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While studying the effects of glutamine deprivation, Boa Kim & team noticed dramatic clustering of glutaminase throughout endothelial cells

The team now report on a mechanism underlying kidney tumor cell growth involving the cancer-driving protein HIF2α that blocks clustering/activation of glutaminase—revealing a new therapeutic target in renal clear cell carcinoma:

The figure shows glutamine deprivation induces GLS1 clustering within mitochondria in HUVEC (top) and HELA (bottom) with mitochondrial protein (green) and GLS (red).

1Department of Medicine, Cardiovascular Institute, and Institute of Diabetes Obesity and Metabolism, and.

2The Abramson Family Cancer Research Institute, Department of Cell and Developmental Biology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, USA.

3McAllister Heart Institute, School of Medicine, University of North Carolina, Chapel Hill, North Carolina, USA.

Cutaneous Melanoma: A Review

The incidence and prevalence of cutaneous melanoma in the US and worldwide have increased over the last 5 decades.

Cutaneous melanoma presents as a new, changing, or irregularly pigmented skin lesion. Risk factors for cutaneous melanoma include UV radiation exposure, skin type, presence of benign and atypical nevi, and personal or family history of melanoma.

This Review summarizes current evidence regarding the epidemiology, pathophysiology, diagnosis, and treatment of cutaneous melanoma.

Improvements in melanoma mortality over the last decade are attributed to the advent of multiple effective therapies,6 including immune checkpoint blockade with anti–cytotoxic T-lymphocyte–associated protein 4 (CTLA-4) antibodies (ipilimumab), anti–programmed cell death protein 1 (PD-1) antibodies (nivolumab, pembrolizumab), and anti–lymphocyte activation gene 3 protein (LAG-3) antibodies (relatlimab), as well as oral combination targeted therapy with B-Raf protein (BRAF) and mitogen-activated extracellular signal-regulated kinase (MEK) inhibitors (eg, encorafenib + binimetinib, vemurafenib + cobimetinib, dabrafenib + trametinib).

This review summarizes current evidence regarding epidemiology and risk factors, clinical presentation, diagnosis, and management of cutaneous melanoma (Box).

Dysfunctions of Circulating Adaptive Immune Cells in End-Stage Liver Disease

End-stage liver disease (ESLD) from acute liver failure to compensated advanced chronic liver disease and decompensated cirrhosis at different stages (chronic decompensation, acute decompensation with or without acute-on-chronic liver failure) has high disease severity and poor patient outcome. Infection is a common complication in patients with ESLD and it is associated with a high mortality rate. Multiple mechanisms are involved in this marked susceptibility to infections, noticeably the inadequate immune response known as immune paresis, as part of cirrhosis-associated immune dysfunction (CAID). Specifically in the adaptive immune arm, lymphocyte impairments—including inadequate activation, reduced ability to secrete effector molecules and enhanced immune suppressive phenotypes—result in compromised systemic immune responses and increased risk of infections.

Boosting One Mitochondrial Protein Increases Lifespan And Slows Aging in Mice

Tiny biological batteries known as mitochondria keep the body’s cells running smoothly, and their gradual decline is linked to a wide range of age-related diseases. Now scientists think they have found a way to keep mitochondria powered for longer.

A protein called COX7RP is key to this discovery from researchers at the Saitama Medical University and Chiba University in Japan. The protein is thought to help mitochondria form supercomplexes, structures that improve energy efficiency.

In the new study, male mice engineered to produce extra COX7RP showed a host of differences compared with controls, including a 6.6 percent increase in average lifespan and indicators of an extended healthspan – being able to live healthier for longer.

Molecular Switch for Repairing Central Nervous System disorders

A molecular switch has the ability to turn on a substance in animals that repairs neurological damage in disorders such as multiple sclerosis (MS), Mayo Clinic researchers discovered. The early research in animal models could advance an already approved Food and Drug Administration therapy and also could lead to new strategies for treating diseases of the central nervous system.

Research by Isobel Scarisbrick, Ph.D., published in the Journal of Neuroscience finds that by genetically switching off a receptor activated by blood proteins, named Protease Activated Receptor 1 (PAR1), the body switches on regeneration of myelin, a fatty substance that coats and protects nerves.

“Myelin regeneration holds tremendous potential to improve function. We showed when we block the PAR1 receptor, neurological healing is much better and happens more quickly. In many cases, the nervous system does have a good capacity for innate repair,” says Dr. Scarisbrick, principal investigator and senior author. “This sets the stage for development of new clinically relevant myelin regeneration strategies.”

Consciousness May Be a Fundamental Force of the Universe, Not a Byproduct

You’ve probably grown up accepting that your thoughts, feelings, and inner awareness all emerge from the firing of neurons in your brain. It’s what science has taught us for decades. Your consciousness is simply what happens when billions of brain cells communicate. Simple enough, right?

What if you’ve been looking at this backwards the whole time? What if the entire universe has been trying to tell you something fundamentally different about the nature of reality itself?

A materials science professor from Uppsala University recently published a framework that proposes an entirely new theory of the origin of the universe. Here’s where things get interesting. This framework presents consciousness not as a byproduct of brain activity, but as a fundamental field underlying everything we experience, including matter, space, time, and life itself.

The mind-bending reality of quantum mechanics — with Jim Al Khalili

Jim Al-Khalili explores emerging technologies powering the future of quantum, and looks at how we got here.

This Discourse was recorded at the Ri on 7 November 2025, in partnership with the Institute of Physics.

Watch the Q&A session for this talk here (exclusively for our Science Supporter members):
Join this channel as a member to get access to perks:
/ @theroyalinstitution.

Physicist and renowned broadcaster Jim Al-Khalili takes a look back at a century of quantum mechanics, the strangest yet most successful theory in all of science, and how it has shaped our world. He also looks forward to the exciting new world of Quantum 2.0 and how a deeper understanding of such counterintuitive concepts as quantum superposition and quantum entanglement is leading to the development of entirely new technologies, from quantum computers and quantum sensors to quantum cryptography and the quantum internet.

The United Nations has proclaimed 2025 as the International Year of Quantum Science and Technology, to celebrate the centenary of quantum mechanics and the revolutionary work of the likes of Werner Heisenberg and Erwin Schrödinger. Together with the Institute of Physics, join us to celebrate the culmination of the International Year of Quantum at the penultimate Discourse of our Discover200 year.

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