treatment enters the tumors by targeting cells called macrophages that guard the cancer cells, disarms these protectors, and opens up the tumor’s gates for the immune system to enter and wipe out the cancer cells.

Shapeshifting materials could power next generation of soft robots

McGill University engineers have developed new ultra-thin materials that can be programmed to move, fold and reshape themselves, much like animated origami. They open the door to softer, safer and more adaptable robots that could be used in medical tools that gently move inside the body, wearable devices that change shape on the skin or smart packaging that reacts to its environment.

The research, jointly led by the laboratories of Hamid Akbarzadeh in the Department of Bioresource Engineering and Marta Cerruti in the Department of Mining and Material Engineering, shows how simple, paper-like sheets made from folded graphene oxide (GO) can be turned into tiny devices that walk, twist, flip and sense their own motion. Two related studies demonstrate how these materials can be made at scale, programmed to change shape and controlled either by humidity or magnetic fields.

The studies are published in Materials Horizons and Advanced Science.

Abstract: Caught in the crossfire: cardiac complications of cancer therapy

In this Review, Emilio Hirsch discuss the mechanisms and therapeutic strategies for cardiotoxicity caused by chemotherapy, targeted agents, and immune modulators.


1Department of Molecular Biotechnology and Health Sciences, Molecular Biotechnology Center “Guido Tarone”, University of Torino, Torino, Italy.

2University of Arizona College of Medicine, Tucson, Arizona, USA.

Address correspondence to: Emilio Hirsch or Alessandra Ghigo, Via Nizza 52, 10126, Turin, Italy. Phone: 39.011.670.6425; Email: [email protected] (EH). Phone: 39.011.670.6335; Email: [email protected] (AG). Or to: Hossein Ardehali, 3,838 North Campbell Avenue, Building 2, Tucson, Arizona 85,719, USA. Phone: 520.626.6453; Email: [email protected].

Computational model discovers new types of neurons hidden in decade-old dataset

“We saw some peculiar brain activity in the model,” Miller says. “There was a group of neurons that predicted the wrong answer, yet they kept getting stronger as the model learned. So we went back to the original macaque data, and the same signal was there, hiding in plain sight. It wasn’t a quirk of the model — the monkeys’ brains were doing it too. Even as their performance improved, both the real and simulated brains maintained a reserve of neurons that continued to predict the incorrect answer.”

The new work, published in Nature Communications, puts a name to these overlooked signals: incongruent neurons, or ICNs, and explores theories as to why a primate brain might want to keep alternate options in mind, even if they’re not the right ones at the moment.

Beyond identifying a previously unrecognized class of neurons involved in learning, the study shows that the model behaves like a brain and generates realistic brain activity, even without being trained on neural data. The findings could have major implications for testing potential neurological drugs and for using computational models to investigate how cognition emerges and functions.

Different gametogenesis states uniquely impact longevity in Caenorhabditis elegans

In Caenorhabditis elegans, ablation of germline stem cells leads to extended lifespan and increased fat storage. Here the authors show that disrupting distinct gametogenesis programs and germline progression in C. elegans triggers molecular responses that affect fat metabolism, stress resilience, and lifespan.

A viable therapeutic target pancreatic ductal adenocarcinoma

This issue’s cover features work by Adrian M. Seifert & team on Nectin-4’s connection to poor outcome and immune suppression in patients with PDAC, and targeting Nectin-4 with the antibody-drug conjugate enfortumab vedotin inhibited tumor growth in PDAC organoids:

The cover image shows high Nectin-4 immunohistochemistry staining (brown) in human PDAC.


1Department of Visceral, Thoracic and Vascular Surgery, University Hospital Carl Gustav Carus, Technische Universität Dresden, Dresden, Germany.

2National Center for Tumor Diseases (NCT), Dresden, Germany.

3German Cancer Research Center (DKFZ), Heidelberg, Germany.

Stress-testing AI vision systems: Rethinking how adversarial images are generated

Deep neural networks (DNNs) have become a cornerstone of modern AI technology, driving a thriving field of research in image-related tasks. These systems have found applications in medical diagnosis, automated data processing, computer vision, and various forms of industrial automation, to name a few.

As reliance on AI models grows, so does the need to test them thoroughly using adversarial examples. Simply put, adversarial examples are images that have been strategically modified with noise to trick an AI into making a mistake. Understanding adversarial image generation techniques is essential for identifying vulnerabilities in DNNs and for developing more secure, reliable systems.

Scientists Say They’ve Made a Pill That Could Let You Live to 150

They’ve been promising eternal youth since the first snake-oil salesman bottled spring water. Now a Chinese biotech startup says it might actually have the chemistry right. Lonvi Biosciences claims its new pill could stretch human life to 150 years.

The Shenzhen-based company, backed by China’s booming longevity sector, says it has developed a pill that could theoretically extend human life to 150 years. The company’s formula targets so-called “zombie cells”—aging cells that refuse to die, triggering inflammation and age-related disease. “This is not just another pill. This is the Holy Grail,” said CEO Ip Zhu, describing the capsule as a breakthrough that could make extreme longevity a reality.

The drug’s key ingredient, procyanidin C1 (PCC1), is derived from grape seeds and has shown lifespan extension in lab animals. In Lonvi’s own mouse trials, the treatment reportedly increased overall lifespan by 9.4 percent and extended life by 64 percent from the first day of treatment. “Living to 150 is definitely realistic,” said Chief Technology Officer Lyu Qinghua in an interview with The New York Times. “In a few years, this will be the reality.”

Overlooked molecule points to new treatments for drug resistant fungal infections

Fungal infections kill millions of people each year, and modern medicine is struggling to keep up. But researchers at McMaster University have identified a molecule that may help turn the tide—butyrolactolA, a chemical compound that targets a deadly, disease-causing fungi called Cryptococcus neoformans.

Infections caused by Cryptococcus are extremely dangerous. The pathogen, which can cause pneumonia-like symptoms, is notoriously drug-resistant, and it often preys on people with weakened immune systems, like cancer patients or those living with HIV. And the same can be said about other fungal pathogens, like Candida auris or Aspergillus fumigatus—both of which, like Cryptococcus, have been declared priority pathogens by the World Health Organization.

Despite the threat, though, doctors have only three treatment options for fungal infections.

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