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Key driver of pancreatic cancer spread identified

A Cornell-led study has revealed how a deadly form of pancreatic cancer enters the bloodstream, solving a long-standing mystery of how the disease spreads and identifying a promising target for therapy.

Pancreatic ductal adenocarcinoma is among the most lethal cancers, with fewer than 10% of patients surviving five years after diagnosis. Its microenvironment is a dense, fibrotic tissue that acts like armor around the tumor. This barrier makes difficult and should, in theory, prevent the tumor from spreading. Yet the cancer metastasizes with striking efficiency—a paradox that has puzzled scientists.

New research published in the journal Molecular Cancer reveals that a biological receptor called ALK7 is responsible, by activating two interconnected pathways that work in tandem. One makes cancer cells more mobile through a process called , and the other produces enzymes that physically break down the .

Enhanced CAR T cells emerge from genetic screening

CAR T cells are patient-derived, genetically engineered immune cells. They are “living drugs” and constitute a milestone in modern medicine. Equipping T cells, a key cell type of the immune system, with a “chimeric antigen receptor” (CAR) enables them to specifically recognize and attack cancer cells.

CAR T cell therapy has demonstrated its potential by curing patients with otherwise untreatable blood cancers. But it still fails for most patients, often due to T cell intrinsic dysfunction. To address their current limitations and to make CAR T cells intrinsically stronger, scientists at the CeMM Research Center for Molecular Medicine of the Austrian Academy of Sciences and the Medical University of Vienna have developed a new method for systematic discovery of genetic boosters of CAR T cell function.

The new study, published in Nature, introduces CELLFIE, a CAR T cell engineering and high-content CRISPR screening platform, enabling researchers to systematically modify CAR T cells and evaluate their therapeutic potential.

Oral bacteria linked to Parkinson’s via the gut-brain axis

Korean researchers have uncovered compelling evidence that oral bacteria, once colonized in the gut, can affect neurons in the brain and potentially trigger Parkinson’s disease.

The joint research team, led by Professor Ara Koh and doctoral candidate Hyunji Park of POSTECH’s Department of Life Sciences, together with Professor Yunjong Lee and doctoral candidate Jiwon Cheon of Sungkyunkwan University School of Medicine, collaborated with Professor Han-Joon Kim of Seoul National University College of Medicine.

They have identified the mechanism by which metabolites produced by in the gut may trigger the development of Parkinson’s disease. The findings were published online in Nature Communications.

Nectandrin B (Found In Nutmeg) Extends Lifespan As Much As Rapamycin

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Some patients could use special eyedrops instead of reading glasses as they age, researcher says

Everybody develops presbyopia as they age—a difficulty in focusing on near objects and text—and often must resort to reading glasses. However, the solution might be as simple as using special eye drops two or three times a day.

A retrospective study of 766 patients presented at the 43rd Congress of the European Society of Cataract and Refractive Surgeons (ESCRS) has found that the majority could read an extra two, three or more lines on the eye chart used for testing near visual acuity (the Jaeger chart) after using specially formulated eye drops. This improvement was sustained for up to two years.

Dr. Giovanna Benozzi, director of the Center for Advanced Research for Presbyopia, in Buenos Aires, Argentina, said, We conducted this research due to the significant unmet medical need in presbyopia management. Current solutions such as reading glasses or surgical interventions have limitations, including inconvenience, social discomfort, and potential risks or complications.

Google’s top AI scientist says ‘learning how to learn’ will be next generation’s most needed skill

Speaking at an ancient Roman theater at the foot of the Acropolis in Athens, Demis Hassabis, CEO of Google’s DeepMind, said rapid technological change demands a new approach to learning and skill development.

“It’s very hard to predict the future, like 10 years from now, in normal cases. It’s even harder today, given how fast AI is changing, even week by week,” Hassabis told the audience. “The only thing you can say for certain is that huge change is coming.”

The neuroscientist and former chess prodigy said artificial general intelligence—a futuristic vision of machines that are as broadly smart as humans or at least can do many things as well as people can—could arrive within a decade. This, he said, will bring dramatic advances and a possible future of “radical abundance” despite acknowledged risks.

AI chips are getting hotter. A microfluidics breakthrough goes straight to the silicon to cool up to three times better

AI is hot – literally.

The chips that datacenters use to run the latest AI breakthroughs generate much more heat than previous generations of silicon. Anybody whose phone or laptop has overheated knows that electronics don’t like to get hot. In the face of rising demand for AI and newer chip designs, the current cooling technology will put a ceiling on progress in just a few years.

To help address this problem, Microsoft has successfully tested a new cooling system that removed heat up to three times better than cold plates, an advanced cooling technology commonly used today. It uses microfluidics, an approach that brings liquid coolant directly inside the silicon – where the heat is. Tiny channels are etched directly on the back of the silicon chip, creating grooves that allow cooling liquid to flow directly onto the chip and more efficiently remove heat. The team also used AI to identify the unique heat signatures on a chip and direct the coolant with more precision.

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